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RJR: Recommended Bibliography 24 Apr 2025 at 01:52 Created:
Human Microbiome
The human microbiome is the set of all microbes that live on or in humans. Together, a human body and its associated microbiomes constitute a human holobiont. Although a human holobiont is mostly mammal by weight, by cell count it is mostly microbial. The number of microbial genes in the associated microbiomes far outnumber the number of human genes in the human genome. Just as humans (and other multicellular eukaryotes) evolved in the constant presence of gravity, so they also evolved in the constant presence of microbes. Consequently, nearly every aspect of human biology has evolved to deal with, and to take advantage of, the existence of associated microbiota. In some cases, the absence of a "normal microbiome" can cause disease, which can be treated by the transplant of a correct microbiome from a healthy donor. For example, fecal transplants are an effective treatment for chronic diarrhea from over abundant Clostridium difficile bacteria in the gut.
Created with PubMed® Query: "human microbiome" NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2025-04-23
Harnessing the Human Microbiome for Innovative Drug Delivery Systems: Exploring Pharmacomicrobiomics and Targeted Therapies.
Current pharmaceutical design pii:CPD-EPUB-147821 [Epub ahead of print].
The human gut microbiome has emerged as a crucial component of health and disease, presenting novel opportunities for the development of drug delivery systems based on microbiome interactions. This paper explores advanced strategies utilizing microorganisms, engineered bacteria, viruses, and bacteria-encapsulated nanoparticles as next-generation therapeutic vehicles. Focusing on analytical approaches to phage therapy and bio-hybrid bacteria for targeted drug delivery, the article highlights recent breakthroughs in colon-specific targeting for gastrointestinal disorders. The study also delves into the emerging field of pharmacomicrobiomics, with an emphasis on applications in cancer, cardiovascular, digestive, and nervous system treatments, specifically targeting key drug classes such as ACE inhibitors, proton-pump inhibitors, and NSAIDs. Challenges related to cytotoxicity and toxicity are addressed, offering proposals for safer therapeutic applications. This review underscores the transformative potential of the microbiome in personalized medicine and targeted drug delivery, with a focus on its integration with advanced technologies to optimize therapeutic outcomes.
Additional Links: PMID-40264322
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PubMed:
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@article {pmid40264322,
year = {2025},
author = {Jain, MS and Prasanthi, S and Bommala, ND and Goudanavar, P and Naveen, NR},
title = {Harnessing the Human Microbiome for Innovative Drug Delivery Systems: Exploring Pharmacomicrobiomics and Targeted Therapies.},
journal = {Current pharmaceutical design},
volume = {},
number = {},
pages = {},
doi = {10.2174/0113816128354250250326045943},
pmid = {40264322},
issn = {1873-4286},
abstract = {The human gut microbiome has emerged as a crucial component of health and disease, presenting novel opportunities for the development of drug delivery systems based on microbiome interactions. This paper explores advanced strategies utilizing microorganisms, engineered bacteria, viruses, and bacteria-encapsulated nanoparticles as next-generation therapeutic vehicles. Focusing on analytical approaches to phage therapy and bio-hybrid bacteria for targeted drug delivery, the article highlights recent breakthroughs in colon-specific targeting for gastrointestinal disorders. The study also delves into the emerging field of pharmacomicrobiomics, with an emphasis on applications in cancer, cardiovascular, digestive, and nervous system treatments, specifically targeting key drug classes such as ACE inhibitors, proton-pump inhibitors, and NSAIDs. Challenges related to cytotoxicity and toxicity are addressed, offering proposals for safer therapeutic applications. This review underscores the transformative potential of the microbiome in personalized medicine and targeted drug delivery, with a focus on its integration with advanced technologies to optimize therapeutic outcomes.},
}
RevDate: 2025-04-22
Recent advances in therapeutic probiotics: insights from human trials.
Clinical microbiology reviews [Epub ahead of print].
SUMMARYRecent advances in therapeutic probiotics have shown promising results across various health conditions, reflecting a growing understanding of the human microbiome's role in health and disease. However, comprehensive reviews integrating the diverse therapeutic effects of probiotics in human subjects have been limited. By analyzing randomized controlled trials (RCTs) and meta-analyses, this review provides a comprehensive overview of key developments in probiotic interventions targeting gut, liver, skin, vaginal, mental, and oral health. Emerging evidence supports the efficacy of specific probiotic strains and combinations in treating a wide range of disorders, from gastrointestinal (GI) and liver diseases to dermatological conditions, bacterial vaginosis, mental disorders, and oral diseases. We discuss the expanding understanding of microbiome-organ connections underlying probiotic mechanisms of action. While many clinical trials demonstrate significant benefits, we acknowledge areas requiring further large-scale studies to establish definitive efficacy and optimal treatment protocols. The review addresses challenges in standardizing probiotic research methodologies and emphasizes the importance of considering individual variations in microbiome composition and host genetics. Additionally, we explore emerging concepts such as the oral-gut-brain axis and future directions, including high-resolution microbiome profiling, host-microbe interaction studies, organoid models, and artificial intelligence applications in probiotic research. Overall, this review offers a comprehensive update on the current state of therapeutic probiotics across multiple domains of human health, providing insights into future directions and the potential for probiotics to revolutionize preventive and therapeutic medicine.
Additional Links: PMID-40261032
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PubMed:
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@article {pmid40261032,
year = {2025},
author = {Cho, M-Y and Eom, J-H and Choi, E-M and Yang, S-J and Lee, D and Kim, YY and Kim, H-S and Hwang, I},
title = {Recent advances in therapeutic probiotics: insights from human trials.},
journal = {Clinical microbiology reviews},
volume = {},
number = {},
pages = {e0024024},
doi = {10.1128/cmr.00240-24},
pmid = {40261032},
issn = {1098-6618},
abstract = {SUMMARYRecent advances in therapeutic probiotics have shown promising results across various health conditions, reflecting a growing understanding of the human microbiome's role in health and disease. However, comprehensive reviews integrating the diverse therapeutic effects of probiotics in human subjects have been limited. By analyzing randomized controlled trials (RCTs) and meta-analyses, this review provides a comprehensive overview of key developments in probiotic interventions targeting gut, liver, skin, vaginal, mental, and oral health. Emerging evidence supports the efficacy of specific probiotic strains and combinations in treating a wide range of disorders, from gastrointestinal (GI) and liver diseases to dermatological conditions, bacterial vaginosis, mental disorders, and oral diseases. We discuss the expanding understanding of microbiome-organ connections underlying probiotic mechanisms of action. While many clinical trials demonstrate significant benefits, we acknowledge areas requiring further large-scale studies to establish definitive efficacy and optimal treatment protocols. The review addresses challenges in standardizing probiotic research methodologies and emphasizes the importance of considering individual variations in microbiome composition and host genetics. Additionally, we explore emerging concepts such as the oral-gut-brain axis and future directions, including high-resolution microbiome profiling, host-microbe interaction studies, organoid models, and artificial intelligence applications in probiotic research. Overall, this review offers a comprehensive update on the current state of therapeutic probiotics across multiple domains of human health, providing insights into future directions and the potential for probiotics to revolutionize preventive and therapeutic medicine.},
}
RevDate: 2025-04-21
Correction: Dietary risk factors in Crohn's disease and ulcerative colitis: a cohort study with paired healthy relatives as controls.
European journal of nutrition, 64(4):161 pii:10.1007/s00394-025-03669-y.
Additional Links: PMID-40257583
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PubMed:
Citation:
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@article {pmid40257583,
year = {2025},
author = {Hu, J and Chen, W and Zhu, R and Yang, F and Xu, J and Xiang, B and Li, Y and Wang, W and Zhu, L and Chen, G and Zhi, M},
title = {Correction: Dietary risk factors in Crohn's disease and ulcerative colitis: a cohort study with paired healthy relatives as controls.},
journal = {European journal of nutrition},
volume = {64},
number = {4},
pages = {161},
doi = {10.1007/s00394-025-03669-y},
pmid = {40257583},
issn = {1436-6215},
}
RevDate: 2025-04-19
Microbiome data management in action workshop: Atlanta, GA, USA, June 12-13, 2024.
Environmental microbiome, 20(1):40.
Microbiome research is revolutionizing human and environmental health, but the value and reuse of microbiome data are significantly hampered by the limited development and adoption of data standards. While several ongoing efforts are aimed at improving microbiome data management, significant gaps still remain in terms of defining and promoting adoption of consensus standards for these datasets. The Strengthening the Organization and Reporting of Microbiome Studies (STORMS) guidelines for human microbiome research have been endorsed and successfully utilized by many research organizations, publishers, and funding agencies, and have been recognized as a consensus community standard. No equivalent effort has occurred for environmental, synthetic, and non-human host-associated microbiomes. To address this growing need within the microbiome research community, we convened the Microbiome Data Management in Action Workshop (June 12-13, 2024, in Atlanta, GA, USA), to bring together key decision makers in microbiome science including researchers, publishers, funders, and data repositories. The 50 attendees, representing the diverse and interdisciplinary nature of microbiome research, discussed recent progress and challenges, and brainstormed actionable recommendations and paths forward for coordinated environmental microbiome data management and the modifications necessary for the STORMS guidelines to be applied to environmental, non-human host, and synthetic microbiomes. The outcomes of this workshop will form the basis of a formalized data management roadmap to be implemented across the field. These best practices will drive scientific innovation now and in years to come as these data continue to be used not only in targeted reanalyses but in large-scale models and machine learning efforts.
Additional Links: PMID-40253432
PubMed:
Citation:
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@article {pmid40253432,
year = {2025},
author = {Kelliher, JM and Aljumaah, M and Bordenstein, SR and Brister, JR and Chain, PSG and Dundore-Arias, JP and Emerson, JB and Fernandes, VMC and Flores, R and Gonzalez, A and Hansen, ZA and Hatcher, EL and Jackson, SA and Kellogg, CA and Madupu, R and Miller, CML and Mirzayi, C and Moustafa, AM and Mungall, C and Oliver, A and Pariente, N and Pett-Ridge, J and Record, S and Reji, L and Reysenbach, AL and Rich, VI and Richardson, L and Schriml, LM and Shabman, RS and Sierra, MA and Sullivan, MB and Sundaramurthy, P and Thibault, KM and Thompson, LR and Tighe, S and Vereen, E and Eloe-Fadrosh, EA},
title = {Microbiome data management in action workshop: Atlanta, GA, USA, June 12-13, 2024.},
journal = {Environmental microbiome},
volume = {20},
number = {1},
pages = {40},
pmid = {40253432},
issn = {2524-6372},
support = {2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; 2422717//Directorate for Biological Sciences/ ; },
abstract = {Microbiome research is revolutionizing human and environmental health, but the value and reuse of microbiome data are significantly hampered by the limited development and adoption of data standards. While several ongoing efforts are aimed at improving microbiome data management, significant gaps still remain in terms of defining and promoting adoption of consensus standards for these datasets. The Strengthening the Organization and Reporting of Microbiome Studies (STORMS) guidelines for human microbiome research have been endorsed and successfully utilized by many research organizations, publishers, and funding agencies, and have been recognized as a consensus community standard. No equivalent effort has occurred for environmental, synthetic, and non-human host-associated microbiomes. To address this growing need within the microbiome research community, we convened the Microbiome Data Management in Action Workshop (June 12-13, 2024, in Atlanta, GA, USA), to bring together key decision makers in microbiome science including researchers, publishers, funders, and data repositories. The 50 attendees, representing the diverse and interdisciplinary nature of microbiome research, discussed recent progress and challenges, and brainstormed actionable recommendations and paths forward for coordinated environmental microbiome data management and the modifications necessary for the STORMS guidelines to be applied to environmental, non-human host, and synthetic microbiomes. The outcomes of this workshop will form the basis of a formalized data management roadmap to be implemented across the field. These best practices will drive scientific innovation now and in years to come as these data continue to be used not only in targeted reanalyses but in large-scale models and machine learning efforts.},
}
RevDate: 2025-04-19
CmpDate: 2025-04-19
Updating the Discontinuity Theory to the Extended Immunity: The Symmunobiome Concept.
European journal of immunology, 55(4):e202451528.
The immune system (IS) is commonly understood as a system composed of specific cells and tissues that have evolved to contrast pathogens and defend the host. By virtue of this capacity, it has come to be considered capable of making an essential distinction, that between self versus non-self, which would contribute to a clear identity of the organism. However, in the wake of evolution and ecology, growing evidence suggests that the so-called immune system, which also evolved from symbiotic interactions with external agents, is not just a defensive system that merely protects the organism but, on the contrary, is involved in many global regulatory and homeostatic functions. Moreover, in performing these many functions, IS is not only an ensemble of host cells and tissues but functionally is constitutively determined by the interaction with a set of associated microorganisms, that is, the human microbiome. In this scenario, it is open-and-shut that the microbiome itself is a functional part of this extended immune system. Organisms and microbiomes together, therefore, form a functional whole, which constitutes a privileged form of biological organization. In light of this evidence showing the inadequacy of traditional accounts, we propose to extend and supplement the current IS conceptualization by introducing the notion of the symmunobiome. With this term, we intend to characterize the microbiome's own and unavoidable component to overall immune functionality. Therefore, we suggest a new immune system determination, articulated in three linked pillars-adaptive immunity, innate immunity, and symmunobiome-to better grasp the diverse functionality of extended immunity.
Additional Links: PMID-40251928
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PubMed:
Citation:
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@article {pmid40251928,
year = {2025},
author = {Boem, F and LamminpÀÀ, I and Amedei, A},
title = {Updating the Discontinuity Theory to the Extended Immunity: The Symmunobiome Concept.},
journal = {European journal of immunology},
volume = {55},
number = {4},
pages = {e202451528},
doi = {10.1002/eji.202451528},
pmid = {40251928},
issn = {1521-4141},
support = {PE0000006//Italian Ministry of University and Research MNESYS/ ; B55F2100//University of Florence-European Union-Next Generation EU-CUP/ ; B83C22003920001//The National Recovery and Resilience Plan, Investment 1.5 Ecosystems of Innovation, Project Tuscany Health Ecosystem (THE), CUP/ ; },
mesh = {Humans ; *Microbiota/immunology ; Animals ; *Immune System/immunology ; Symbiosis/immunology ; Homeostasis/immunology ; *Immunity ; Biological Evolution ; Immunity, Innate ; Adaptive Immunity ; },
abstract = {The immune system (IS) is commonly understood as a system composed of specific cells and tissues that have evolved to contrast pathogens and defend the host. By virtue of this capacity, it has come to be considered capable of making an essential distinction, that between self versus non-self, which would contribute to a clear identity of the organism. However, in the wake of evolution and ecology, growing evidence suggests that the so-called immune system, which also evolved from symbiotic interactions with external agents, is not just a defensive system that merely protects the organism but, on the contrary, is involved in many global regulatory and homeostatic functions. Moreover, in performing these many functions, IS is not only an ensemble of host cells and tissues but functionally is constitutively determined by the interaction with a set of associated microorganisms, that is, the human microbiome. In this scenario, it is open-and-shut that the microbiome itself is a functional part of this extended immune system. Organisms and microbiomes together, therefore, form a functional whole, which constitutes a privileged form of biological organization. In light of this evidence showing the inadequacy of traditional accounts, we propose to extend and supplement the current IS conceptualization by introducing the notion of the symmunobiome. With this term, we intend to characterize the microbiome's own and unavoidable component to overall immune functionality. Therefore, we suggest a new immune system determination, articulated in three linked pillars-adaptive immunity, innate immunity, and symmunobiome-to better grasp the diverse functionality of extended immunity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota/immunology
Animals
*Immune System/immunology
Symbiosis/immunology
Homeostasis/immunology
*Immunity
Biological Evolution
Immunity, Innate
Adaptive Immunity
RevDate: 2025-04-17
CmpDate: 2025-04-17
Similarity of drug targets to human microbiome metaproteome promotes pharmacological promiscuity.
The pharmacogenomics journal, 25(3):9.
Similarity between candidate drug targets and human proteins is commonly assessed to minimize the occurrence of side effects. Although numerous drugs have been found to disrupt the health of the human microbiome, no comprehensive comparison between established drug targets and the human microbiome metaproteome has yet been conducted. Therefore, herein, sequence and structure alignments between human and pathogen drug targets and representative human gut, oral, and vaginal microbiome metaproteomes were performed. Both human and pathogen drug targets were found to be similar in sequence, function, structure, and drug binding capacity to proteins in diverse pathogenic and non-pathogenic bacteria from all three microbiomes. The gut metaproteome was identified as particularly susceptible overall to off-target effects. Certain symptoms, such as infections and immune disorders, may be more common among drugs that non-selectively target host microbiota. These findings suggest that similarities between human microbiome metaproteomes and drug target candidates should be routinely checked.
Additional Links: PMID-40246834
PubMed:
Citation:
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@article {pmid40246834,
year = {2025},
author = {Beaudoin, CA and Norget, S and Omran, Z and Hala, S and Daqeeq, AH and Burnet, PWJ and Blundell, TL and van Tonder, AJ},
title = {Similarity of drug targets to human microbiome metaproteome promotes pharmacological promiscuity.},
journal = {The pharmacogenomics journal},
volume = {25},
number = {3},
pages = {9},
pmid = {40246834},
issn = {1473-1150},
support = {ANTSRG 01/2019//Antibiotic Research UK (ANTRUK)/ ; },
mesh = {Humans ; Female ; *Microbiota/drug effects/genetics ; *Proteome/genetics ; *Gastrointestinal Microbiome/drug effects ; Vagina/microbiology ; Proteomics/methods ; Mouth/microbiology ; Bacteria/drug effects/genetics/metabolism ; },
abstract = {Similarity between candidate drug targets and human proteins is commonly assessed to minimize the occurrence of side effects. Although numerous drugs have been found to disrupt the health of the human microbiome, no comprehensive comparison between established drug targets and the human microbiome metaproteome has yet been conducted. Therefore, herein, sequence and structure alignments between human and pathogen drug targets and representative human gut, oral, and vaginal microbiome metaproteomes were performed. Both human and pathogen drug targets were found to be similar in sequence, function, structure, and drug binding capacity to proteins in diverse pathogenic and non-pathogenic bacteria from all three microbiomes. The gut metaproteome was identified as particularly susceptible overall to off-target effects. Certain symptoms, such as infections and immune disorders, may be more common among drugs that non-selectively target host microbiota. These findings suggest that similarities between human microbiome metaproteomes and drug target candidates should be routinely checked.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Microbiota/drug effects/genetics
*Proteome/genetics
*Gastrointestinal Microbiome/drug effects
Vagina/microbiology
Proteomics/methods
Mouth/microbiology
Bacteria/drug effects/genetics/metabolism
RevDate: 2025-04-17
Fructose activates a stress response shared by methylglyoxal and hydrogen peroxide in Streptococcus mutans.
mBio [Epub ahead of print].
Fructose catabolism by Streptococcus mutans is initiated by three phosphotransferase (PTS) transporters yielding fructose-1-phosphate (F-1-P) or fructose-6-phosphate. Deletion of one such F-1-P-generating PTS, fruI, was shown to reduce the cariogenicity of S. mutans in rats fed a high-sucrose diet. Moreover, a recent study linked fructose metabolism in S. mutans to a reactive electrophile species methylglyoxal. Here, we conducted a comparative transcriptomic analysis of S. mutans treated briefly with 50 mM fructose, 50 mM glucose, 5 mM methylglyoxal, or 0.5 mM hydrogen peroxide (H2O2). The results revealed a striking overlap between the fructose and methylglyoxal transcriptomes, totaling 176 genes, 61 of which were also shared with the H2O2 transcriptome. This core of 61 genes encompassed many of the same pathways affected by exposure to low pH or zinc intoxication. Consistent with these findings, fructose negatively impacted the metal homeostasis of a mutant deficient in zinc expulsion and the growth of a mutant of the major oxidative stress regulator SpxA1. Importantly, fructose metabolism lowered culture pH at a faster pace, allowed better survival under acidic and nutrient-depleted conditions, and enhanced the competitiveness of S. mutans against Streptococcus sanguinis, although a moderated level of F-1-P might further boost some of these benefits. Conversely, several commensal streptococcal species displayed a greater sensitivity to fructose that may negatively affect their persistence and competitiveness in dental biofilm. In conclusion, fructose metabolism is integrated into the stress core of S. mutans and regulates critical functions required for survival and its ability to induce dysbiosis in the oral cavity.IMPORTANCEFructose is a common monosaccharide in the biosphere, yet its overconsumption has been linked to various health problems in humans including insulin resistance, obesity, diabetes, non-alcoholic liver diseases, and even cancer. These effects are in large part attributable to the unique biochemical characteristics and metabolic responses associated with the degradation of fructose. Yet, an understanding of the effects of fructose on the physiology of bacteria and its implications for the human microbiome is severely lacking. Here, we performed a series of analyses on the gene regulation of a dental pathogen Streptococcus mutans by exposing it to fructose and other important stress agents. Further supported by growth, persistence, and competition assays, our findings revealed the ability of fructose to activate a set of stress-related functions that may prove critical to the ability of the bacterium to persist and cause diseases both within and without the oral cavity.
Additional Links: PMID-40243330
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PubMed:
Citation:
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@article {pmid40243330,
year = {2025},
author = {Walker, AR and Pham, DN and Noeparvar, P and Peterson, AM and Lipp, MK and Lemos, JA and Zeng, L},
title = {Fructose activates a stress response shared by methylglyoxal and hydrogen peroxide in Streptococcus mutans.},
journal = {mBio},
volume = {},
number = {},
pages = {e0048525},
doi = {10.1128/mbio.00485-25},
pmid = {40243330},
issn = {2150-7511},
abstract = {Fructose catabolism by Streptococcus mutans is initiated by three phosphotransferase (PTS) transporters yielding fructose-1-phosphate (F-1-P) or fructose-6-phosphate. Deletion of one such F-1-P-generating PTS, fruI, was shown to reduce the cariogenicity of S. mutans in rats fed a high-sucrose diet. Moreover, a recent study linked fructose metabolism in S. mutans to a reactive electrophile species methylglyoxal. Here, we conducted a comparative transcriptomic analysis of S. mutans treated briefly with 50 mM fructose, 50 mM glucose, 5 mM methylglyoxal, or 0.5 mM hydrogen peroxide (H2O2). The results revealed a striking overlap between the fructose and methylglyoxal transcriptomes, totaling 176 genes, 61 of which were also shared with the H2O2 transcriptome. This core of 61 genes encompassed many of the same pathways affected by exposure to low pH or zinc intoxication. Consistent with these findings, fructose negatively impacted the metal homeostasis of a mutant deficient in zinc expulsion and the growth of a mutant of the major oxidative stress regulator SpxA1. Importantly, fructose metabolism lowered culture pH at a faster pace, allowed better survival under acidic and nutrient-depleted conditions, and enhanced the competitiveness of S. mutans against Streptococcus sanguinis, although a moderated level of F-1-P might further boost some of these benefits. Conversely, several commensal streptococcal species displayed a greater sensitivity to fructose that may negatively affect their persistence and competitiveness in dental biofilm. In conclusion, fructose metabolism is integrated into the stress core of S. mutans and regulates critical functions required for survival and its ability to induce dysbiosis in the oral cavity.IMPORTANCEFructose is a common monosaccharide in the biosphere, yet its overconsumption has been linked to various health problems in humans including insulin resistance, obesity, diabetes, non-alcoholic liver diseases, and even cancer. These effects are in large part attributable to the unique biochemical characteristics and metabolic responses associated with the degradation of fructose. Yet, an understanding of the effects of fructose on the physiology of bacteria and its implications for the human microbiome is severely lacking. Here, we performed a series of analyses on the gene regulation of a dental pathogen Streptococcus mutans by exposing it to fructose and other important stress agents. Further supported by growth, persistence, and competition assays, our findings revealed the ability of fructose to activate a set of stress-related functions that may prove critical to the ability of the bacterium to persist and cause diseases both within and without the oral cavity.},
}
RevDate: 2025-04-16
CmpDate: 2025-04-16
Zero inflated high dimensional compositional data with DeepInsight.
PloS one, 20(4):e0320832 pii:PONE-D-24-49284.
Through the Human Microbiome Project, research on human-associated microbiomes has been conducted in various fields. New sequencing techniques such as Next Generation Sequencing (NGS) and High-Throughput Sequencing (HTS) have enabled the inclusion of a wide range of features of the microbiome. These advancements have also contributed to the development of numerical proxies like Operational Taxonomic Units (OTUs) and Amplicon Sequence Variants (ASVs). Studies involving such microbiome data often encounter zero-inflated and high-dimensional problems. Based on the need to address these two issues and the recent emphasis on compositional interpretation of microbiome data, we conducted our research. To solve the zero-inflated problem in compositional microbiome data, we transformed the data onto the surface of the hypersphere using a square root transformation. Then, to solve the high-dimensional problem, we modified DeepInsight, an image-generating method using Convolutional Neural Networks (CNNs), to fit the hypersphere space. Furthermore, to resolve the common issue of distinguishing between true zero values and fake zero values in zero-inflated images, we added a small value to the true zero values. We validated our approach using pediatric inflammatory bowel disease (IBD) fecal sample data and achieved an area under the curve (AUC) value of 0.847, which is higher than the previous study's result of 0.83.
Additional Links: PMID-40238826
Publisher:
PubMed:
Citation:
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@article {pmid40238826,
year = {2025},
author = {Lee, J and Kim, B},
title = {Zero inflated high dimensional compositional data with DeepInsight.},
journal = {PloS one},
volume = {20},
number = {4},
pages = {e0320832},
doi = {10.1371/journal.pone.0320832},
pmid = {40238826},
issn = {1932-6203},
mesh = {Humans ; High-Throughput Nucleotide Sequencing/methods ; *Microbiota/genetics ; Neural Networks, Computer ; Inflammatory Bowel Diseases/microbiology ; Child ; },
abstract = {Through the Human Microbiome Project, research on human-associated microbiomes has been conducted in various fields. New sequencing techniques such as Next Generation Sequencing (NGS) and High-Throughput Sequencing (HTS) have enabled the inclusion of a wide range of features of the microbiome. These advancements have also contributed to the development of numerical proxies like Operational Taxonomic Units (OTUs) and Amplicon Sequence Variants (ASVs). Studies involving such microbiome data often encounter zero-inflated and high-dimensional problems. Based on the need to address these two issues and the recent emphasis on compositional interpretation of microbiome data, we conducted our research. To solve the zero-inflated problem in compositional microbiome data, we transformed the data onto the surface of the hypersphere using a square root transformation. Then, to solve the high-dimensional problem, we modified DeepInsight, an image-generating method using Convolutional Neural Networks (CNNs), to fit the hypersphere space. Furthermore, to resolve the common issue of distinguishing between true zero values and fake zero values in zero-inflated images, we added a small value to the true zero values. We validated our approach using pediatric inflammatory bowel disease (IBD) fecal sample data and achieved an area under the curve (AUC) value of 0.847, which is higher than the previous study's result of 0.83.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
High-Throughput Nucleotide Sequencing/methods
*Microbiota/genetics
Neural Networks, Computer
Inflammatory Bowel Diseases/microbiology
Child
RevDate: 2025-04-16
The human phageome: niche-specific distribution of bacteriophages and their clinical implications.
Applied and environmental microbiology [Epub ahead of print].
Bacteriophages (phages) play a crucial role in shaping the composition and diversity of the human microbiome across various body niches. Recent advancements in high-throughput sequencing technologies have enabled comprehensive analysis of the human phageome in different body sites. This review comprehensively analyzes phage populations across major human body niches, examining their distribution and dynamics through recent metagenomic discoveries. We explore how phage-bacteria interactions within different body sites contribute to homeostasis and disease development. Emerging evidence demonstrates that phageome perturbations can serve as early indicators of various disorders, particularly in the gut microbiome. Understanding these complex microbial interactions offers promising opportunities for developing novel diagnostic markers and therapeutic approaches. However, the causal relationship between phages, bacteria, and disease development remains unclear. Further research is needed to elucidate the role of phages in human health and disease and to explore their potential as diagnostic or therapeutic tools. Understanding the intricate interactions between phages, bacteria, and the human host is crucial for unraveling the complexities of the human microbiome and its impact on health and disease.
Additional Links: PMID-40237489
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PubMed:
Citation:
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@article {pmid40237489,
year = {2025},
author = {Rybicka, I and KaΕΊmierczak, Z},
title = {The human phageome: niche-specific distribution of bacteriophages and their clinical implications.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0178824},
doi = {10.1128/aem.01788-24},
pmid = {40237489},
issn = {1098-5336},
abstract = {Bacteriophages (phages) play a crucial role in shaping the composition and diversity of the human microbiome across various body niches. Recent advancements in high-throughput sequencing technologies have enabled comprehensive analysis of the human phageome in different body sites. This review comprehensively analyzes phage populations across major human body niches, examining their distribution and dynamics through recent metagenomic discoveries. We explore how phage-bacteria interactions within different body sites contribute to homeostasis and disease development. Emerging evidence demonstrates that phageome perturbations can serve as early indicators of various disorders, particularly in the gut microbiome. Understanding these complex microbial interactions offers promising opportunities for developing novel diagnostic markers and therapeutic approaches. However, the causal relationship between phages, bacteria, and disease development remains unclear. Further research is needed to elucidate the role of phages in human health and disease and to explore their potential as diagnostic or therapeutic tools. Understanding the intricate interactions between phages, bacteria, and the human host is crucial for unraveling the complexities of the human microbiome and its impact on health and disease.},
}
RevDate: 2025-04-16
The case for microbiome stewardship: what it is and how to get there.
mSystems [Epub ahead of print].
Microbiomes are essential for human, animal, plant, and ecosystem health. Despite widespread recognition of the importance of microbiomes, there is little attention paid to monitoring and safeguarding microbial ecologies on policy levels. We observe that microbiomes are deteriorating owing to practices at societal levels such as pesticide use in agriculture, air and water pollution, and overuse of antibiotics. Potential policy on these issues would cross multiple domains such as public health, environmental protection, and agriculture. We propose microbiome stewardship as a foundational concept that can act across policy domains to facilitate healthy microbiomes for human and ecosystem health. We examine challenges to be addressed and steps to take toward developing meaningful microbiome stewardship.
Additional Links: PMID-40237447
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PubMed:
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@article {pmid40237447,
year = {2025},
author = {Choudoir, MJ and Ishaq, SL and Beiko, RG and Silva, DS and Allen-Vercoe, E and O'Doherty, KC},
title = {The case for microbiome stewardship: what it is and how to get there.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0006225},
doi = {10.1128/msystems.00062-25},
pmid = {40237447},
issn = {2379-5077},
abstract = {Microbiomes are essential for human, animal, plant, and ecosystem health. Despite widespread recognition of the importance of microbiomes, there is little attention paid to monitoring and safeguarding microbial ecologies on policy levels. We observe that microbiomes are deteriorating owing to practices at societal levels such as pesticide use in agriculture, air and water pollution, and overuse of antibiotics. Potential policy on these issues would cross multiple domains such as public health, environmental protection, and agriculture. We propose microbiome stewardship as a foundational concept that can act across policy domains to facilitate healthy microbiomes for human and ecosystem health. We examine challenges to be addressed and steps to take toward developing meaningful microbiome stewardship.},
}
RevDate: 2025-04-16
Preconception maternal gut dysbiosis affects enteric nervous system development and disease susceptibility in offspring via the GPR41-GDNF/RET/SOX10 signaling pathway.
iMeta, 4(2):e70012.
Maternal health, specifically changes in the gut microbiota, can profoundly impact offspring health; however, our understanding of how gut microbiota alterations during the preconception period influence the offspring remains limited. In this study, we investigated the impact and mechanisms of preconception maternal gut dysbiosis on the development of the enteric nervous system (ENS) in mice. We found that preconception maternal exposure to antibiotics led to the abnormal development of the ENS in offspring, increasing their susceptibility to water avoidance stress at the adult stage. Metagenomic, targeted metabolomic, and transcriptomic analyses revealed that preconception antibiotic exposure disrupted the expression of genes crucial for embryonic ENS development by altering maternal gut microbiota composition. Multi-omics analysis combined with Limosilactobacillus reuteri and propionate gestational supplementation demonstrated that the maternal gut microbiota and metabolites may influence embryonic ENS development via the GPR41-GDNF/RET/SOX10 signaling pathway. Our findings highlight the critical importance of maintaining a healthy maternal gut microbiota before conception to support normal ENS development in offspring.
Additional Links: PMID-40236770
PubMed:
Citation:
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@article {pmid40236770,
year = {2025},
author = {Zhang, C and Chen, Y and Duan, R and Zhang, Y and Zheng, H and Zhang, J and Zhang, T and Xu, J and Li, K and Pei, F and Duan, L},
title = {Preconception maternal gut dysbiosis affects enteric nervous system development and disease susceptibility in offspring via the GPR41-GDNF/RET/SOX10 signaling pathway.},
journal = {iMeta},
volume = {4},
number = {2},
pages = {e70012},
pmid = {40236770},
issn = {2770-596X},
abstract = {Maternal health, specifically changes in the gut microbiota, can profoundly impact offspring health; however, our understanding of how gut microbiota alterations during the preconception period influence the offspring remains limited. In this study, we investigated the impact and mechanisms of preconception maternal gut dysbiosis on the development of the enteric nervous system (ENS) in mice. We found that preconception maternal exposure to antibiotics led to the abnormal development of the ENS in offspring, increasing their susceptibility to water avoidance stress at the adult stage. Metagenomic, targeted metabolomic, and transcriptomic analyses revealed that preconception antibiotic exposure disrupted the expression of genes crucial for embryonic ENS development by altering maternal gut microbiota composition. Multi-omics analysis combined with Limosilactobacillus reuteri and propionate gestational supplementation demonstrated that the maternal gut microbiota and metabolites may influence embryonic ENS development via the GPR41-GDNF/RET/SOX10 signaling pathway. Our findings highlight the critical importance of maintaining a healthy maternal gut microbiota before conception to support normal ENS development in offspring.},
}
RevDate: 2025-04-16
Machine learning determines the incidence of Alzheimer's disease based on population gut microbiome profile.
Brain communications, 7(2):fcaf059.
The human microbiome is a complex and dynamic community of microbes, thought to have symbiotic benefit to its host. Influences of the gut microbiome on brain microglia have been identified as a potential mechanism contributing to neurodegenerative diseases, such as Alzheimer's disease, motor neurone disease and Parkinson's disease (Boddy SL, Giovannelli I, Sassani M, et al. The gut microbiome: A key player in the complexity of amyotrophic lateral sclerosis (ALS). BMC Med. 2021;19(1):13). We hypothesize that population level differences in the gut microbiome will predict the incidence of Alzheimer's disease using machine learning methods. Cross-sectional analyses were performed in R, using two large, open-access microbiome datasets (n = 959 and n = 2012). Countries in these datasets were grouped based on Alzheimer's disease incidence and the gut microbiome profiles compared. In countries with a high incidence of Alzheimer's disease, there is a significantly lower diversity of the gut microbiome (P < 0.05). A permutational analysis of variance test (P < 0.05) revealed significant differences in the microbiome profile between countries with high versus low incidence of Alzheimer's disease with several contributing taxa identified: at a species level Escherichia coli, and at a genus level Haemophilus and Akkermansia were found to be reproducibly protective in both datasets. Additionally, using machine learning, we were able to predict the incidence of Alzheimer's disease within a country based on the microbiome profile (mean area under the curve 0.889 and 0.927). We conclude that differences in the microbiome can predict the varying incidence of Alzheimer's disease between countries. Our results support a key role of the gut microbiome in neurodegeneration at a population level.
Additional Links: PMID-40235960
PubMed:
Citation:
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@article {pmid40235960,
year = {2025},
author = {Basgaran, A and Lymberopoulos, E and Burchill, E and Reis-Dehabadi, M and Sharma, N},
title = {Machine learning determines the incidence of Alzheimer's disease based on population gut microbiome profile.},
journal = {Brain communications},
volume = {7},
number = {2},
pages = {fcaf059},
pmid = {40235960},
issn = {2632-1297},
abstract = {The human microbiome is a complex and dynamic community of microbes, thought to have symbiotic benefit to its host. Influences of the gut microbiome on brain microglia have been identified as a potential mechanism contributing to neurodegenerative diseases, such as Alzheimer's disease, motor neurone disease and Parkinson's disease (Boddy SL, Giovannelli I, Sassani M, et al. The gut microbiome: A key player in the complexity of amyotrophic lateral sclerosis (ALS). BMC Med. 2021;19(1):13). We hypothesize that population level differences in the gut microbiome will predict the incidence of Alzheimer's disease using machine learning methods. Cross-sectional analyses were performed in R, using two large, open-access microbiome datasets (n = 959 and n = 2012). Countries in these datasets were grouped based on Alzheimer's disease incidence and the gut microbiome profiles compared. In countries with a high incidence of Alzheimer's disease, there is a significantly lower diversity of the gut microbiome (P < 0.05). A permutational analysis of variance test (P < 0.05) revealed significant differences in the microbiome profile between countries with high versus low incidence of Alzheimer's disease with several contributing taxa identified: at a species level Escherichia coli, and at a genus level Haemophilus and Akkermansia were found to be reproducibly protective in both datasets. Additionally, using machine learning, we were able to predict the incidence of Alzheimer's disease within a country based on the microbiome profile (mean area under the curve 0.889 and 0.927). We conclude that differences in the microbiome can predict the varying incidence of Alzheimer's disease between countries. Our results support a key role of the gut microbiome in neurodegeneration at a population level.},
}
RevDate: 2025-04-16
Exploring the dark side of probiotics to pursue light: Intrinsic and extrinsic risks to be opportunistic pathogens.
Current research in food science, 10:101044.
Probiotics, live microorganisms with multiple health benefits, have gained popularity for their roles in maintaining daily health and treating a variety of diseases. However, they have the potential to be opportunistic pathogens in some conditions. This review delves into the intrinsic and extrinsic risks associated with probiotics. Intrinsic risks involve the production of harmful substances, such as toxins and invasive factors, biofilm formation, bacteria emboli, antibiotic resistance with relevant genetic materials, genetic plasticity, and metabolic issues, while extrinsic risks include problems in regulatory oversight and public awareness, host health status and appropriately administration. It emphasizes the need for a balanced view of their therapeutic benefits and potential hazards, advocating for further research to understand the complex interactions between probiotics and the human microbiome, to optimize the safety and efficacy of probiotics.
Additional Links: PMID-40235735
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Citation:
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@article {pmid40235735,
year = {2025},
author = {Xu, R and Yu, Y and Chen, T},
title = {Exploring the dark side of probiotics to pursue light: Intrinsic and extrinsic risks to be opportunistic pathogens.},
journal = {Current research in food science},
volume = {10},
number = {},
pages = {101044},
pmid = {40235735},
issn = {2665-9271},
abstract = {Probiotics, live microorganisms with multiple health benefits, have gained popularity for their roles in maintaining daily health and treating a variety of diseases. However, they have the potential to be opportunistic pathogens in some conditions. This review delves into the intrinsic and extrinsic risks associated with probiotics. Intrinsic risks involve the production of harmful substances, such as toxins and invasive factors, biofilm formation, bacteria emboli, antibiotic resistance with relevant genetic materials, genetic plasticity, and metabolic issues, while extrinsic risks include problems in regulatory oversight and public awareness, host health status and appropriately administration. It emphasizes the need for a balanced view of their therapeutic benefits and potential hazards, advocating for further research to understand the complex interactions between probiotics and the human microbiome, to optimize the safety and efficacy of probiotics.},
}
RevDate: 2025-04-15
Protein O-glycosylation in the Bacteroidota phylum.
FEBS open bio [Epub ahead of print].
Glycans play crucial roles in bacteria, such as providing structural integrity or enabling interactions with the ecosystem. They can be linked to lipids, peptides, or proteins. In proteins, they modify either asparagine (N-glycosylation) or serine or threonine (O-glycosylation). Species of the Bacteroidota phylum, a major component of the human microbiome and marine and soil ecosystems, have a unique type of O-glycosylation that modifies multiple noncytoplasmic proteins containing a specific amino acid sequence. Only a small number of species have currently been characterized, but within one species, generally all proteins are modified with the same glycan structure. Most species share a common inner part but differ in the sugar composition and branching of the outer part of their glycan. This suggests that the biosynthesis of the glycan occurs in two separate steps. Both the inner core and the outer glycan are likely assembled from nucleotide-activated monosaccharides on undecaprenyl phosphate on the cytoplasmic side of the inner membrane, prior to being flipped to the periplasm and transferred to the protein. A genomic locus responsible for the biosynthesis of the outer glycan has been identified, containing some conserved genes across species. Despite substantial progress in the characterization of this O-glycosylation system, its function, the overall diversity of glycan structures across the phylum, and the complete biosynthetic pathway remain mostly unknown. Due to the importance of this group of species for the human gut microbiome, elucidating these aspects can open up strategies to modulate the composition of the microbiome community toward a healthy state.
Additional Links: PMID-40231347
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PubMed:
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@article {pmid40231347,
year = {2025},
author = {Hoffmanns, L and Svedberg, D and Mateus, A},
title = {Protein O-glycosylation in the Bacteroidota phylum.},
journal = {FEBS open bio},
volume = {},
number = {},
pages = {},
doi = {10.1002/2211-5463.70041},
pmid = {40231347},
issn = {2211-5463},
support = {Wallenberg Academy Fellows 2025//Knut och Alice Wallenbergs Stiftelse/ ; 2021-06602//Vetenskapsrådet/ ; 2022-02958//Vetenskapsrådet/ ; ProFITGut-101076015//H2020 European Research Council/ ; },
abstract = {Glycans play crucial roles in bacteria, such as providing structural integrity or enabling interactions with the ecosystem. They can be linked to lipids, peptides, or proteins. In proteins, they modify either asparagine (N-glycosylation) or serine or threonine (O-glycosylation). Species of the Bacteroidota phylum, a major component of the human microbiome and marine and soil ecosystems, have a unique type of O-glycosylation that modifies multiple noncytoplasmic proteins containing a specific amino acid sequence. Only a small number of species have currently been characterized, but within one species, generally all proteins are modified with the same glycan structure. Most species share a common inner part but differ in the sugar composition and branching of the outer part of their glycan. This suggests that the biosynthesis of the glycan occurs in two separate steps. Both the inner core and the outer glycan are likely assembled from nucleotide-activated monosaccharides on undecaprenyl phosphate on the cytoplasmic side of the inner membrane, prior to being flipped to the periplasm and transferred to the protein. A genomic locus responsible for the biosynthesis of the outer glycan has been identified, containing some conserved genes across species. Despite substantial progress in the characterization of this O-glycosylation system, its function, the overall diversity of glycan structures across the phylum, and the complete biosynthetic pathway remain mostly unknown. Due to the importance of this group of species for the human gut microbiome, elucidating these aspects can open up strategies to modulate the composition of the microbiome community toward a healthy state.},
}
RevDate: 2025-04-14
CmpDate: 2025-04-14
Pneumocystis jirovecii is a potential pivotal ecological driver contributing to shifts in microbial equilibrium during the early-life lower airway microbiome assembly.
Communications biology, 8(1):609.
Early life gut microbiota is being increasingly recognized as a major contributor to short and/or long-term human health and diseases. However, little is known about these early-life events in the human microbiome of the lower respiratory tract. This study aims to investigate fungal and bacterial colonization in the lower airways over the first year of life by analyzing lung tissue from autopsied infants. The fungal and bacterial communities of lung tissue samples from 53 autopsied infants were characterized by Next-Generation Sequencing (NGS), based on universal PCR amplification of the ITS region and the 16S rRNA gene, respectively. Our study highlights a high degree of inter-individual variability in both fungal and bacterial communities inhabiting the infant lung. The lower respiratory tract microbiota is mainly composed of transient microorganisms that likely travel from the upper respiratory tract and do not establish permanent residence. However, it could also contain some genera identified as long-term inhabitants of the lung, which could potentially play a role in lung physiology or disease. At 3-4 months of age, important dynamic changes to the microbial community were observed, which might correspond to a transitional time period in the maturation of the lung microbiome. This timeframe represents a susceptibility period for the colonization of pathogens such as Pneumocystis. The asymptomatic colonization of Pneumocystis was associated with changes in the fungal and bacterial communities. These findings suggest that the period of 2-4 months of age is a "critical window" early in life. Pneumocystis jirovecii could be a potential pivotal ecological driver contributing to shifts in microbial equilibrium during the early-life lower airway microbiome assembly, and to the future health of children.
Additional Links: PMID-40229539
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Citation:
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@article {pmid40229539,
year = {2025},
author = {Magne, F and Ruiz-Ruiz, S and PΓ©rez-Brocal, V and Ponce, CA and Bustamante, R and Martin, VS and Gutierrez, M and Gatti, G and Vargas, SL and Moya, A},
title = {Pneumocystis jirovecii is a potential pivotal ecological driver contributing to shifts in microbial equilibrium during the early-life lower airway microbiome assembly.},
journal = {Communications biology},
volume = {8},
number = {1},
pages = {609},
pmid = {40229539},
issn = {2399-3642},
mesh = {Humans ; Infant ; *Microbiota ; *Lung/microbiology ; Female ; *Pneumocystis carinii/physiology/genetics ; Male ; RNA, Ribosomal, 16S/genetics ; Bacteria/genetics/classification ; Infant, Newborn ; },
abstract = {Early life gut microbiota is being increasingly recognized as a major contributor to short and/or long-term human health and diseases. However, little is known about these early-life events in the human microbiome of the lower respiratory tract. This study aims to investigate fungal and bacterial colonization in the lower airways over the first year of life by analyzing lung tissue from autopsied infants. The fungal and bacterial communities of lung tissue samples from 53 autopsied infants were characterized by Next-Generation Sequencing (NGS), based on universal PCR amplification of the ITS region and the 16S rRNA gene, respectively. Our study highlights a high degree of inter-individual variability in both fungal and bacterial communities inhabiting the infant lung. The lower respiratory tract microbiota is mainly composed of transient microorganisms that likely travel from the upper respiratory tract and do not establish permanent residence. However, it could also contain some genera identified as long-term inhabitants of the lung, which could potentially play a role in lung physiology or disease. At 3-4 months of age, important dynamic changes to the microbial community were observed, which might correspond to a transitional time period in the maturation of the lung microbiome. This timeframe represents a susceptibility period for the colonization of pathogens such as Pneumocystis. The asymptomatic colonization of Pneumocystis was associated with changes in the fungal and bacterial communities. These findings suggest that the period of 2-4 months of age is a "critical window" early in life. Pneumocystis jirovecii could be a potential pivotal ecological driver contributing to shifts in microbial equilibrium during the early-life lower airway microbiome assembly, and to the future health of children.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Infant
*Microbiota
*Lung/microbiology
Female
*Pneumocystis carinii/physiology/genetics
Male
RNA, Ribosomal, 16S/genetics
Bacteria/genetics/classification
Infant, Newborn
RevDate: 2025-04-14
Exploring the Microbiome's Impact on Glioma and Brain Metastases: Insights into Development, Progression, and Treatment Response-A Scoping Review.
Cancers, 17(7): pii:cancers17071228.
Background: The human microbiome plays a crucial role in health and disease. Dysbiosis, an imbalance of microorganisms, has been implicated in cancer development and treatment response, including in primary brain tumors and brain metastases, through interactions mediated by the gut-brain axis. This scoping review synthesizes current evidence on the relationship between the human microbiome and brain tumors. Methods: A systematic search of five electronic databases was conducted by an expert librarian, using controlled vocabulary and keywords. A targeted grey literature search in Google Scholar and clinical trial registries was also undertaken. Eligible studies included primary research involving human patients, or in vivo, or in vitro models of glioma or brain metastasis, with a focus on the microbiome's role in tumor development, treatment response, and outcomes. Results: Out of 584 citations screened, 40 studies met inclusion criteria, comprising 24 articles and 16 conference abstracts. These included 12 human studies, 16 using mouse models, 7 combining both, and 5 employing large datasets or next-generation sequencing of tumor samples. Thirty-one studies focused on primary brain tumors, six on brain metastases, and three on both. Of the 20 studies examining dysbiosis in tumor development, 95% (n = 19) found an association with tumor growth. Additionally, 71.4% (n = 5/7) of studies reported that microbiome alterations influenced treatment efficacy. Conclusions: Although the role of the gut-brain axis in brain tumors is still emerging and is characterized by heterogeneity across studies, existing evidence consistently supports a relationship between the gut microbiome and both brain tumor development and treatment outcomes.
Additional Links: PMID-40227812
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PubMed:
Citation:
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@article {pmid40227812,
year = {2025},
author = {Leigh, J and Skidmore, B and Wong, A and Maleki Vareki, S and Ng, TL},
title = {Exploring the Microbiome's Impact on Glioma and Brain Metastases: Insights into Development, Progression, and Treatment Response-A Scoping Review.},
journal = {Cancers},
volume = {17},
number = {7},
pages = {},
doi = {10.3390/cancers17071228},
pmid = {40227812},
issn = {2072-6694},
abstract = {Background: The human microbiome plays a crucial role in health and disease. Dysbiosis, an imbalance of microorganisms, has been implicated in cancer development and treatment response, including in primary brain tumors and brain metastases, through interactions mediated by the gut-brain axis. This scoping review synthesizes current evidence on the relationship between the human microbiome and brain tumors. Methods: A systematic search of five electronic databases was conducted by an expert librarian, using controlled vocabulary and keywords. A targeted grey literature search in Google Scholar and clinical trial registries was also undertaken. Eligible studies included primary research involving human patients, or in vivo, or in vitro models of glioma or brain metastasis, with a focus on the microbiome's role in tumor development, treatment response, and outcomes. Results: Out of 584 citations screened, 40 studies met inclusion criteria, comprising 24 articles and 16 conference abstracts. These included 12 human studies, 16 using mouse models, 7 combining both, and 5 employing large datasets or next-generation sequencing of tumor samples. Thirty-one studies focused on primary brain tumors, six on brain metastases, and three on both. Of the 20 studies examining dysbiosis in tumor development, 95% (n = 19) found an association with tumor growth. Additionally, 71.4% (n = 5/7) of studies reported that microbiome alterations influenced treatment efficacy. Conclusions: Although the role of the gut-brain axis in brain tumors is still emerging and is characterized by heterogeneity across studies, existing evidence consistently supports a relationship between the gut microbiome and both brain tumor development and treatment outcomes.},
}
RevDate: 2025-04-12
The role of bacteriophage in inflammatory bowel disease and its therapeutic potential.
Critical reviews in microbiology [Epub ahead of print].
Inflammatory bowel disease (IBD) refers to a group of chronic inflammatory disorders impacting the gastrointestinal (GI) tract. It represents a significant public health challenge due to its rising global incidence and substantial impact on patients' quality of life. Emerging research suggests a pivotal role of the human microbiome in IBD pathogenesis. Bacteriophages, integral components of the human microbiome, are indicated to influence the disease onset, progression, and therapeutic strategies. Here, we review the effect of bacteriophages on the pathogenesis of IBD and, more specifically, on the gut bacteria, the systemic immunity, and the susceptibility genes. Additionally, we explore the potential therapeutic use of the bacteriophages to modify gut microbiota and improve the health outcomes of IBD patients. This review highlights the potential of therapeutic bacteriophages in regulating gut microbiota and modulating the immune response to improve health outcomes in IBD patients. Future studies on personalized bacteriophage therapy and its integration into clinical practice could advance treatment strategies for IBD.
Additional Links: PMID-40219702
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@article {pmid40219702,
year = {2025},
author = {Xiao, Y and Yue, X and Zhang, X and Yang, Y and Zhang, Y and Sun, L},
title = {The role of bacteriophage in inflammatory bowel disease and its therapeutic potential.},
journal = {Critical reviews in microbiology},
volume = {},
number = {},
pages = {1-15},
doi = {10.1080/1040841X.2025.2492154},
pmid = {40219702},
issn = {1549-7828},
abstract = {Inflammatory bowel disease (IBD) refers to a group of chronic inflammatory disorders impacting the gastrointestinal (GI) tract. It represents a significant public health challenge due to its rising global incidence and substantial impact on patients' quality of life. Emerging research suggests a pivotal role of the human microbiome in IBD pathogenesis. Bacteriophages, integral components of the human microbiome, are indicated to influence the disease onset, progression, and therapeutic strategies. Here, we review the effect of bacteriophages on the pathogenesis of IBD and, more specifically, on the gut bacteria, the systemic immunity, and the susceptibility genes. Additionally, we explore the potential therapeutic use of the bacteriophages to modify gut microbiota and improve the health outcomes of IBD patients. This review highlights the potential of therapeutic bacteriophages in regulating gut microbiota and modulating the immune response to improve health outcomes in IBD patients. Future studies on personalized bacteriophage therapy and its integration into clinical practice could advance treatment strategies for IBD.},
}
RevDate: 2025-04-11
CmpDate: 2025-04-11
Insights into Autophagy in Microbiome Therapeutic Approaches for Drug-Resistant Tuberculosis.
Cells, 14(7): pii:cells14070540.
Tuberculosis, primarily caused by Mycobacterium tuberculosis, is an airborne lung disease and continues to pose a significant global health threat, resulting in millions of deaths annually. The current treatment for tuberculosis involves a prolonged regimen of antibiotics, which leads to complications such as recurrence, drug resistance, reinfection, and a range of side effects. This scenario underscores the urgent need for novel therapeutic strategies to combat this lethal pathogen. Over the last two decades, microbiome therapeutics have emerged as promising next-generation drug candidates, offering advantages over traditional medications. In 2022, the Food and Drug Administration approved the first microbiome therapeutic for recurrent Clostridium infections, and extensive research is underway on microbiome treatments for various challenging diseases, including metabolic disorders and cancer. Research on microbiomes concerning tuberculosis commenced roughly a decade ago, and the scope of this research has broadened considerably over the last five years, with microbiome therapeutics now viewed as viable options for managing drug-resistant tuberculosis. Nevertheless, the understanding of their mechanisms is still in its infancy. Although autophagy has been extensively studied in other diseases, research into its role in tuberculosis is just beginning, with preliminary developments in progress. Against this backdrop, this comprehensive review begins by succinctly outlining tuberculosis' characteristics and assessing existing treatments' strengths and weaknesses, followed by a detailed examination of microbiome-based therapeutic approaches for drug-resistant tuberculosis. Additionally, this review focuses on establishing a basic understanding of microbiome treatments for tuberculosis, mainly through the lens of autophagy as a mechanism of action. Ultimately, this review aims to contribute to the foundational comprehension of microbiome-based therapies for tuberculosis, thereby setting the stage for the further advancement of microbiome therapeutics for drug-resistant tuberculosis.
Additional Links: PMID-40214493
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@article {pmid40214493,
year = {2025},
author = {Rahim, MA and Seo, H and Barman, I and Hossain, MS and Shuvo, MSH and Song, HY},
title = {Insights into Autophagy in Microbiome Therapeutic Approaches for Drug-Resistant Tuberculosis.},
journal = {Cells},
volume = {14},
number = {7},
pages = {},
doi = {10.3390/cells14070540},
pmid = {40214493},
issn = {2073-4409},
support = {RS-2023-00219563//National Research Foundation of Korea/ ; P248400003//Korea Institute for Advancement of Technology (KIAT)/ ; Soonchunhyang University Research Fund//Soonchunhyang University/ ; },
mesh = {Humans ; *Autophagy ; *Tuberculosis, Multidrug-Resistant/therapy/microbiology ; *Microbiota ; Mycobacterium tuberculosis/drug effects ; Animals ; Antitubercular Agents/therapeutic use/pharmacology ; },
abstract = {Tuberculosis, primarily caused by Mycobacterium tuberculosis, is an airborne lung disease and continues to pose a significant global health threat, resulting in millions of deaths annually. The current treatment for tuberculosis involves a prolonged regimen of antibiotics, which leads to complications such as recurrence, drug resistance, reinfection, and a range of side effects. This scenario underscores the urgent need for novel therapeutic strategies to combat this lethal pathogen. Over the last two decades, microbiome therapeutics have emerged as promising next-generation drug candidates, offering advantages over traditional medications. In 2022, the Food and Drug Administration approved the first microbiome therapeutic for recurrent Clostridium infections, and extensive research is underway on microbiome treatments for various challenging diseases, including metabolic disorders and cancer. Research on microbiomes concerning tuberculosis commenced roughly a decade ago, and the scope of this research has broadened considerably over the last five years, with microbiome therapeutics now viewed as viable options for managing drug-resistant tuberculosis. Nevertheless, the understanding of their mechanisms is still in its infancy. Although autophagy has been extensively studied in other diseases, research into its role in tuberculosis is just beginning, with preliminary developments in progress. Against this backdrop, this comprehensive review begins by succinctly outlining tuberculosis' characteristics and assessing existing treatments' strengths and weaknesses, followed by a detailed examination of microbiome-based therapeutic approaches for drug-resistant tuberculosis. Additionally, this review focuses on establishing a basic understanding of microbiome treatments for tuberculosis, mainly through the lens of autophagy as a mechanism of action. Ultimately, this review aims to contribute to the foundational comprehension of microbiome-based therapies for tuberculosis, thereby setting the stage for the further advancement of microbiome therapeutics for drug-resistant tuberculosis.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Autophagy
*Tuberculosis, Multidrug-Resistant/therapy/microbiology
*Microbiota
Mycobacterium tuberculosis/drug effects
Animals
Antitubercular Agents/therapeutic use/pharmacology
RevDate: 2025-04-11
Standardizing the approach to clinical-based human microbiome research: from clinical information collection to microbiome profiling and human resource utilization.
Osong public health and research perspectives pii:j.phrp.2024.0319 [Epub ahead of print].
OBJECTIVES: This study presents the standardized protocols developed by the Clinical-Based Human Microbiome Research and Development Project (cHMP) in the Republic of Korea.
METHODS: It addresses clinical metadata collection, specimen handling, DNA extraction, sequencing methods, and quality control measures for microbiome research.
RESULTS: The cHMP involves collecting samples from healthy individuals and patients across various body sites, including the gastrointestinal tract, oral cavity, respiratory system, urogenital tract, and skin. These standardized procedures ensure consistent data quality through controlled specimen collection, storage, transportation, DNA extraction, and sequencing. Sequencing encompasses both amplicon and whole metagenome methods, followed by stringent quality checks. The protocols conform to international guidelines, ensuring that the data generated are both reliable and comparable across microbiome studies.
CONCLUSION: The cHMP underscores the importance of methodological standardization in enhancing data integrity, reproducibility, and advancing microbiome-based research with potential applications for improving human health outcomes.
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@article {pmid40211685,
year = {2025},
author = {Kim, JW and Choi, EC and Lee, KJ},
title = {Standardizing the approach to clinical-based human microbiome research: from clinical information collection to microbiome profiling and human resource utilization.},
journal = {Osong public health and research perspectives},
volume = {},
number = {},
pages = {},
doi = {10.24171/j.phrp.2024.0319},
pmid = {40211685},
issn = {2210-9099},
abstract = {OBJECTIVES: This study presents the standardized protocols developed by the Clinical-Based Human Microbiome Research and Development Project (cHMP) in the Republic of Korea.
METHODS: It addresses clinical metadata collection, specimen handling, DNA extraction, sequencing methods, and quality control measures for microbiome research.
RESULTS: The cHMP involves collecting samples from healthy individuals and patients across various body sites, including the gastrointestinal tract, oral cavity, respiratory system, urogenital tract, and skin. These standardized procedures ensure consistent data quality through controlled specimen collection, storage, transportation, DNA extraction, and sequencing. Sequencing encompasses both amplicon and whole metagenome methods, followed by stringent quality checks. The protocols conform to international guidelines, ensuring that the data generated are both reliable and comparable across microbiome studies.
CONCLUSION: The cHMP underscores the importance of methodological standardization in enhancing data integrity, reproducibility, and advancing microbiome-based research with potential applications for improving human health outcomes.},
}
RevDate: 2025-04-10
Pseudomonas aeruginosa population dynamics in a vancomycin-induced murine model of gastrointestinal carriage.
mBio [Epub ahead of print].
UNLABELLED: Pseudomonas aeruginosa is a common nosocomial pathogen and a major cause of morbidity and mortality in hospitalized patients. Multiple reports highlight that P. aeruginosa gastrointestinal colonization may precede systemic infections by this pathogen. Gaining a deeper insight into the dynamics of P. aeruginosa gastrointestinal carriage is an essential step in managing gastrointestinal colonization and could contribute to preventing bacterial transmission and progression to systemic infection. Here, we present a clinically relevant mouse model relying on parenteral vancomycin pretreatment and a single orogastric gavage of a controlled dose of P. aeruginosa. Robust carriage was observed with multiple clinical isolates, and carriage persisted for up to 60 days. Histological and microbiological examination of mice indicated that this model indeed represented carriage and not infection. We then used a barcoded P. aeruginosa library along with the sequence tag-based analysis of microbial populations (STAMPR) analytic pipeline to quantify bacterial population dynamics and bottlenecks during the establishment of the gastrointestinal carriage. Analysis indicated that most of the P. aeruginosa population was rapidly eliminated in the stomach, but the few bacteria that moved to the small intestine and the cecum expanded rapidly. Hence, the stomach constitutes a significant barrier against gastrointestinal carriage of P. aeruginosa, which may have clinical implications for hospitalized patients.
IMPORTANCE: While Pseudomonas aeruginosa is rarely part of the normal human microbiome, carriage of the bacterium is quite frequent in hospitalized patients and residents of long-term care facilities. P. aeruginosa carriage is a precursor to infection. Options for treating infections caused by difficult-to-treat P. aeruginosa strains are dwindling, underscoring the urgency to better understand and impede pre-infection stages, such as colonization. Here, we use vancomycin-treated mice to model antibiotic-treated patients who become colonized with P. aeruginosa in their gastrointestinal tracts. We identify the stomach as a major barrier to the establishment of gastrointestinal carriage. These findings suggest that efforts to prevent gastrointestinal colonization should focus not only on judicious use of antibiotics but also on investigation into how the stomach eliminates orally ingested P. aeruginosa.
Additional Links: PMID-40207916
Publisher:
PubMed:
Citation:
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@article {pmid40207916,
year = {2025},
author = {Lebrun-Corbin, M and Cheung, BH and Hullahalli, K and Dailey, KG and Bailey, K and Waldor, MK and Wunderink, RG and Bachta, KER and Hauser, AR},
title = {Pseudomonas aeruginosa population dynamics in a vancomycin-induced murine model of gastrointestinal carriage.},
journal = {mBio},
volume = {},
number = {},
pages = {e0313624},
doi = {10.1128/mbio.03136-24},
pmid = {40207916},
issn = {2150-7511},
abstract = {UNLABELLED: Pseudomonas aeruginosa is a common nosocomial pathogen and a major cause of morbidity and mortality in hospitalized patients. Multiple reports highlight that P. aeruginosa gastrointestinal colonization may precede systemic infections by this pathogen. Gaining a deeper insight into the dynamics of P. aeruginosa gastrointestinal carriage is an essential step in managing gastrointestinal colonization and could contribute to preventing bacterial transmission and progression to systemic infection. Here, we present a clinically relevant mouse model relying on parenteral vancomycin pretreatment and a single orogastric gavage of a controlled dose of P. aeruginosa. Robust carriage was observed with multiple clinical isolates, and carriage persisted for up to 60 days. Histological and microbiological examination of mice indicated that this model indeed represented carriage and not infection. We then used a barcoded P. aeruginosa library along with the sequence tag-based analysis of microbial populations (STAMPR) analytic pipeline to quantify bacterial population dynamics and bottlenecks during the establishment of the gastrointestinal carriage. Analysis indicated that most of the P. aeruginosa population was rapidly eliminated in the stomach, but the few bacteria that moved to the small intestine and the cecum expanded rapidly. Hence, the stomach constitutes a significant barrier against gastrointestinal carriage of P. aeruginosa, which may have clinical implications for hospitalized patients.
IMPORTANCE: While Pseudomonas aeruginosa is rarely part of the normal human microbiome, carriage of the bacterium is quite frequent in hospitalized patients and residents of long-term care facilities. P. aeruginosa carriage is a precursor to infection. Options for treating infections caused by difficult-to-treat P. aeruginosa strains are dwindling, underscoring the urgency to better understand and impede pre-infection stages, such as colonization. Here, we use vancomycin-treated mice to model antibiotic-treated patients who become colonized with P. aeruginosa in their gastrointestinal tracts. We identify the stomach as a major barrier to the establishment of gastrointestinal carriage. These findings suggest that efforts to prevent gastrointestinal colonization should focus not only on judicious use of antibiotics but also on investigation into how the stomach eliminates orally ingested P. aeruginosa.},
}
RevDate: 2025-04-10
Pathogen exclusion from intestinal mucus and antimicrobial susceptibility of Bifidobacterium spp. strains from fecal donors.
Microbiome research reports, 4(1):5.
Aim: To study the ability of bifidobacterial strains isolated from fecal donors to prevent pathogens from adhering to intestinal mucus, along with their antimicrobial susceptibility. Methods: Pathogen prevention was assessed through an in vitro adhesion assay using immobilized porcine mucus. Subsequently, bifidobacterial RNA-Seq data were analyzed to pinpoint glycoside hydrolases and glycosyltransferases possibly involved in mucus degradation affecting pathogen adhesion. The antimicrobial susceptibility of bifidobacterial strains was evaluated using in vitro susceptibility testing, followed by analysis of whole-genome sequencing data to reveal antimicrobial resistance genes. Results: Bifidobacterial strains inhibited pathogen adhesion to intestinal mucus, with most strains reducing the adhesion levels of pathogens like Escherichia coli, Listeria monocytogenes, Salmonella Typhimurium, and Staphylococcus aureus by at least 70%. None of the strains significantly affected Pseudomonas aeruginosa, but they moderately reduced the adhesion of Yersinia enterocolitica. Gene expression analysis indicated that the more effective strains expressed higher levels of glycoside hydrolases, correlating with their pathogen exclusion capabilities. Antimicrobial susceptibility testing revealed that most strains were sensitive to several antibiotics, though some exhibited resistance to tobramycin, trimethoprim, and ciprofloxacin. Notably, one strain carried the tetW gene, conferring resistance to tetracycline. Conclusion: The bifidobacterial strains characterized in this study show potential for bacteriotherapeutic applications due to their strong ability to interfere with the adhesion of pathogenic bacteria and their lack of alarming antimicrobial resistance patterns.
Additional Links: PMID-40207286
PubMed:
Citation:
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@article {pmid40207286,
year = {2025},
author = {Ronkainen, A and Khan, I and Satokari, R},
title = {Pathogen exclusion from intestinal mucus and antimicrobial susceptibility of Bifidobacterium spp. strains from fecal donors.},
journal = {Microbiome research reports},
volume = {4},
number = {1},
pages = {5},
pmid = {40207286},
issn = {2771-5965},
abstract = {Aim: To study the ability of bifidobacterial strains isolated from fecal donors to prevent pathogens from adhering to intestinal mucus, along with their antimicrobial susceptibility. Methods: Pathogen prevention was assessed through an in vitro adhesion assay using immobilized porcine mucus. Subsequently, bifidobacterial RNA-Seq data were analyzed to pinpoint glycoside hydrolases and glycosyltransferases possibly involved in mucus degradation affecting pathogen adhesion. The antimicrobial susceptibility of bifidobacterial strains was evaluated using in vitro susceptibility testing, followed by analysis of whole-genome sequencing data to reveal antimicrobial resistance genes. Results: Bifidobacterial strains inhibited pathogen adhesion to intestinal mucus, with most strains reducing the adhesion levels of pathogens like Escherichia coli, Listeria monocytogenes, Salmonella Typhimurium, and Staphylococcus aureus by at least 70%. None of the strains significantly affected Pseudomonas aeruginosa, but they moderately reduced the adhesion of Yersinia enterocolitica. Gene expression analysis indicated that the more effective strains expressed higher levels of glycoside hydrolases, correlating with their pathogen exclusion capabilities. Antimicrobial susceptibility testing revealed that most strains were sensitive to several antibiotics, though some exhibited resistance to tobramycin, trimethoprim, and ciprofloxacin. Notably, one strain carried the tetW gene, conferring resistance to tetracycline. Conclusion: The bifidobacterial strains characterized in this study show potential for bacteriotherapeutic applications due to their strong ability to interfere with the adhesion of pathogenic bacteria and their lack of alarming antimicrobial resistance patterns.},
}
RevDate: 2025-04-10
Potential effects of probiotics on atherosclerosis.
Microbiome research reports, 4(1):11.
The rising global incidence of atherosclerosis highlights the inadequacies in our understanding of the pathophysiology and treatment of the disease. Increasing evidence outlines the importance of the intestinal microbiome in atherosclerosis, wherein gut-derived uremic toxins (GDUTs) may be of concern. Plasma levels of the GDUTs trimethylamine n-oxide (TMAO), p-cresyl sulfate, and indoxyl sulfate are associated with accelerated renal function decline and increased cardiovascular risk. Thus, reducing the amount of GDUTs in circulation is expected to benefit patients with atherosclerosis. Because some beneficial bacteria can clear GDUTs in vitro and in vivo, orally administered probiotics targeting the intestinal tract represent a promising way to bring about these changes. Atherosclerosis such, this perspective reviews the potential use of probiotics to treat atherosclerosis, particularly in patients with non-traditional risk factors and/or impaired renal function.
Additional Links: PMID-40207282
PubMed:
Citation:
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@article {pmid40207282,
year = {2025},
author = {Stuivenberg, GA and Poon, A and Burton, JP and Spence, JD},
title = {Potential effects of probiotics on atherosclerosis.},
journal = {Microbiome research reports},
volume = {4},
number = {1},
pages = {11},
pmid = {40207282},
issn = {2771-5965},
abstract = {The rising global incidence of atherosclerosis highlights the inadequacies in our understanding of the pathophysiology and treatment of the disease. Increasing evidence outlines the importance of the intestinal microbiome in atherosclerosis, wherein gut-derived uremic toxins (GDUTs) may be of concern. Plasma levels of the GDUTs trimethylamine n-oxide (TMAO), p-cresyl sulfate, and indoxyl sulfate are associated with accelerated renal function decline and increased cardiovascular risk. Thus, reducing the amount of GDUTs in circulation is expected to benefit patients with atherosclerosis. Because some beneficial bacteria can clear GDUTs in vitro and in vivo, orally administered probiotics targeting the intestinal tract represent a promising way to bring about these changes. Atherosclerosis such, this perspective reviews the potential use of probiotics to treat atherosclerosis, particularly in patients with non-traditional risk factors and/or impaired renal function.},
}
RevDate: 2025-04-10
A microbial symphony: a literature review of the factors that orchestrate the colonization dynamics of the human colonic microbiome during infancy and implications for future health.
Microbiome research reports, 4(1):1.
Since the advent of new sequencing and bioinformatic technologies, our understanding of the human microbiome has expanded rapidly over recent years. Numerous studies have indicated causal links between alterations to the microbiome and a range of pathological conditions. Furthermore, a large body of epidemiological data is starting to suggest that exposure, or lack thereof, to specific microbial species during the first five years of life has key implications for long-term health outcomes. These include chronic inflammatory and metabolic conditions such as diabetes, asthma, inflammatory bowel disease (IBD), and obesity, with the effects lasting into adulthood. Human microbial colonisation during these first five years of life is a highly dynamic process, with multiple environmental exposures recently being characterised to have influence before the microbiome stabilises and resembles that of an adult at 3-5 years. This short period of time, known as the window of opportunity, appears to "prime" immunoregulation for later life. Understanding and appreciating this aspect of human physiology is therefore crucial for clinicians, scientists, and public health officials. This review outlines the most recent evidence for the pre- and post-natal environments that order the development of the microbiome, how these influences metabolic and immunoregulatory pathways, and their associated health outcomes. It also discusses the limitations of the current knowledge base, and describes the potential microbiome-mediated interventions and public health measures that may have therapeutic potential in the future.
Additional Links: PMID-40207275
PubMed:
Citation:
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@article {pmid40207275,
year = {2025},
author = {Horwell, E and Bearn, P and Cutting, SM},
title = {A microbial symphony: a literature review of the factors that orchestrate the colonization dynamics of the human colonic microbiome during infancy and implications for future health.},
journal = {Microbiome research reports},
volume = {4},
number = {1},
pages = {1},
pmid = {40207275},
issn = {2771-5965},
abstract = {Since the advent of new sequencing and bioinformatic technologies, our understanding of the human microbiome has expanded rapidly over recent years. Numerous studies have indicated causal links between alterations to the microbiome and a range of pathological conditions. Furthermore, a large body of epidemiological data is starting to suggest that exposure, or lack thereof, to specific microbial species during the first five years of life has key implications for long-term health outcomes. These include chronic inflammatory and metabolic conditions such as diabetes, asthma, inflammatory bowel disease (IBD), and obesity, with the effects lasting into adulthood. Human microbial colonisation during these first five years of life is a highly dynamic process, with multiple environmental exposures recently being characterised to have influence before the microbiome stabilises and resembles that of an adult at 3-5 years. This short period of time, known as the window of opportunity, appears to "prime" immunoregulation for later life. Understanding and appreciating this aspect of human physiology is therefore crucial for clinicians, scientists, and public health officials. This review outlines the most recent evidence for the pre- and post-natal environments that order the development of the microbiome, how these influences metabolic and immunoregulatory pathways, and their associated health outcomes. It also discusses the limitations of the current knowledge base, and describes the potential microbiome-mediated interventions and public health measures that may have therapeutic potential in the future.},
}
RevDate: 2025-04-10
Host-microbiota interactions in the infant gut revealed by daily faecal sample time series.
Microbiome research reports, 4(1):13.
Aim: This study aims to explore the interplay between host immune factors and gut microbiota in human infants in vivo using time-series daily stool samples and identify biomarkers of host-microbe interactions. Methods: 216 faecal samples collected from infants aged 5-6 or 11-12 months were analysed for gut microbiota composition, total bacterial load, and biomarkers of immune function. Results: We identified indications of microbial stimulation of eosinophil cationic protein (ECP), IgA, calprotectin (Cal), intestinal alkaline phosphatase (IAP), and Bactericidal/permeability-increasing protein (BPI) at 6 and 12 months, as well as stimulation of lipocalin 2 (LCN2), lactoferrin (LTF), and alpha-defensin-5 only at 6 months. The associations between biomarker concentrations and bacterial population growth were primarily positive at 6 months and mostly negative at 12 months, suggesting increasing host regulation of the microbiota with age. The exceptions were IAP, which was predictive of declining bacterial populations at both time points, and Cal, whose associations changed from negative at 6 months to positive at 12 months. Conclusion: There is an age-associated development in the correlation pattern between bacterial population growth and the biomarker concentrations, suggesting that host-microbe interactions change during early development. Albumin appeared as a potential marker of gut permeability, while LCN2 seemed to correlate with gut transit time. Mucin degradation appeared to decrease with age. Mucin2 and IAP emerged as potentially important regulators of the bacterial populations in the infant gut. The study demonstrates the utility of biomarker and bacteria profiling from daily stool samples for analysing in vivo associations between the immune system and the gut microbiota and provides evidence of host regulation of the microbiota in infants.
Additional Links: PMID-40207273
PubMed:
Citation:
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@article {pmid40207273,
year = {2025},
author = {van Beek, N and Katavisto, I and Lehto, M and Kolho, KL and de Vos, WM and Salonen, A and Korpela, K},
title = {Host-microbiota interactions in the infant gut revealed by daily faecal sample time series.},
journal = {Microbiome research reports},
volume = {4},
number = {1},
pages = {13},
pmid = {40207273},
issn = {2771-5965},
abstract = {Aim: This study aims to explore the interplay between host immune factors and gut microbiota in human infants in vivo using time-series daily stool samples and identify biomarkers of host-microbe interactions. Methods: 216 faecal samples collected from infants aged 5-6 or 11-12 months were analysed for gut microbiota composition, total bacterial load, and biomarkers of immune function. Results: We identified indications of microbial stimulation of eosinophil cationic protein (ECP), IgA, calprotectin (Cal), intestinal alkaline phosphatase (IAP), and Bactericidal/permeability-increasing protein (BPI) at 6 and 12 months, as well as stimulation of lipocalin 2 (LCN2), lactoferrin (LTF), and alpha-defensin-5 only at 6 months. The associations between biomarker concentrations and bacterial population growth were primarily positive at 6 months and mostly negative at 12 months, suggesting increasing host regulation of the microbiota with age. The exceptions were IAP, which was predictive of declining bacterial populations at both time points, and Cal, whose associations changed from negative at 6 months to positive at 12 months. Conclusion: There is an age-associated development in the correlation pattern between bacterial population growth and the biomarker concentrations, suggesting that host-microbe interactions change during early development. Albumin appeared as a potential marker of gut permeability, while LCN2 seemed to correlate with gut transit time. Mucin degradation appeared to decrease with age. Mucin2 and IAP emerged as potentially important regulators of the bacterial populations in the infant gut. The study demonstrates the utility of biomarker and bacteria profiling from daily stool samples for analysing in vivo associations between the immune system and the gut microbiota and provides evidence of host regulation of the microbiota in infants.},
}
RevDate: 2025-04-08
CmpDate: 2025-04-08
Lactobacillus acidophilus potentiates oncolytic virotherapy through modulating gut microbiota homeostasis in hepatocellular carcinoma.
Nature communications, 16(1):3315.
Oncolytic viruses (OVs) hold promise for cancer treatment. However, the antitumor efficacy is limited. Microbiota plays a pivotal role in cancer treatment and its impact on oncolytic virotherapy is unknown. Here, we show that VSVΞ51 has higher antitumor efficacy for hepatocellular carcinoma in the absence of microbiota in female mouse models. VSVΞ51 infection causes microbiota dysbiosis, increasing most of the gut bacteria abundance, while decreasing the commensal Lactobacillus. VSVΞ51 reduced intestinal expression of SLC20A1 that binds to Lactobacillus acidophilus (L. acidophilus) CdpA cell wall protein through IL6-JAK-STAT3 signaling, thereby attenuating attachment and colonization of L. acidophilus. L. acidophilus supplementation confers sensitivity to VSVΞ51 through restoring gut barrier integrity and microbiota homeostasis destroyed by VSVΞ51. In this work, we show that targeting microbiota homostasis holds substantial potential in improving therapeutic outcomes of oncolytic virotherapy.
Additional Links: PMID-40195307
PubMed:
Citation:
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@article {pmid40195307,
year = {2025},
author = {Zhang, J and Yang, J and Luo, J and Wu, W and Luo, H and Wei, W and Lyu, H and Wang, Y and Yi, H and Zhang, Y and Fan, Z and Lyu, H and Kanakaveti, VP and Qin, B and Yuan, P and Yang, R and Zhang, H and Zuo, T and Felsher, DW and Lee, MH and Li, K},
title = {Lactobacillus acidophilus potentiates oncolytic virotherapy through modulating gut microbiota homeostasis in hepatocellular carcinoma.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {3315},
pmid = {40195307},
issn = {2041-1723},
support = {2023A1515030245//Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation)/ ; 2023A1515010737//Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation)/ ; 82473321//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82204411//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82373139//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Lactobacillus acidophilus/metabolism/physiology ; *Carcinoma, Hepatocellular/therapy/microbiology ; *Liver Neoplasms/therapy/microbiology ; *Oncolytic Virotherapy/methods ; Mice ; Female ; Homeostasis ; Humans ; Oncolytic Viruses/genetics ; Mice, Inbred C57BL ; Dysbiosis/microbiology ; Cell Line, Tumor ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; },
abstract = {Oncolytic viruses (OVs) hold promise for cancer treatment. However, the antitumor efficacy is limited. Microbiota plays a pivotal role in cancer treatment and its impact on oncolytic virotherapy is unknown. Here, we show that VSVΞ51 has higher antitumor efficacy for hepatocellular carcinoma in the absence of microbiota in female mouse models. VSVΞ51 infection causes microbiota dysbiosis, increasing most of the gut bacteria abundance, while decreasing the commensal Lactobacillus. VSVΞ51 reduced intestinal expression of SLC20A1 that binds to Lactobacillus acidophilus (L. acidophilus) CdpA cell wall protein through IL6-JAK-STAT3 signaling, thereby attenuating attachment and colonization of L. acidophilus. L. acidophilus supplementation confers sensitivity to VSVΞ51 through restoring gut barrier integrity and microbiota homeostasis destroyed by VSVΞ51. In this work, we show that targeting microbiota homostasis holds substantial potential in improving therapeutic outcomes of oncolytic virotherapy.},
}
MeSH Terms:
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Animals
*Gastrointestinal Microbiome/physiology
*Lactobacillus acidophilus/metabolism/physiology
*Carcinoma, Hepatocellular/therapy/microbiology
*Liver Neoplasms/therapy/microbiology
*Oncolytic Virotherapy/methods
Mice
Female
Homeostasis
Humans
Oncolytic Viruses/genetics
Mice, Inbred C57BL
Dysbiosis/microbiology
Cell Line, Tumor
STAT3 Transcription Factor/metabolism
Signal Transduction
RevDate: 2025-04-07
CmpDate: 2025-04-07
MetaDAVis: An R shiny application for metagenomic data analysis and visualization.
PloS one, 20(4):e0319949 pii:PONE-D-24-54435.
The human microbiome exerts tremendous influence on maintaining a balance between human health and disease. High-throughput sequencing has enabled the study of microbial communities at an unprecedented resolution. Generation of massive amounts of sequencing data has also presented novel challenges to analyzing and visualizing data to make biologically relevant interpretations. We have developed an interactive Metagenome Data Analysis and Visualization (MetaDAVis) tool for 16S rRNA as well as the whole genome sequencing data analysis and visualization to address these challenges using an R Shiny application. MetaDAVis can perform six different types of analyses that include: i) Taxonomic abundance distribution; ii) Alpha and beta diversity analyses; iii) Dimension reduction tasks using PCA, t-SNE, and UMAP; iv) Correlation analysis using taxa- or sample-based data; v) Heatmap generation; and vi) Differential abundance analysis. MetaDAVis creates interactive and dynamic figures and tables from multiple methods enabling users to easily understand their data using different variables. Our program is user-friendly and easily customizable allowing those without any programming background to perform comprehensive data analyses using a standalone or web-based interface.
Additional Links: PMID-40193328
Publisher:
PubMed:
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@article {pmid40193328,
year = {2025},
author = {Jagadesan, S and Guda, C},
title = {MetaDAVis: An R shiny application for metagenomic data analysis and visualization.},
journal = {PloS one},
volume = {20},
number = {4},
pages = {e0319949},
doi = {10.1371/journal.pone.0319949},
pmid = {40193328},
issn = {1932-6203},
mesh = {*Metagenomics/methods ; Humans ; RNA, Ribosomal, 16S/genetics ; *Software ; *Metagenome ; Microbiota/genetics ; High-Throughput Nucleotide Sequencing ; },
abstract = {The human microbiome exerts tremendous influence on maintaining a balance between human health and disease. High-throughput sequencing has enabled the study of microbial communities at an unprecedented resolution. Generation of massive amounts of sequencing data has also presented novel challenges to analyzing and visualizing data to make biologically relevant interpretations. We have developed an interactive Metagenome Data Analysis and Visualization (MetaDAVis) tool for 16S rRNA as well as the whole genome sequencing data analysis and visualization to address these challenges using an R Shiny application. MetaDAVis can perform six different types of analyses that include: i) Taxonomic abundance distribution; ii) Alpha and beta diversity analyses; iii) Dimension reduction tasks using PCA, t-SNE, and UMAP; iv) Correlation analysis using taxa- or sample-based data; v) Heatmap generation; and vi) Differential abundance analysis. MetaDAVis creates interactive and dynamic figures and tables from multiple methods enabling users to easily understand their data using different variables. Our program is user-friendly and easily customizable allowing those without any programming background to perform comprehensive data analyses using a standalone or web-based interface.},
}
MeSH Terms:
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*Metagenomics/methods
Humans
RNA, Ribosomal, 16S/genetics
*Software
*Metagenome
Microbiota/genetics
High-Throughput Nucleotide Sequencing
RevDate: 2025-04-07
Strategic use of nanomaterials as double-edged therapeutics to control carcinogenesis via regulation of dysbiosis and bacterial infection: current status and future prospects.
Journal of materials chemistry. B [Epub ahead of print].
The human microbiome plays a crucial role in modulating health and disease susceptibility through a complex network of interactions with the host. When the delicate balance of this microbial ecosystem is disrupted, it often correlates with the onset of systemic diseases. An over-abundance of pathogenic microorganisms within the microbiome has been implicated as a driving factor in the development of disease conditions such as diabetes, obesity, and chronic infections. It has been observed that microbiome dysbiosis perturbs metabolic, inflammatory, and immunological pathways, potentially facilitating carcinogenesis. Furthermore, the metabolites associated with microbial dysbiosis exert multifaceted effects, including metabolic interference, host DNA damage, and tumor promotion, further underscoring the microbiome's significance in several of the cancers. This new exploration of microbiome involvement in carcinogenesis needs additional patient sample analysis, which could provide new insights into cancer diagnosis and treatment. However, treating these diseases using drugs, traditional methods, etc. has resulted in multi-drug resistance, and this has eventually made the situation worrisome. This review highlights the importance of nanotechnology, which may tackle these pathogenic conditions simultaneously by targeting common receptors present in bacteria and cancer. Herein, we have explained how nanotechnology may come to the forefront for these treatments. It explores the potential of non-antibiotic disinfectants, i.e., nanoparticles (NPs) with dual targeting capabilities against microbes and cancer cells, using mechanisms such as ROS generation and DNA damage while minimizing the chances of drug resistance.
Additional Links: PMID-40192037
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PubMed:
Citation:
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@article {pmid40192037,
year = {2025},
author = {Verma, M and Randhawa, S and Bathla, M and Teji, N and Acharya, A},
title = {Strategic use of nanomaterials as double-edged therapeutics to control carcinogenesis via regulation of dysbiosis and bacterial infection: current status and future prospects.},
journal = {Journal of materials chemistry. B},
volume = {},
number = {},
pages = {},
doi = {10.1039/d4tb02409e},
pmid = {40192037},
issn = {2050-7518},
abstract = {The human microbiome plays a crucial role in modulating health and disease susceptibility through a complex network of interactions with the host. When the delicate balance of this microbial ecosystem is disrupted, it often correlates with the onset of systemic diseases. An over-abundance of pathogenic microorganisms within the microbiome has been implicated as a driving factor in the development of disease conditions such as diabetes, obesity, and chronic infections. It has been observed that microbiome dysbiosis perturbs metabolic, inflammatory, and immunological pathways, potentially facilitating carcinogenesis. Furthermore, the metabolites associated with microbial dysbiosis exert multifaceted effects, including metabolic interference, host DNA damage, and tumor promotion, further underscoring the microbiome's significance in several of the cancers. This new exploration of microbiome involvement in carcinogenesis needs additional patient sample analysis, which could provide new insights into cancer diagnosis and treatment. However, treating these diseases using drugs, traditional methods, etc. has resulted in multi-drug resistance, and this has eventually made the situation worrisome. This review highlights the importance of nanotechnology, which may tackle these pathogenic conditions simultaneously by targeting common receptors present in bacteria and cancer. Herein, we have explained how nanotechnology may come to the forefront for these treatments. It explores the potential of non-antibiotic disinfectants, i.e., nanoparticles (NPs) with dual targeting capabilities against microbes and cancer cells, using mechanisms such as ROS generation and DNA damage while minimizing the chances of drug resistance.},
}
RevDate: 2025-04-07
CmpDate: 2025-04-07
Patients with post-COVID-19 condition show minor blood transcriptomic changes, with altered erythrocyte gene expression in a male subgroup.
Frontiers in immunology, 16:1500997.
BACKGROUND: The mechanisms underlying persistent symptoms after non-severe COVID-19 remain unclear. This study aimed to investigate transcriptomic changes in peripheral blood cells of patients with post-COVID-19 condition (PCC) and assess if distinct clinical subtypes with specific gene signatures could be identified.
METHODS: The cohort included 111 PCC patients from the SARS-CoV-2 Omicron variant era, with 57 recovered (Recov) and 54 having prolonged symptoms indicative of PCC. The results were compared to 63 healthy controls (Ctrl) without known SARS-CoV-2 infection. Clinical data included patient assessments, laboratory results, comorbidities, and questionnaires on quality of life and functioning. Transcriptomic analysis and cellular deconvolution methods were used on total RNA from peripheral blood mononuclear cells (PBMCs).
RESULTS: PCC patients had more comorbidities (mean 1.3) and more frequently (59%) at least one comorbidity than recovered patients (31%) and controls (24%). Overall, past COVID-19 illness or current PCC symptoms caused minimal changes in the blood cell transcriptome, with only 3-6 differentially expressed genes (DEGs) identified across comparisons. However, a subset of male PCC patients exhibited an increased fraction of deconvoluted erythroblasts and significant genome-wide gene expression changes, with 399 DEGs compared to recovered and control males. These genes were enriched in pathways related to heme metabolism and gas exchange in erythrocytes.
CONCLUSIONS: Persistent symptoms in PCC are multifactorial and not directly linked to peripheral blood cell gene expression changes. However, a subgroup of male PCC patients shows distinct erythrocyte responses that may contribute to long-term symptoms.
Additional Links: PMID-40191210
PubMed:
Citation:
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@article {pmid40191210,
year = {2025},
author = {Karisola, P and Kanerva, M and Vuokko, A and Liira, H and Wang, S and KvarnstrΓΆm, K and Varonen, M and Suojalehto, H and Alenius, H},
title = {Patients with post-COVID-19 condition show minor blood transcriptomic changes, with altered erythrocyte gene expression in a male subgroup.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1500997},
pmid = {40191210},
issn = {1664-3224},
mesh = {Humans ; *COVID-19/genetics/blood/immunology/complications ; Male ; Middle Aged ; *Transcriptome ; *SARS-CoV-2 ; Aged ; *Erythrocytes/metabolism ; Female ; Adult ; Gene Expression Profiling ; Leukocytes, Mononuclear/metabolism ; Quality of Life ; },
abstract = {BACKGROUND: The mechanisms underlying persistent symptoms after non-severe COVID-19 remain unclear. This study aimed to investigate transcriptomic changes in peripheral blood cells of patients with post-COVID-19 condition (PCC) and assess if distinct clinical subtypes with specific gene signatures could be identified.
METHODS: The cohort included 111 PCC patients from the SARS-CoV-2 Omicron variant era, with 57 recovered (Recov) and 54 having prolonged symptoms indicative of PCC. The results were compared to 63 healthy controls (Ctrl) without known SARS-CoV-2 infection. Clinical data included patient assessments, laboratory results, comorbidities, and questionnaires on quality of life and functioning. Transcriptomic analysis and cellular deconvolution methods were used on total RNA from peripheral blood mononuclear cells (PBMCs).
RESULTS: PCC patients had more comorbidities (mean 1.3) and more frequently (59%) at least one comorbidity than recovered patients (31%) and controls (24%). Overall, past COVID-19 illness or current PCC symptoms caused minimal changes in the blood cell transcriptome, with only 3-6 differentially expressed genes (DEGs) identified across comparisons. However, a subset of male PCC patients exhibited an increased fraction of deconvoluted erythroblasts and significant genome-wide gene expression changes, with 399 DEGs compared to recovered and control males. These genes were enriched in pathways related to heme metabolism and gas exchange in erythrocytes.
CONCLUSIONS: Persistent symptoms in PCC are multifactorial and not directly linked to peripheral blood cell gene expression changes. However, a subgroup of male PCC patients shows distinct erythrocyte responses that may contribute to long-term symptoms.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*COVID-19/genetics/blood/immunology/complications
Male
Middle Aged
*Transcriptome
*SARS-CoV-2
Aged
*Erythrocytes/metabolism
Female
Adult
Gene Expression Profiling
Leukocytes, Mononuclear/metabolism
Quality of Life
RevDate: 2025-04-07
Hand-to-surface bacterial transfer and healthcare-associated infections prevention: a pilot study on skin microbiome in a molecular biology laboratory.
Frontiers in medicine, 12:1546298.
BACKGROUND: Healthcare-associated infections (HAIs) are a major global public health problem, contributing significantly to patient morbidity and mortality. This study analyses differences in type and amounts of bacteria transferred from volunteers' dominant palm to two healthcare-relevant surfaces (glass and laminate table), both before and after hand washing with water and antibacterial soap. The aim was to understand hand-to-surface microbial contamination and support the development of HAI prevention strategies.
METHODS: Microbial DNA was extracted and sequenced to identify bacteria species. Taxonomic and statistical analyses were performed to evaluate bacterial diversity and abundance across the experimental groups.
RESULTS: The results confirmed greater bacteria abundance and species richness on palm compared to surfaces, with a significant reduction after hand washing, especially on glass. Taxa analysis highlighted the increased persistence of Gram-negative HAIs-related bacteria on laminate surface, while Gram-positive opportunistic bacteria were more abundant on palms and glass surface. Beta diversity confirmed significant differences in microbial composition between the groups, highlighting the importance of bacteria-surface characteristics in designing preventive measures.
CONCLUSION: Despite some limitations, our study emphasizes the importance of microbiological surveillance for all opportunistic bacteria with pathogenic potential. These findings can contribute to more effective guidelines for surface disinfection and hand washing, key elements in preventing HAIs.
Additional Links: PMID-40190580
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@article {pmid40190580,
year = {2025},
author = {Delicati, A and Marcante, B and Catelan, D and Biggeri, A and Caenazzo, L and Tozzo, P},
title = {Hand-to-surface bacterial transfer and healthcare-associated infections prevention: a pilot study on skin microbiome in a molecular biology laboratory.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1546298},
pmid = {40190580},
issn = {2296-858X},
abstract = {BACKGROUND: Healthcare-associated infections (HAIs) are a major global public health problem, contributing significantly to patient morbidity and mortality. This study analyses differences in type and amounts of bacteria transferred from volunteers' dominant palm to two healthcare-relevant surfaces (glass and laminate table), both before and after hand washing with water and antibacterial soap. The aim was to understand hand-to-surface microbial contamination and support the development of HAI prevention strategies.
METHODS: Microbial DNA was extracted and sequenced to identify bacteria species. Taxonomic and statistical analyses were performed to evaluate bacterial diversity and abundance across the experimental groups.
RESULTS: The results confirmed greater bacteria abundance and species richness on palm compared to surfaces, with a significant reduction after hand washing, especially on glass. Taxa analysis highlighted the increased persistence of Gram-negative HAIs-related bacteria on laminate surface, while Gram-positive opportunistic bacteria were more abundant on palms and glass surface. Beta diversity confirmed significant differences in microbial composition between the groups, highlighting the importance of bacteria-surface characteristics in designing preventive measures.
CONCLUSION: Despite some limitations, our study emphasizes the importance of microbiological surveillance for all opportunistic bacteria with pathogenic potential. These findings can contribute to more effective guidelines for surface disinfection and hand washing, key elements in preventing HAIs.},
}
RevDate: 2025-04-06
CmpDate: 2025-04-06
Therapeutic potential of microbiome modulation in reproductive cancers.
Medical oncology (Northwood, London, England), 42(5):152.
The human microbiome, a complex ecosystem of microbial communities, plays a crucial role in physiological processes, and emerging research indicates a potential link between it and reproductive cancers. This connection highlights the significance of understanding the microbiome's influence on cancer development and treatment. A comprehensive review of current literature was conducted, focusing on studies that investigate the relationship between microbiome composition, reproductive cancer progression, and potential therapeutic approaches to modulate the microbiome. Evidence suggests that imbalances in the microbiome, known as dysbiosis, may contribute to the development and progression of reproductive cancers. Specific microbial populations have been associated with inflammatory responses, immune modulation, and even resistance to conventional therapies. Interventions such as probiotics, dietary modifications, and fecal microbiota transplantation have shown promise in restoring healthy microbiome function and improving cancer outcomes in pre-clinical models, with pilot studies in humans indicating potential benefits. This review explores the therapeutic potential of microbiome modulation in the management of reproductive cancers, discussing the mechanisms involved and the evidence supporting microbiome-targeted therapies. Future research is warranted to unravel the complex interactions between the microbiome and reproductive cancer pathophysiology, paving the way for innovative approaches.
Additional Links: PMID-40188410
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Citation:
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@article {pmid40188410,
year = {2025},
author = {Oyovwi, MO and Ben-Azu, B and Babawale, KH},
title = {Therapeutic potential of microbiome modulation in reproductive cancers.},
journal = {Medical oncology (Northwood, London, England)},
volume = {42},
number = {5},
pages = {152},
pmid = {40188410},
issn = {1559-131X},
mesh = {Humans ; *Microbiota ; Probiotics/therapeutic use ; Female ; Dysbiosis/microbiology/therapy ; *Genital Neoplasms, Female/microbiology/therapy ; Fecal Microbiota Transplantation/methods ; Animals ; Gastrointestinal Microbiome ; },
abstract = {The human microbiome, a complex ecosystem of microbial communities, plays a crucial role in physiological processes, and emerging research indicates a potential link between it and reproductive cancers. This connection highlights the significance of understanding the microbiome's influence on cancer development and treatment. A comprehensive review of current literature was conducted, focusing on studies that investigate the relationship between microbiome composition, reproductive cancer progression, and potential therapeutic approaches to modulate the microbiome. Evidence suggests that imbalances in the microbiome, known as dysbiosis, may contribute to the development and progression of reproductive cancers. Specific microbial populations have been associated with inflammatory responses, immune modulation, and even resistance to conventional therapies. Interventions such as probiotics, dietary modifications, and fecal microbiota transplantation have shown promise in restoring healthy microbiome function and improving cancer outcomes in pre-clinical models, with pilot studies in humans indicating potential benefits. This review explores the therapeutic potential of microbiome modulation in the management of reproductive cancers, discussing the mechanisms involved and the evidence supporting microbiome-targeted therapies. Future research is warranted to unravel the complex interactions between the microbiome and reproductive cancer pathophysiology, paving the way for innovative approaches.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
Probiotics/therapeutic use
Female
Dysbiosis/microbiology/therapy
*Genital Neoplasms, Female/microbiology/therapy
Fecal Microbiota Transplantation/methods
Animals
Gastrointestinal Microbiome
RevDate: 2025-04-03
Unlocking the healthy human microbiome: Redefining core microbial signatures.
Acta pharmaceutica Sinica. B, 15(2):1189-1192.
Additional Links: PMID-40177558
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@article {pmid40177558,
year = {2025},
author = {Xia, S and Jiang, D and Zhou, Q and Lyu, H and Voigt, AY and Zhou, X and Zhou, Z and Huang, Y},
title = {Unlocking the healthy human microbiome: Redefining core microbial signatures.},
journal = {Acta pharmaceutica Sinica. B},
volume = {15},
number = {2},
pages = {1189-1192},
doi = {10.1016/j.apsb.2025.01.001},
pmid = {40177558},
issn = {2211-3835},
}
RevDate: 2025-04-02
Embracing the unknown: Proteomic insights into the human microbiome.
Cell metabolism, 37(4):799-801.
Protein-level investigations into the human microbiome provide insights into active microbial functions. Recently, ValdΓ©s-Mas et al.[1] introduced a metagenome-informed metaproteomics approach to functionally explore species-level microbiome-host interactions and quantify the dietary exposome. Its potential has been implemented in mice and humans to uncover proteomic signatures of health and inflammatory bowel disease.
Additional Links: PMID-40174574
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@article {pmid40174574,
year = {2025},
author = {Zeng, S and Almeida, A and Mu, D and Wang, S},
title = {Embracing the unknown: Proteomic insights into the human microbiome.},
journal = {Cell metabolism},
volume = {37},
number = {4},
pages = {799-801},
doi = {10.1016/j.cmet.2025.02.003},
pmid = {40174574},
issn = {1932-7420},
abstract = {Protein-level investigations into the human microbiome provide insights into active microbial functions. Recently, ValdΓ©s-Mas et al.[1] introduced a metagenome-informed metaproteomics approach to functionally explore species-level microbiome-host interactions and quantify the dietary exposome. Its potential has been implemented in mice and humans to uncover proteomic signatures of health and inflammatory bowel disease.},
}
RevDate: 2025-04-02
CmpDate: 2025-04-02
Modulation of Host Immunity by Microbiome-Derived Indole-3-Propionic Acid and Other Bacterial Metabolites.
European journal of immunology, 55(4):e202451594.
In recent years, we have witnessed a rapidly growing interest in the intricate communications between intestinal microorganisms and the host immune system. Research on the human microbiome is evolving from merely descriptive and correlative studies to a deeper mechanistic understanding of the bidirectional interactions between gut microbiota and the mucosal immune system. Despite numerous challenges, it has become increasingly evident that an imbalance in gut microbiota composition, known as dysbiosis, is associated with the development and progression of various metabolic, immune, cancer, and neurodegenerative disorders. A growing body of evidence highlights the importance of small molecules produced by intestinal commensal bacteria, collectively referred to as gut microbial metabolites. These metabolites serve as crucial diffusible messengers, translating the microbial language to host cells. This review aims to explore the complex and not yet fully understood molecular mechanisms through which microbiota-derived metabolites influence the activity of the immune cells and shape immune reactions in the gut and other organs. Specifically, we will discuss recent research that reveals the close relationship between microbial indole-3-propionic acid (IPA) and mucosal immunity. Furthermore, we will emphasize the beneficial effects of IPA on intestinal inflammation and discuss its potential clinical implications.
Additional Links: PMID-40170399
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PubMed:
Citation:
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@article {pmid40170399,
year = {2025},
author = {SchΓΌtz, B and Krause, FF and Taudte, RV and Zaiss, MM and Luu, M and Visekruna, A},
title = {Modulation of Host Immunity by Microbiome-Derived Indole-3-Propionic Acid and Other Bacterial Metabolites.},
journal = {European journal of immunology},
volume = {55},
number = {4},
pages = {e202451594},
doi = {10.1002/eji.202451594},
pmid = {40170399},
issn = {1521-4141},
support = {VI562/7-1//Deutsche Forschungsgemeinschaft/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Indoles/immunology ; Animals ; Immunity, Mucosal/immunology ; Dysbiosis/immunology ; Bacteria/immunology/metabolism ; Propionates ; },
abstract = {In recent years, we have witnessed a rapidly growing interest in the intricate communications between intestinal microorganisms and the host immune system. Research on the human microbiome is evolving from merely descriptive and correlative studies to a deeper mechanistic understanding of the bidirectional interactions between gut microbiota and the mucosal immune system. Despite numerous challenges, it has become increasingly evident that an imbalance in gut microbiota composition, known as dysbiosis, is associated with the development and progression of various metabolic, immune, cancer, and neurodegenerative disorders. A growing body of evidence highlights the importance of small molecules produced by intestinal commensal bacteria, collectively referred to as gut microbial metabolites. These metabolites serve as crucial diffusible messengers, translating the microbial language to host cells. This review aims to explore the complex and not yet fully understood molecular mechanisms through which microbiota-derived metabolites influence the activity of the immune cells and shape immune reactions in the gut and other organs. Specifically, we will discuss recent research that reveals the close relationship between microbial indole-3-propionic acid (IPA) and mucosal immunity. Furthermore, we will emphasize the beneficial effects of IPA on intestinal inflammation and discuss its potential clinical implications.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/immunology
*Indoles/immunology
Animals
Immunity, Mucosal/immunology
Dysbiosis/immunology
Bacteria/immunology/metabolism
Propionates
RevDate: 2025-04-01
Prophages as a source of antimicrobial resistance genes in the human microbiome.
bioRxiv : the preprint server for biology pii:2025.03.19.644263.
UNLABELLED: Prophages-viruses that integrate into bacterial genomes-are ubiquitous in the microbial realm. Prophages contribute significantly to horizontal gene transfer, including the potential spread of antimicrobial resistance (AMR) genes, because they can collect host genes. Understanding their role in the human microbiome is essential for fully understanding AMR dynamics and possible clinical implications. We analysed almost 15,000 bacterial genomes for prophages and AMR genes. The bacteria were isolated from diverse human body sites and geographical regions, and their genomes were retrieved from GenBank. AMR genes were detected in 6.6% of bacterial genomes, with a higher prevalence in people with symptomatic diseases. We found a wide variety of AMR genes combating multiple drug classes. We discovered AMR genes previously associated with plasmids, such as blaOXA-23 in Acinetobacter baumannii prophages or genes found in prophages in species they had not been previously described in, such as mefA-msrD in Gardnerella prophages, suggesting prophage-mediated gene transfer of AMR genes. Prophages encoding AMR genes were found at varying frequencies across body sites and geographical regions, with Asia showing the highest diversity of AMR genes.
IMPORTANCE: Antimicrobial resistance (AMR) is a growing threat to public health, and understanding how resistance genes spread between bacteria is essential for controlling their dissemination. Bacteriophages, viruses that infect bacteria, have been recognised as potential vehicles for transferring these resistance genes, but their role in the human microbiome remains poorly understood. We examined nearly 15,000 bacterial genomes from various human body sites and regions worldwide to investigate how often prophages carry AMR genes in the human microbiome. Although AMR genes were uncommon in prophages, we identified diverse resistance genes across multiple bacterial species and drug classes, including some typically associated with plasmids. These findings reveal that prophages may contribute to the spread of resistance genes, highlighting an overlooked mechanism in the dynamics of AMR transmission. Ongoing monitoring of prophages is critical to fully understanding the pathways through which resistance genes move within microbial communities and impact human health.
Additional Links: PMID-40166311
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@article {pmid40166311,
year = {2025},
author = {Inglis, LK and Grigson, SR and Roach, MJ and Edwards, RA},
title = {Prophages as a source of antimicrobial resistance genes in the human microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.03.19.644263},
pmid = {40166311},
issn = {2692-8205},
abstract = {UNLABELLED: Prophages-viruses that integrate into bacterial genomes-are ubiquitous in the microbial realm. Prophages contribute significantly to horizontal gene transfer, including the potential spread of antimicrobial resistance (AMR) genes, because they can collect host genes. Understanding their role in the human microbiome is essential for fully understanding AMR dynamics and possible clinical implications. We analysed almost 15,000 bacterial genomes for prophages and AMR genes. The bacteria were isolated from diverse human body sites and geographical regions, and their genomes were retrieved from GenBank. AMR genes were detected in 6.6% of bacterial genomes, with a higher prevalence in people with symptomatic diseases. We found a wide variety of AMR genes combating multiple drug classes. We discovered AMR genes previously associated with plasmids, such as blaOXA-23 in Acinetobacter baumannii prophages or genes found in prophages in species they had not been previously described in, such as mefA-msrD in Gardnerella prophages, suggesting prophage-mediated gene transfer of AMR genes. Prophages encoding AMR genes were found at varying frequencies across body sites and geographical regions, with Asia showing the highest diversity of AMR genes.
IMPORTANCE: Antimicrobial resistance (AMR) is a growing threat to public health, and understanding how resistance genes spread between bacteria is essential for controlling their dissemination. Bacteriophages, viruses that infect bacteria, have been recognised as potential vehicles for transferring these resistance genes, but their role in the human microbiome remains poorly understood. We examined nearly 15,000 bacterial genomes from various human body sites and regions worldwide to investigate how often prophages carry AMR genes in the human microbiome. Although AMR genes were uncommon in prophages, we identified diverse resistance genes across multiple bacterial species and drug classes, including some typically associated with plasmids. These findings reveal that prophages may contribute to the spread of resistance genes, highlighting an overlooked mechanism in the dynamics of AMR transmission. Ongoing monitoring of prophages is critical to fully understanding the pathways through which resistance genes move within microbial communities and impact human health.},
}
RevDate: 2025-04-01
FRUCTOSE ACTIVATES A STRESS RESPONSE SHARED BY METHYLGLYOXAL AND HYDROGEN PEROXIDE IN STREPTOCOCCUS MUTANS.
bioRxiv : the preprint server for biology pii:2024.10.26.620100.
Fructose catabolism by Streptococcus mutans is initiated by three PTS transporters yielding either fructose-1-phoshate (F-1-P) or fructose-6-phosphate (F-6-P). Deletion of one such F-1-P-generating PTS, fruI, has been shown to reduce the cariogenicity of S. mutans in rats fed a high-sucrose diet. Moreover, a recent study linked fructose metabolism in S. mutans to a reactive electrophile species (RES) methylglyoxal. Here, we conducted a comparative transcriptomic analysis of exponentially grown S. mutans shocked with 50 mM fructose, 50 mM glucose, 5 mM methylglyoxal, or 0.5 mM hydrogen peroxide (H2O2). The results revealed a striking overlap between the fructose and methylglyoxal transcriptomes, totaling 176 genes, 61 of which were also shared with the H2O2 transcriptome. This core of 61 genes encompassed many of the same pathways affected by exposure to low pH or zinc intoxication. Consistent with these findings, fructose negatively impacted metal homeostasis of a mutant deficient in zinc expulsion and the growth of a mutant of the major oxidative stress regulator SpxA1. We further demonstrated the induction of the superoxide dismutase (sodA) and the fruRKI operon by different levels of fructose. Finally, fructose metabolism lowered culture pH at a faster pace, allowed better survival under acidic and nutrient-depleted conditions, and enhanced the competitiveness of S. mutans against Streptococcus sanguinis, although a moderated level of F-1-P might further boost some of these benefits. In conclusion, fructose metabolism is integrated into the stress core of S. mutans and regulates critical functions required for survival in both the oral cavity and during systemic infections. Importance. Fructose is a common monosaccharide in the biosphere, yet its overconsumption has been linked to various health problems in humans including insulin resistance, obesity, diabetes, and non-alcoholic liver diseases. These effects are in large part attributed to the unique biochemical characteristics and metabolic responses associated with the degradation of fructose. Yet, an understanding of the effects of fructose on the physiology of bacteria and its implications to the human microbiome is severely lacking. Here we performed a series of analyses on the gene regulation of a dental pathogen Streptococcus mutans by exposing it to fructose and other important stress agents. Further supported by growth, persistence, and competition assays, our findings revealed the ability of fructose to activate a set of cellular functions that may prove critical to the ability of the bacterium to persist and cause diseases both within and without of the oral cavity.
Additional Links: PMID-40166302
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@article {pmid40166302,
year = {2025},
author = {Walker, AR and Pham, DN and Noeparvar, P and Peterson, AM and Lipp, MK and Lemos, JA and Zeng, L},
title = {FRUCTOSE ACTIVATES A STRESS RESPONSE SHARED BY METHYLGLYOXAL AND HYDROGEN PEROXIDE IN STREPTOCOCCUS MUTANS.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.10.26.620100},
pmid = {40166302},
issn = {2692-8205},
abstract = {Fructose catabolism by Streptococcus mutans is initiated by three PTS transporters yielding either fructose-1-phoshate (F-1-P) or fructose-6-phosphate (F-6-P). Deletion of one such F-1-P-generating PTS, fruI, has been shown to reduce the cariogenicity of S. mutans in rats fed a high-sucrose diet. Moreover, a recent study linked fructose metabolism in S. mutans to a reactive electrophile species (RES) methylglyoxal. Here, we conducted a comparative transcriptomic analysis of exponentially grown S. mutans shocked with 50 mM fructose, 50 mM glucose, 5 mM methylglyoxal, or 0.5 mM hydrogen peroxide (H2O2). The results revealed a striking overlap between the fructose and methylglyoxal transcriptomes, totaling 176 genes, 61 of which were also shared with the H2O2 transcriptome. This core of 61 genes encompassed many of the same pathways affected by exposure to low pH or zinc intoxication. Consistent with these findings, fructose negatively impacted metal homeostasis of a mutant deficient in zinc expulsion and the growth of a mutant of the major oxidative stress regulator SpxA1. We further demonstrated the induction of the superoxide dismutase (sodA) and the fruRKI operon by different levels of fructose. Finally, fructose metabolism lowered culture pH at a faster pace, allowed better survival under acidic and nutrient-depleted conditions, and enhanced the competitiveness of S. mutans against Streptococcus sanguinis, although a moderated level of F-1-P might further boost some of these benefits. In conclusion, fructose metabolism is integrated into the stress core of S. mutans and regulates critical functions required for survival in both the oral cavity and during systemic infections. Importance. Fructose is a common monosaccharide in the biosphere, yet its overconsumption has been linked to various health problems in humans including insulin resistance, obesity, diabetes, and non-alcoholic liver diseases. These effects are in large part attributed to the unique biochemical characteristics and metabolic responses associated with the degradation of fructose. Yet, an understanding of the effects of fructose on the physiology of bacteria and its implications to the human microbiome is severely lacking. Here we performed a series of analyses on the gene regulation of a dental pathogen Streptococcus mutans by exposing it to fructose and other important stress agents. Further supported by growth, persistence, and competition assays, our findings revealed the ability of fructose to activate a set of cellular functions that may prove critical to the ability of the bacterium to persist and cause diseases both within and without of the oral cavity.},
}
RevDate: 2025-03-31
Comparative analysis of oral microbiome in molar-incisor-hypomineralization vs healthy age-matched controls.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: Molar-incisor-hypomineralization (MIH) is one of the most challenging dental diseases in children. While the association of oral microbiomes with caries and periodontitis has been studied thoroughly, limited data on the microbial composition in MIH and its clinical significance exist. This cross-sectional study aimed to compare the supragingival plaque microbiome between children and adolescents affected by MIH and a healthy age-matched control group. Ninety-five patients aged 7-17 years were recruited at the Department of Conservative Dentistry, Heidelberg University Hospital. The final sample included 29 participants with a confirmed diagnosis of MIH, treated preventively and restoratively, and 35 orally healthy controls. Clinical data were obtained, and supragingival plaque samples were collected using OMNIgene ORAL OMR-110 (DNA Genotek Inc.), followed by 16S rRNA amplicon sequencing. The microbiome composition was analyzed using Ξ±-diversity (Shannon index) and evenness (Pielou index), with group differences assessed using permutational multivariate analysis of variance (PERMANOVA) and MaAsLin2. The overall microbiome composition showed mostly similarities between both groups (PERMANOVA: R[2] = 0.019, P-value = 0.287), indicating no major dysbiosis. However, a significant decrease in Ξ±-diversity and evenness was observed with an increasing number of MIH-affected teeth. Pronounced positive correlations were found between ASV0055 (Streptococcus spp.), caries experience, and MIH severity. ASV0100 (Mannheimia sp.) increased significantly with the increasing number of MIH-affected teeth, whereas ASV0053 (Bergeyella sp.) decreased with higher caries experience. In summary, the oral microbiome of children and adolescents with MIH exhibits no significant differences from healthy children and adolescents of the same age group. Depending on MIH severity, the presence of early plaque-forming species and cariogenic biofilm may increase, requiring intensive, tailored preventive care and appropriate restorative treatment to achieve microbial homeostasis.
IMPORTANCE: Molar-incisor-hypomineralization (MIH) represents a significant burden for affected children and adolescents, playing an increasingly important role in pediatric dentistry worldwide. Despite its high global prevalence, data on the microbiome of MIH patients remains limited. This study is the first to compare the oral microbiome composition of MIH patients with a healthy control group, making a significant contribution to pediatric dentistry and microbiology. Our results indicate that the oral microbiome of children with MIH is similar to that of healthy children of the same age. Although this structural anomaly predisposes patients to caries, effective preventive and restorative treatments can help maintain microbial homeostasis. However, MIH-affected children remain high-risk patients, as the disease severity may reduce microbial diversity. Furthermore, the increased abundance of Streptococcus spp. in MIH patients indicates a higher caries susceptibility, emphasizing the need for targeted dental care focusing on plaque control and topical fluoride use.
Additional Links: PMID-40162761
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PubMed:
Citation:
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@article {pmid40162761,
year = {2025},
author = {Jung, M and Boutin, S and Simon, MM and Frese, C},
title = {Comparative analysis of oral microbiome in molar-incisor-hypomineralization vs healthy age-matched controls.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0289724},
doi = {10.1128/spectrum.02897-24},
pmid = {40162761},
issn = {2165-0497},
abstract = {UNLABELLED: Molar-incisor-hypomineralization (MIH) is one of the most challenging dental diseases in children. While the association of oral microbiomes with caries and periodontitis has been studied thoroughly, limited data on the microbial composition in MIH and its clinical significance exist. This cross-sectional study aimed to compare the supragingival plaque microbiome between children and adolescents affected by MIH and a healthy age-matched control group. Ninety-five patients aged 7-17 years were recruited at the Department of Conservative Dentistry, Heidelberg University Hospital. The final sample included 29 participants with a confirmed diagnosis of MIH, treated preventively and restoratively, and 35 orally healthy controls. Clinical data were obtained, and supragingival plaque samples were collected using OMNIgene ORAL OMR-110 (DNA Genotek Inc.), followed by 16S rRNA amplicon sequencing. The microbiome composition was analyzed using Ξ±-diversity (Shannon index) and evenness (Pielou index), with group differences assessed using permutational multivariate analysis of variance (PERMANOVA) and MaAsLin2. The overall microbiome composition showed mostly similarities between both groups (PERMANOVA: R[2] = 0.019, P-value = 0.287), indicating no major dysbiosis. However, a significant decrease in Ξ±-diversity and evenness was observed with an increasing number of MIH-affected teeth. Pronounced positive correlations were found between ASV0055 (Streptococcus spp.), caries experience, and MIH severity. ASV0100 (Mannheimia sp.) increased significantly with the increasing number of MIH-affected teeth, whereas ASV0053 (Bergeyella sp.) decreased with higher caries experience. In summary, the oral microbiome of children and adolescents with MIH exhibits no significant differences from healthy children and adolescents of the same age group. Depending on MIH severity, the presence of early plaque-forming species and cariogenic biofilm may increase, requiring intensive, tailored preventive care and appropriate restorative treatment to achieve microbial homeostasis.
IMPORTANCE: Molar-incisor-hypomineralization (MIH) represents a significant burden for affected children and adolescents, playing an increasingly important role in pediatric dentistry worldwide. Despite its high global prevalence, data on the microbiome of MIH patients remains limited. This study is the first to compare the oral microbiome composition of MIH patients with a healthy control group, making a significant contribution to pediatric dentistry and microbiology. Our results indicate that the oral microbiome of children with MIH is similar to that of healthy children of the same age. Although this structural anomaly predisposes patients to caries, effective preventive and restorative treatments can help maintain microbial homeostasis. However, MIH-affected children remain high-risk patients, as the disease severity may reduce microbial diversity. Furthermore, the increased abundance of Streptococcus spp. in MIH patients indicates a higher caries susceptibility, emphasizing the need for targeted dental care focusing on plaque control and topical fluoride use.},
}
RevDate: 2025-03-31
Assessment of ecological fidelity of human microbiome-associated mice in observational studies and an interventional trial.
bioRxiv : the preprint server for biology pii:2025.03.11.642547.
UNLABELLED: Composition and function of the gut microbiome is associated with diverse health conditions and treatment responses. Human microbiota-associated (HMA) mouse models are used to establish causal links for these associations but have important limitations. We assessed the fidelity of HMA mouse models to recapitulate ecological responses to a microbial consortium using stools collected from a human clinical trial. HMA mice were generated using different routes of consortium exposure and their ecological features were compared to human donors by metagenomic sequencing. HMA mice were more similar in gut composition to other mice than their respective human donors, with taxa including Akkermansia muciniphila and Bacteroides species enriched in mouse recipients. A limited repertoire of microbes was able to engraft into HMA mice regardless of route of consortium exposure. In publicly available HMA mouse datasets from four distinct health conditions, we confirmed our observation that a taxonomically restricted set of microbes reproducibly engrafts in HMA mice and observed that stool microbiome composition of HMA mice were more like other mice than their human donor. Our data suggest that HMA mice are limited models to assess the ecological impact of microbial consortia, with ecological effects in HMA mice being more strongly associated with host species than donor stool ecology or ecological responses to treatment in humans. Comparisons to published studies suggest this may be due to comparatively large host-species effects that overwhelm ecological effects of treatment in humans that HMA models aim to recapitulate.
IMPORTANCE: Human microbiota-associated (HMA) mice are models that better represent human gut ecology compared to conventional laboratory mice and are commonly used to test the effect of the gut microbiome on disease or treatment response. We evaluated the fidelity of using HMA mice as avatars of ecological response to a human microbial consortium, MET4. Our results show that HMA mice in our cohort and across other published studies are more similar to each other than the human donors or inoculum they are derived from and harbour a taxonomically restricted gut microbiome. These findings highlight the limitations of HMA mice in evaluating the ecological effects of complex human microbiome-targeting interventions, such as microbial consortia.
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@article {pmid40161742,
year = {2025},
author = {Wong, MK and Armstrong, E and Heirali, AA and Schneeberger, PHH and Chen, H and Cochrane, K and Sherriff, K and Allen-Vercoe, E and Siu, LL and Spreafico, A and Coburn, B},
title = {Assessment of ecological fidelity of human microbiome-associated mice in observational studies and an interventional trial.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.03.11.642547},
pmid = {40161742},
issn = {2692-8205},
abstract = {UNLABELLED: Composition and function of the gut microbiome is associated with diverse health conditions and treatment responses. Human microbiota-associated (HMA) mouse models are used to establish causal links for these associations but have important limitations. We assessed the fidelity of HMA mouse models to recapitulate ecological responses to a microbial consortium using stools collected from a human clinical trial. HMA mice were generated using different routes of consortium exposure and their ecological features were compared to human donors by metagenomic sequencing. HMA mice were more similar in gut composition to other mice than their respective human donors, with taxa including Akkermansia muciniphila and Bacteroides species enriched in mouse recipients. A limited repertoire of microbes was able to engraft into HMA mice regardless of route of consortium exposure. In publicly available HMA mouse datasets from four distinct health conditions, we confirmed our observation that a taxonomically restricted set of microbes reproducibly engrafts in HMA mice and observed that stool microbiome composition of HMA mice were more like other mice than their human donor. Our data suggest that HMA mice are limited models to assess the ecological impact of microbial consortia, with ecological effects in HMA mice being more strongly associated with host species than donor stool ecology or ecological responses to treatment in humans. Comparisons to published studies suggest this may be due to comparatively large host-species effects that overwhelm ecological effects of treatment in humans that HMA models aim to recapitulate.
IMPORTANCE: Human microbiota-associated (HMA) mice are models that better represent human gut ecology compared to conventional laboratory mice and are commonly used to test the effect of the gut microbiome on disease or treatment response. We evaluated the fidelity of using HMA mice as avatars of ecological response to a human microbial consortium, MET4. Our results show that HMA mice in our cohort and across other published studies are more similar to each other than the human donors or inoculum they are derived from and harbour a taxonomically restricted gut microbiome. These findings highlight the limitations of HMA mice in evaluating the ecological effects of complex human microbiome-targeting interventions, such as microbial consortia.},
}
RevDate: 2025-03-30
Unraveling the potential of bioengineered microbiome-based strategies to enhance cancer immunotherapy.
Microbiological research, 296:128156 pii:S0944-5013(25)00112-0 [Epub ahead of print].
The human microbiome plays a pivotal role in the field of cancer immunotherapy. The microbial communities that inhabit the gastrointestinal tract, as well as the bacterial populations within tumors, have been identified as key modulators of therapeutic outcomes, affecting immune responses and reprogramming the tumor microenvironment. Advances in synthetic biology have made it possible to reprogram and engineer these microorganisms to improve antitumor activity, enhance T-cell function, and enable targeted delivery of therapies to neoplasms. This review discusses the role of the microbiome in modulating both innate and adaptive immune mechanisms-ranging from the initiation of cytokine production and antigen presentation to the regulation of immune checkpoints-and discusses how these mechanisms improve the efficacy of immune checkpoint inhibitors. We highlight significant advances with bioengineered strains like Escherichia coli Nissle 1917, Lactococcus lactis, Bifidobacterium, and Bacteroides, which have shown promising antitumor efficacy in preclinical models. These engineered microorganisms not only efficiently colonize tumor tissues but also help overcome resistance to standard therapies by reprogramming the local immune environment. Nevertheless, several challenges remain, such as the requirement for genetic stability, effective tumor colonization, and the control of potential safety issues. In the future, the ongoing development of genetic engineering tools and the optimization of bacterial delivery systems are crucial for the translation of microbiome-based therapies into the clinic. This review highlights the potential of bioengineered microbiota as an innovative, personalized approach in cancer immunotherapy, bringing hope for more effective and personalized treatment options for patients with advanced malignancies.
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@article {pmid40158322,
year = {2025},
author = {Hamza, M and Wang, S and Liu, Y and Li, K and Zhu, M and Chen, L},
title = {Unraveling the potential of bioengineered microbiome-based strategies to enhance cancer immunotherapy.},
journal = {Microbiological research},
volume = {296},
number = {},
pages = {128156},
doi = {10.1016/j.micres.2025.128156},
pmid = {40158322},
issn = {1618-0623},
abstract = {The human microbiome plays a pivotal role in the field of cancer immunotherapy. The microbial communities that inhabit the gastrointestinal tract, as well as the bacterial populations within tumors, have been identified as key modulators of therapeutic outcomes, affecting immune responses and reprogramming the tumor microenvironment. Advances in synthetic biology have made it possible to reprogram and engineer these microorganisms to improve antitumor activity, enhance T-cell function, and enable targeted delivery of therapies to neoplasms. This review discusses the role of the microbiome in modulating both innate and adaptive immune mechanisms-ranging from the initiation of cytokine production and antigen presentation to the regulation of immune checkpoints-and discusses how these mechanisms improve the efficacy of immune checkpoint inhibitors. We highlight significant advances with bioengineered strains like Escherichia coli Nissle 1917, Lactococcus lactis, Bifidobacterium, and Bacteroides, which have shown promising antitumor efficacy in preclinical models. These engineered microorganisms not only efficiently colonize tumor tissues but also help overcome resistance to standard therapies by reprogramming the local immune environment. Nevertheless, several challenges remain, such as the requirement for genetic stability, effective tumor colonization, and the control of potential safety issues. In the future, the ongoing development of genetic engineering tools and the optimization of bacterial delivery systems are crucial for the translation of microbiome-based therapies into the clinic. This review highlights the potential of bioengineered microbiota as an innovative, personalized approach in cancer immunotherapy, bringing hope for more effective and personalized treatment options for patients with advanced malignancies.},
}
RevDate: 2025-03-29
CmpDate: 2025-03-29
Modeling microbiome-trait associations with taxonomy-adaptive neural networks.
Microbiome, 13(1):87.
The human microbiome, a complex ecosystem of microorganisms inhabiting the body, plays a critical role in human health. Investigating its association with host traits is essential for understanding its impact on various diseases. Although shotgun metagenomic sequencing technologies have produced vast amounts of microbiome data, analyzing such data is highly challenging due to its sparsity, noisiness, and high feature dimensionality. Here, we develop MIOSTONE, an accurate and interpretable neural network model for microbiome-disease association that simulates a real taxonomy by encoding the relationships among microbial features. The taxonomy-encoding architecture provides a natural bridge from variations in microbial taxa abundance to variations in traits, encompassing increasingly coarse scales from species to domains. MIOSTONE has the ability to determine whether taxa within the corresponding taxonomic group provide a better explanation in a data-driven manner. MIOSTONE serves as an effective predictive model, as it not only accurately predicts microbiome-trait associations across extensive simulated and real datasets but also offers interpretability for scientific discovery. Both attributes are crucial for facilitating in silico investigations into the biological mechanisms underlying such associations among microbial taxa. Video Abstract.
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@article {pmid40158141,
year = {2025},
author = {Jiang, Y and Aton, M and Zhu, Q and Lu, YY},
title = {Modeling microbiome-trait associations with taxonomy-adaptive neural networks.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {87},
pmid = {40158141},
issn = {2049-2618},
support = {RGPIN-03270-2023//Canadian NSERC Discovery Grant/ ; RGPIN-03270-2023//Canadian NSERC Discovery Grant/ ; },
mesh = {Humans ; *Neural Networks, Computer ; *Microbiota ; Metagenomics/methods ; Bacteria/classification/genetics ; Computer Simulation ; },
abstract = {The human microbiome, a complex ecosystem of microorganisms inhabiting the body, plays a critical role in human health. Investigating its association with host traits is essential for understanding its impact on various diseases. Although shotgun metagenomic sequencing technologies have produced vast amounts of microbiome data, analyzing such data is highly challenging due to its sparsity, noisiness, and high feature dimensionality. Here, we develop MIOSTONE, an accurate and interpretable neural network model for microbiome-disease association that simulates a real taxonomy by encoding the relationships among microbial features. The taxonomy-encoding architecture provides a natural bridge from variations in microbial taxa abundance to variations in traits, encompassing increasingly coarse scales from species to domains. MIOSTONE has the ability to determine whether taxa within the corresponding taxonomic group provide a better explanation in a data-driven manner. MIOSTONE serves as an effective predictive model, as it not only accurately predicts microbiome-trait associations across extensive simulated and real datasets but also offers interpretability for scientific discovery. Both attributes are crucial for facilitating in silico investigations into the biological mechanisms underlying such associations among microbial taxa. Video Abstract.},
}
MeSH Terms:
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Humans
*Neural Networks, Computer
*Microbiota
Metagenomics/methods
Bacteria/classification/genetics
Computer Simulation
RevDate: 2025-03-29
Travel to low- and middle-income countries and travellers' diarrhoea increase risk of mismatching antimicrobial therapy for urinary tract infection.
Journal of travel medicine pii:8099361 [Epub ahead of print].
BACKGROUND: Travel to low- and middle-income countries (LMICs) increases the risk of urinary tract infections (UTIs), including those caused by extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-PE). Focusing on international travel, we explored resistance profiles of urinary ESBL-PE and non-ESBL-PE isolates in a low antimicrobial resistance prevalence country and factors associated with UTI treatment failure.
METHODS: During 2015-19, we recruited 18-65-year-old individuals with recent ESBL-PE UTI and a respective cohort of those with non-ESBL-PE UTI to complete questionnaires on symptoms, antibiotic therapies, and treatment failure risk factors. We compared uropathogens' resistance profiles among patients with or without LMIC travel history and conducted multivariable analyses to identify factors contributing to mismatching antimicrobial treatment (uropathogen resistant to the initial antimicrobial used) and clinical failure.
RESULTS: Among non-ESBL-PE UTI patients (n = 187), trimethoprim resistance was more common in isolates from individuals with recent LMIC travel (8/19, 42.1%) compared to those without (30/167, 18.0%) (OR 3.3, CI95% 1.2-9.0). ESBL-PE isolates (n = 130) showed no differences in resistance profiles with respect to LMIC travel history.In the group non-ESBL-PE UTI, risk factors included microbiological mismatching recent LMIC travel (AOR 3.6, CI95% 1.0-12.7) and travellers' diarrhoea (AOR 7.1, CI95% 1.1-45.6); no factors were significantly associated with mismatching in the group ESBL-PE UTI. As risk factors for clinical failure, in the group non-ESBL-PE UTI, we identified microbiological mismatching (AOR 15.2, CI95% 4.0-57.9), and renal/bladder disease (AOR 5.2, CI95% 1.1-23.2), and in the group ESBL-PE UTI, microbiological mismatching (AOR 8.1, CI95% 2.6-24.7).
CONCLUSIONS: LMIC travel increases the risk of nonmatching empiric antimicrobials, concurring with increased trimethoprim resistance rates among the non-ESBL-PE isolates. Our data suggest that UTI patients with recent LMIC travel should not be empirically treated with trimethoprim and, when possible, urinary culturing is warranted.
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@article {pmid40156096,
year = {2025},
author = {Patjas, A and Kantele, A},
title = {Travel to low- and middle-income countries and travellers' diarrhoea increase risk of mismatching antimicrobial therapy for urinary tract infection.},
journal = {Journal of travel medicine},
volume = {},
number = {},
pages = {},
doi = {10.1093/jtm/taaf025},
pmid = {40156096},
issn = {1708-8305},
abstract = {BACKGROUND: Travel to low- and middle-income countries (LMICs) increases the risk of urinary tract infections (UTIs), including those caused by extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-PE). Focusing on international travel, we explored resistance profiles of urinary ESBL-PE and non-ESBL-PE isolates in a low antimicrobial resistance prevalence country and factors associated with UTI treatment failure.
METHODS: During 2015-19, we recruited 18-65-year-old individuals with recent ESBL-PE UTI and a respective cohort of those with non-ESBL-PE UTI to complete questionnaires on symptoms, antibiotic therapies, and treatment failure risk factors. We compared uropathogens' resistance profiles among patients with or without LMIC travel history and conducted multivariable analyses to identify factors contributing to mismatching antimicrobial treatment (uropathogen resistant to the initial antimicrobial used) and clinical failure.
RESULTS: Among non-ESBL-PE UTI patients (n = 187), trimethoprim resistance was more common in isolates from individuals with recent LMIC travel (8/19, 42.1%) compared to those without (30/167, 18.0%) (OR 3.3, CI95% 1.2-9.0). ESBL-PE isolates (n = 130) showed no differences in resistance profiles with respect to LMIC travel history.In the group non-ESBL-PE UTI, risk factors included microbiological mismatching recent LMIC travel (AOR 3.6, CI95% 1.0-12.7) and travellers' diarrhoea (AOR 7.1, CI95% 1.1-45.6); no factors were significantly associated with mismatching in the group ESBL-PE UTI. As risk factors for clinical failure, in the group non-ESBL-PE UTI, we identified microbiological mismatching (AOR 15.2, CI95% 4.0-57.9), and renal/bladder disease (AOR 5.2, CI95% 1.1-23.2), and in the group ESBL-PE UTI, microbiological mismatching (AOR 8.1, CI95% 2.6-24.7).
CONCLUSIONS: LMIC travel increases the risk of nonmatching empiric antimicrobials, concurring with increased trimethoprim resistance rates among the non-ESBL-PE isolates. Our data suggest that UTI patients with recent LMIC travel should not be empirically treated with trimethoprim and, when possible, urinary culturing is warranted.},
}
RevDate: 2025-03-29
CmpDate: 2025-03-29
Large-scale biosynthetic analysis of human microbiomes reveals diverse protective ribosomal peptides.
Nature communications, 16(1):3054.
The human microbiome produces diverse metabolites that influence host health, yet the chemical landscape of ribosomally synthesized and post-translationally modified peptides (RiPPs)-a versatile class of bioactive compounds-remains underexplored. Here, we conduct a large-scale biosynthetic analysis of 306,481 microbial genomes from human-associated microbiomes, uncovering a broad array of yet-to-be-discovered RiPPs. These RiPPs are distributed across various body sites but show a specific enrichment in the gut and oral microbiome. Big data omics analysis reveals that numerous RiPP families are inversely related to various diseases, suggesting their potential protective effects on health. For a proof of principle study, we apply the synthetic-bioinformatic natural product (syn-BNP) approach to RiPPs and chemically synthesize nine autoinducing peptides (AIPs) for in vitro and ex vivo assay. Our findings reveal that five AIPs effectively inhibit the biofilm formation of disease-associated pathogens. Furthermore, when ex vivo testing gut microbiota from mice with inflammatory bowel disease, we observe that two AIPs can regulate the microbial community and reduce harmful species. These findings highlight the vast potential of human microbial RiPPs in regulating microbial communities and maintaining human health, emphasizing their potential for therapeutic development.
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@article {pmid40155374,
year = {2025},
author = {Zhang, J and Zhang, D and Xu, Y and Zhang, J and Liu, R and Gao, Y and Shi, Y and Cai, P and Zhong, Z and He, B and Li, X and Zhou, H and Chen, M and Li, YX},
title = {Large-scale biosynthetic analysis of human microbiomes reveals diverse protective ribosomal peptides.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {3054},
pmid = {40155374},
issn = {2041-1723},
support = {C7014-24GF//Research Grants Council, University Grants Committee (RGC, UGC)/ ; },
mesh = {Humans ; Animals ; Mice ; *Gastrointestinal Microbiome ; *Peptides/metabolism/chemistry ; *Microbiota ; *Ribosomes/metabolism ; *Protein Processing, Post-Translational ; Biofilms ; Inflammatory Bowel Diseases/microbiology ; Biological Products/metabolism ; Genome, Bacterial ; Mice, Inbred C57BL ; Ribosomal Proteins/metabolism/genetics ; },
abstract = {The human microbiome produces diverse metabolites that influence host health, yet the chemical landscape of ribosomally synthesized and post-translationally modified peptides (RiPPs)-a versatile class of bioactive compounds-remains underexplored. Here, we conduct a large-scale biosynthetic analysis of 306,481 microbial genomes from human-associated microbiomes, uncovering a broad array of yet-to-be-discovered RiPPs. These RiPPs are distributed across various body sites but show a specific enrichment in the gut and oral microbiome. Big data omics analysis reveals that numerous RiPP families are inversely related to various diseases, suggesting their potential protective effects on health. For a proof of principle study, we apply the synthetic-bioinformatic natural product (syn-BNP) approach to RiPPs and chemically synthesize nine autoinducing peptides (AIPs) for in vitro and ex vivo assay. Our findings reveal that five AIPs effectively inhibit the biofilm formation of disease-associated pathogens. Furthermore, when ex vivo testing gut microbiota from mice with inflammatory bowel disease, we observe that two AIPs can regulate the microbial community and reduce harmful species. These findings highlight the vast potential of human microbial RiPPs in regulating microbial communities and maintaining human health, emphasizing their potential for therapeutic development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Animals
Mice
*Gastrointestinal Microbiome
*Peptides/metabolism/chemistry
*Microbiota
*Ribosomes/metabolism
*Protein Processing, Post-Translational
Biofilms
Inflammatory Bowel Diseases/microbiology
Biological Products/metabolism
Genome, Bacterial
Mice, Inbred C57BL
Ribosomal Proteins/metabolism/genetics
RevDate: 2025-03-27
Translational Implications of The Gut Microbiome in Women with A Benign or Malignant Pelvic Mass.
Annals of obstetrics and gynecology, 8(1):.
OBJECTIVE: The role of the gut microbiome in non-gastrointestinal cancers has generated growing interest in the field of gynecologic oncology. Our objective was to characterize the gut microbiome in women with a pelvic mass suspicious for ovarian cancer. We hypothesized that (1) women with a pelvic mass would have reduced gut microbiota bacterial diversity compared to healthy controls and (2) gut microbial diversity would differ between benign disease compared to ovarian cancer.
METHODS: In this case-control observational study, patients who presented with a suspicious pelvic mass were recruited from university affiliated gynecologic oncology clinics for fecal biospecimen donation. Fecal samples that were obtained from patients underwent 16S rRNA gene sequencing for microbial evaluation and statistical analysis. We used the Human Microbiome Project (HMP) Data Portal to compare gut microbiota profiles for our study to that of healthy female controls.
RESULTS: Fifteen patients with a pelvic mass were included ages 24-75 years. When comparing the gut microbiomes of these patients to 82 healthy females from the HMP Dataset, those with a pelvic mass had a significantly lower microbiota gut bacterial diversity. On the final pathology, 8 of the 15 patients with a suspicious pelvic mass had ovarian cancer and 7 had benign disease. Although not statistically significant, the alpha diversity was marginally reduced in patients with ovarian cancer compared to those with benign disease.
CONCLUSION: These findings underscore the necessity for validation in larger patient cohorts for clinical translation as a potential tool for disease diagnostics and disease prediction in diverse populations.
Additional Links: PMID-40144639
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@article {pmid40144639,
year = {2025},
author = {Sabu, P and Pathak, HB and Nissen, E and Chalise, P and Koestler, DC and Godwin, AK and Umar, S and Spoozak, L and Jewell, A and Mahoney, DE},
title = {Translational Implications of The Gut Microbiome in Women with A Benign or Malignant Pelvic Mass.},
journal = {Annals of obstetrics and gynecology},
volume = {8},
number = {1},
pages = {},
pmid = {40144639},
issn = {2641-6522},
abstract = {OBJECTIVE: The role of the gut microbiome in non-gastrointestinal cancers has generated growing interest in the field of gynecologic oncology. Our objective was to characterize the gut microbiome in women with a pelvic mass suspicious for ovarian cancer. We hypothesized that (1) women with a pelvic mass would have reduced gut microbiota bacterial diversity compared to healthy controls and (2) gut microbial diversity would differ between benign disease compared to ovarian cancer.
METHODS: In this case-control observational study, patients who presented with a suspicious pelvic mass were recruited from university affiliated gynecologic oncology clinics for fecal biospecimen donation. Fecal samples that were obtained from patients underwent 16S rRNA gene sequencing for microbial evaluation and statistical analysis. We used the Human Microbiome Project (HMP) Data Portal to compare gut microbiota profiles for our study to that of healthy female controls.
RESULTS: Fifteen patients with a pelvic mass were included ages 24-75 years. When comparing the gut microbiomes of these patients to 82 healthy females from the HMP Dataset, those with a pelvic mass had a significantly lower microbiota gut bacterial diversity. On the final pathology, 8 of the 15 patients with a suspicious pelvic mass had ovarian cancer and 7 had benign disease. Although not statistically significant, the alpha diversity was marginally reduced in patients with ovarian cancer compared to those with benign disease.
CONCLUSION: These findings underscore the necessity for validation in larger patient cohorts for clinical translation as a potential tool for disease diagnostics and disease prediction in diverse populations.},
}
RevDate: 2025-03-27
Culturable Human Microorganisms and the Impact of Transportation Conditions on Cultivability.
Microorganisms, 13(3): pii:microorganisms13030549.
The composition of the human microbiome is a critical health indicator, and culture-independent methodologies have substantially advanced our understanding of human-associated microorganisms. However, precise identification and characterization of microbial strains require culture-based techniques. Recently, the resurgence of culturomics, combined with high-throughput sequencing technology, has reduced the high labor demand of pure culture methods, facilitating a more efficient and comprehensive acquisition of culturable microbial strains. This study employed an integrated approach combining culturomic and high-throughput sequencing to identify culturable microorganisms on the human scalp and in human saliva and feces. Several Staphylococcus strains were identified from the scalp, whereas anaerobic microorganisms were dominant in the saliva and fecal samples. Additionally, the study highlighted the beneficial effects of transportation conditions (liquid nitrogen treatment, dry ice transport, and dimethyl sulfoxide [DMSO] buffer) in preserving culturable microorganisms. A robust methodology was developed for the large-scale acquisition of culturable microorganisms with optimized transport conditions that enhance the potential for isolating a greater diversity of culturable strains.
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@article {pmid40142442,
year = {2025},
author = {Fan, X and Lv, N and Quan, Z},
title = {Culturable Human Microorganisms and the Impact of Transportation Conditions on Cultivability.},
journal = {Microorganisms},
volume = {13},
number = {3},
pages = {},
doi = {10.3390/microorganisms13030549},
pmid = {40142442},
issn = {2076-2607},
support = {2021YFA1301000//the National Key Research and Development Program of China/ ; 2017SHZDZX01//Shanghai Municipal Science and Technology Major Project/ ; 32470099//the National Natural Foundation of China/ ; },
abstract = {The composition of the human microbiome is a critical health indicator, and culture-independent methodologies have substantially advanced our understanding of human-associated microorganisms. However, precise identification and characterization of microbial strains require culture-based techniques. Recently, the resurgence of culturomics, combined with high-throughput sequencing technology, has reduced the high labor demand of pure culture methods, facilitating a more efficient and comprehensive acquisition of culturable microbial strains. This study employed an integrated approach combining culturomic and high-throughput sequencing to identify culturable microorganisms on the human scalp and in human saliva and feces. Several Staphylococcus strains were identified from the scalp, whereas anaerobic microorganisms were dominant in the saliva and fecal samples. Additionally, the study highlighted the beneficial effects of transportation conditions (liquid nitrogen treatment, dry ice transport, and dimethyl sulfoxide [DMSO] buffer) in preserving culturable microorganisms. A robust methodology was developed for the large-scale acquisition of culturable microorganisms with optimized transport conditions that enhance the potential for isolating a greater diversity of culturable strains.},
}
RevDate: 2025-03-27
CmpDate: 2025-03-27
Gut virome and its implications in the pathogenesis and therapeutics of inflammatory bowel disease.
BMC medicine, 23(1):183.
Inflammatory bowel disease (IBD) refers to chronic, recurrent inflammatory intestinal disorders, primarily including Crohn's disease (CD) and Ulcerative colitis (UC). Numerous studies have elucidated the importance of the gut microbiome in IBD. Recently, numerous studies have focused on the gut virome, an intriguing and enigmatic aspect of the gut microbiome. Alterations in the composition of phages, eukaryotic viruses, and human endogenous retroviruses that occur in IBD suggest potential involvement of the gut virome in IBD. Nevertheless, the mechanisms by which it maintains intestinal homeostasis and interacts with diseases are only beginning to be understood. Here, we thoroughly reviewed the composition of the gut virome in both healthy individuals and IBD patients, emphasizing the key viruses implicated in the onset and progression of IBD. Furthermore, the complex connections between the gut virome and the intestinal barrier, immunity, and gut microbiome were dissected to advance the interpretation of IBD pathogenesis. The updated discussion of the evidence regarding the gut virome will advance our knowledge in gut virome and chronic gastrointestinal diseases. Targeting the gut virome is a promising avenue for IBD treatment in future.
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@article {pmid40140901,
year = {2025},
author = {Wu, Y and Cheng, R and Lin, H and Li, L and Jia, Y and Philips, A and Zuo, T and Zhang, H},
title = {Gut virome and its implications in the pathogenesis and therapeutics of inflammatory bowel disease.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {183},
pmid = {40140901},
issn = {1741-7015},
support = {2023YFS0279//Sichuan Science and Technology Program/ ; },
mesh = {Humans ; *Inflammatory Bowel Diseases/therapy/microbiology/virology ; *Virome ; *Gastrointestinal Microbiome ; },
abstract = {Inflammatory bowel disease (IBD) refers to chronic, recurrent inflammatory intestinal disorders, primarily including Crohn's disease (CD) and Ulcerative colitis (UC). Numerous studies have elucidated the importance of the gut microbiome in IBD. Recently, numerous studies have focused on the gut virome, an intriguing and enigmatic aspect of the gut microbiome. Alterations in the composition of phages, eukaryotic viruses, and human endogenous retroviruses that occur in IBD suggest potential involvement of the gut virome in IBD. Nevertheless, the mechanisms by which it maintains intestinal homeostasis and interacts with diseases are only beginning to be understood. Here, we thoroughly reviewed the composition of the gut virome in both healthy individuals and IBD patients, emphasizing the key viruses implicated in the onset and progression of IBD. Furthermore, the complex connections between the gut virome and the intestinal barrier, immunity, and gut microbiome were dissected to advance the interpretation of IBD pathogenesis. The updated discussion of the evidence regarding the gut virome will advance our knowledge in gut virome and chronic gastrointestinal diseases. Targeting the gut virome is a promising avenue for IBD treatment in future.},
}
MeSH Terms:
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Humans
*Inflammatory Bowel Diseases/therapy/microbiology/virology
*Virome
*Gastrointestinal Microbiome
RevDate: 2025-03-27
Environmental factors and rheumatic diseases.
Best practice & research. Clinical rheumatology pii:S1521-6942(25)00021-X [Epub ahead of print].
The pathogenesis and pathophysiology of rheumatic diseases is complex and relies on the interaction of different factors. The common view is that the pathological autoimmunity develops in genetically predisposed individuals upon exposure to an environmental trigger. This highlights the importance of recognizing and deconstructing the effects of environmental agents in rheumatic diseases. Several factors have been identified in the last decades, with detrimental or protective effects, impacting not only on disease onset, but also on its natural history. Cigarette smoking has been identified as one of the strongest environmental risk factors, being associated with disease development and severity for several rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthropathies. Moreover, other airborne pollutants, such as silica, solvents, asbestos and metals are recognized risk factors for rheumatic diseases. The effect of some other agents is however not straightforward, of which a remarkable example is alcohol consumption. Alcohol has been associated with both pro- and anti-inflammatory effects, exerting a variable effect on rheumatic diseases depending on quantity and frequency of consumption, as well as sex and ethnicity. Similarly, ultraviolet light exposure has been associated with a higher risk of SLE but lower risk of RA. The relationship between microbial exposure and autoimmunity is also complex: while some infectious agents increase the risk of rheumatic diseases, it is widely accepted that less exposure to microbial agents, particularly during immune system development, increases the risk of autoimmunity. Furthermore, in recent years the spotlight has switched to the human microbiome, as alterations in organ-specific microbiome composition are anticipated to be early participants in the onset of immune-mediated illnesses. The aim of this review is to highlight the most relevant environmental factors and their role in Rheumatology, with a specific focus on proposed pathophysiological effect and correlation with clinical outcomes.
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@article {pmid40140341,
year = {2025},
author = {Rodolfi, S and Selmi, C},
title = {Environmental factors and rheumatic diseases.},
journal = {Best practice & research. Clinical rheumatology},
volume = {},
number = {},
pages = {102053},
doi = {10.1016/j.berh.2025.102053},
pmid = {40140341},
issn = {1532-1770},
abstract = {The pathogenesis and pathophysiology of rheumatic diseases is complex and relies on the interaction of different factors. The common view is that the pathological autoimmunity develops in genetically predisposed individuals upon exposure to an environmental trigger. This highlights the importance of recognizing and deconstructing the effects of environmental agents in rheumatic diseases. Several factors have been identified in the last decades, with detrimental or protective effects, impacting not only on disease onset, but also on its natural history. Cigarette smoking has been identified as one of the strongest environmental risk factors, being associated with disease development and severity for several rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthropathies. Moreover, other airborne pollutants, such as silica, solvents, asbestos and metals are recognized risk factors for rheumatic diseases. The effect of some other agents is however not straightforward, of which a remarkable example is alcohol consumption. Alcohol has been associated with both pro- and anti-inflammatory effects, exerting a variable effect on rheumatic diseases depending on quantity and frequency of consumption, as well as sex and ethnicity. Similarly, ultraviolet light exposure has been associated with a higher risk of SLE but lower risk of RA. The relationship between microbial exposure and autoimmunity is also complex: while some infectious agents increase the risk of rheumatic diseases, it is widely accepted that less exposure to microbial agents, particularly during immune system development, increases the risk of autoimmunity. Furthermore, in recent years the spotlight has switched to the human microbiome, as alterations in organ-specific microbiome composition are anticipated to be early participants in the onset of immune-mediated illnesses. The aim of this review is to highlight the most relevant environmental factors and their role in Rheumatology, with a specific focus on proposed pathophysiological effect and correlation with clinical outcomes.},
}
RevDate: 2025-03-26
CmpDate: 2025-03-26
Unlocking the Interactions Between the Whole-Body Microbiome and HPV Infection: A Literature Review.
Pathogens (Basel, Switzerland), 14(3): pii:pathogens14030293.
The human microbiome plays a vital role in maintaining human homeostasis, acting as a key regulator of host immunity and defense mechanisms. However, dysbiotic microbial communities may cause disruption of the symbiotic relationship between the host and the local microbiota, leading to the pathogenesis of various diseases, including viral infections and cancers. One of the most common infectious agents causing cancer is the human papilloma virus (HPV), which accounts for more than 90% of cervical cancers. In most cases, the host immune system is activated and clears HPV, whereas in some cases, the infection persists and can lead to precancerous lesions. Over the last two decades, the advent of next-generation sequencing (NGS) technology and bioinformatics has allowed a thorough and in-depth analysis of the microbial composition in various anatomical niches, allowing researchers to unveil the interactions and the underlying mechanisms through which the human microbiota could affect HPV infection establishment, persistence, and progression. Accordingly, the present narrative review aims to shed light on our understanding of the role of the human microbiome in the context of HPV infection and its progression, mainly to cervical cancer. Furthermore, we explore the mechanisms by which the composition and balance of microbial communities exert potential pathogenic or protective effects, leading to either HPV persistence and disease outcomes or clearance. Special interest is given to how the microbiome can modulate host immunity to HPV infection. Lastly, we summarize the latest findings on the therapeutic efficacy of probiotics and prebiotics in preventing and/or treating HPV infections and the potential of vaginal microbiota transplantation while highlighting the significance of personalized medicine approaches emerging from NGS-based microbiome profiling and artificial intelligence (AI) for the optimal management of HPV-related diseases.
Additional Links: PMID-40137778
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PubMed:
Citation:
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@article {pmid40137778,
year = {2025},
author = {Papamentzelopoulou, M and Pitiriga, VC},
title = {Unlocking the Interactions Between the Whole-Body Microbiome and HPV Infection: A Literature Review.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/pathogens14030293},
pmid = {40137778},
issn = {2076-0817},
mesh = {Humans ; *Papillomavirus Infections/immunology/virology ; *Microbiota/physiology ; Female ; Papillomaviridae/genetics ; Uterine Cervical Neoplasms/virology/immunology/microbiology ; Dysbiosis/immunology ; },
abstract = {The human microbiome plays a vital role in maintaining human homeostasis, acting as a key regulator of host immunity and defense mechanisms. However, dysbiotic microbial communities may cause disruption of the symbiotic relationship between the host and the local microbiota, leading to the pathogenesis of various diseases, including viral infections and cancers. One of the most common infectious agents causing cancer is the human papilloma virus (HPV), which accounts for more than 90% of cervical cancers. In most cases, the host immune system is activated and clears HPV, whereas in some cases, the infection persists and can lead to precancerous lesions. Over the last two decades, the advent of next-generation sequencing (NGS) technology and bioinformatics has allowed a thorough and in-depth analysis of the microbial composition in various anatomical niches, allowing researchers to unveil the interactions and the underlying mechanisms through which the human microbiota could affect HPV infection establishment, persistence, and progression. Accordingly, the present narrative review aims to shed light on our understanding of the role of the human microbiome in the context of HPV infection and its progression, mainly to cervical cancer. Furthermore, we explore the mechanisms by which the composition and balance of microbial communities exert potential pathogenic or protective effects, leading to either HPV persistence and disease outcomes or clearance. Special interest is given to how the microbiome can modulate host immunity to HPV infection. Lastly, we summarize the latest findings on the therapeutic efficacy of probiotics and prebiotics in preventing and/or treating HPV infections and the potential of vaginal microbiota transplantation while highlighting the significance of personalized medicine approaches emerging from NGS-based microbiome profiling and artificial intelligence (AI) for the optimal management of HPV-related diseases.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Papillomavirus Infections/immunology/virology
*Microbiota/physiology
Female
Papillomaviridae/genetics
Uterine Cervical Neoplasms/virology/immunology/microbiology
Dysbiosis/immunology
RevDate: 2025-03-26
Primary Actinomycosis of the Stomach: A Review of the Literature for A Rare Entity.
Journal of personalized medicine, 15(3): pii:jpm15030116.
Background/Objectives: Primary gastric actinomycosis is extremely rare and only a limited number of cases are published in the literature. Actinomycosis is caused by anaerobic Gram-positive bacteria; these microorganisms are members of the normal human microbiome and occasionally lead to infection, especially in immunocompromised patients or patients subjected to abdominal surgery. Advances in personalized medicine, including tailored antimicrobial therapy based on individual patient profiles, may enhance treatment efficacy and reduce unnecessary interventions. Methods: A review was performed through a literature search of the PubMed/MedLine and Scopus databases. Results: A total of 27 patients were included, 15 males (55.56%) and 12 (44.44%) females, with a mean age of 55.11 Β± 17.48 years. Among the included patients, 25.93% had a history of abdominal surgery. Abdominal pain (73.08%), weight loss (40.74%), nausea or vomiting (30.77%) and fever (19.23%) constitute the most commonly reported clinical manifestations. Endoscopy (59.26%), computed tomography (48.15%), ultrasonography (22.22%) and magnetic resonance imaging (11.11%) assisted in indicating the primary lesion. Diagnosis was achieved preoperatively in 66.66% of patients, via endoscopy and biopsy (51.85%) or via cultures (14.81%), while nine cases (33.33%) were diagnosed postoperatively. The therapeutic approaches included antimicrobial administration (32%), surgery (24%) or both (44%). The most widely used antimicrobial was penicillin (77.78%) and the mean duration of antimicrobial treatment was 5.85 months. The protocol for this review was registered in Prospero (ID:CRD42025649532). Conclusions: Due to the divergent clinical presentation of primary gastric actinomycosis, clinicians should be aware of this rare entity in order to establish diagnosis in a timely manner and provide prompt and effective treatment.
Additional Links: PMID-40137432
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PubMed:
Citation:
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@article {pmid40137432,
year = {2025},
author = {Ziogou, A and Giannakodimos, I and Giannakodimos, A and Mitakidi, E and Charalampakis, N and Ioannou, P},
title = {Primary Actinomycosis of the Stomach: A Review of the Literature for A Rare Entity.},
journal = {Journal of personalized medicine},
volume = {15},
number = {3},
pages = {},
doi = {10.3390/jpm15030116},
pmid = {40137432},
issn = {2075-4426},
abstract = {Background/Objectives: Primary gastric actinomycosis is extremely rare and only a limited number of cases are published in the literature. Actinomycosis is caused by anaerobic Gram-positive bacteria; these microorganisms are members of the normal human microbiome and occasionally lead to infection, especially in immunocompromised patients or patients subjected to abdominal surgery. Advances in personalized medicine, including tailored antimicrobial therapy based on individual patient profiles, may enhance treatment efficacy and reduce unnecessary interventions. Methods: A review was performed through a literature search of the PubMed/MedLine and Scopus databases. Results: A total of 27 patients were included, 15 males (55.56%) and 12 (44.44%) females, with a mean age of 55.11 Β± 17.48 years. Among the included patients, 25.93% had a history of abdominal surgery. Abdominal pain (73.08%), weight loss (40.74%), nausea or vomiting (30.77%) and fever (19.23%) constitute the most commonly reported clinical manifestations. Endoscopy (59.26%), computed tomography (48.15%), ultrasonography (22.22%) and magnetic resonance imaging (11.11%) assisted in indicating the primary lesion. Diagnosis was achieved preoperatively in 66.66% of patients, via endoscopy and biopsy (51.85%) or via cultures (14.81%), while nine cases (33.33%) were diagnosed postoperatively. The therapeutic approaches included antimicrobial administration (32%), surgery (24%) or both (44%). The most widely used antimicrobial was penicillin (77.78%) and the mean duration of antimicrobial treatment was 5.85 months. The protocol for this review was registered in Prospero (ID:CRD42025649532). Conclusions: Due to the divergent clinical presentation of primary gastric actinomycosis, clinicians should be aware of this rare entity in order to establish diagnosis in a timely manner and provide prompt and effective treatment.},
}
RevDate: 2025-03-25
CmpDate: 2025-03-25
Temporal dynamics and metagenomics of phosphorothioate epigenomes in the human gut microbiome.
Microbiome, 13(1):81.
BACKGROUND: Epigenetic regulation of gene expression and host defense is well established in microbial communities, with dozens of DNA modifications comprising the epigenomes of prokaryotes and bacteriophage. Phosphorothioation (PT) of DNA, in which a chemically reactive sulfur atom replaces a non-bridging oxygen in the sugar-phosphate backbone, is catalyzed by dnd and ssp gene families widespread in bacteria and archaea. However, little is known about the role of PTs or other microbial epigenetic modifications in the human microbiome. Here we optimized and applied fecal DNA extraction, mass spectrometric, and metagenomics technologies to characterize the landscape and temporal dynamics of gut microbes possessing PT modifications.
RESULTS: Exploiting the nuclease-resistance of PTs, mass spectrometric analysis of limit digests of PT-containing DNA reveals PT dinucleotides as part of genomic consensus sequences, with 16 possible dinucleotide combinations. Analysis of mouse fecal DNA revealed a highly uniform spectrum of 11 PT dinucleotides in all littermates, with PTs estimated to occur in 5-10% of gut microbes. Though at similar levels, PT dinucleotides in fecal DNA from 11 healthy humans possessed signature combinations and levels of individual PTs. Comparison with a widely distributed microbial epigenetic mark, m[6]dA, suggested temporal dynamics consistent with expectations for gut microbial communities based on Taylor's Power Law. Application of PT-seq for site-specific metagenomic analysis of PT-containing bacteria in one fecal donor revealed the larger consensus sequences for the PT dinucleotides in Bacteroidota, Bacillota (formerly Firmicutes), Actinomycetota (formerly Actinobacteria), and Pseudomonadota (formerly Proteobacteria), which differed from unbiased metagenomics and suggested that the abundance of PT-containing bacteria did not simply mirror the spectrum of gut bacteria. PT-seq further revealed low abundance PT sites not detected as dinucleotides by mass spectrometry, attesting to the complementarity of the technologies. Video Abstract CONCLUSIONS: The results of our studies provide a benchmark for understanding the behavior of an abundant and chemically reactive epigenetic mark in the human gut microbiome, with implications for inflammatory conditions of the gut.
Additional Links: PMID-40128848
PubMed:
Citation:
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@article {pmid40128848,
year = {2025},
author = {Byrne, SR and DeMott, MS and Yuan, Y and Ghanegolmohammadi, F and Kaiser, S and Fox, JG and Alm, EJ and Dedon, PC},
title = {Temporal dynamics and metagenomics of phosphorothioate epigenomes in the human gut microbiome.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {81},
pmid = {40128848},
issn = {2049-2618},
support = {T32-ES007020//NIEHS Training Grant in Environmental Toxicology/ ; R01-OD028099-01//NIH Transformative Award/ ; R01-OD028099-01//NIH Transformative Award/ ; P30-ES002109//NIEHS Core Center Grant/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; *Metagenomics/methods ; *Feces/microbiology ; *Bacteria/genetics/classification/metabolism ; Mice ; Animals ; Epigenesis, Genetic ; Epigenome ; Female ; Male ; Phosphates/metabolism ; },
abstract = {BACKGROUND: Epigenetic regulation of gene expression and host defense is well established in microbial communities, with dozens of DNA modifications comprising the epigenomes of prokaryotes and bacteriophage. Phosphorothioation (PT) of DNA, in which a chemically reactive sulfur atom replaces a non-bridging oxygen in the sugar-phosphate backbone, is catalyzed by dnd and ssp gene families widespread in bacteria and archaea. However, little is known about the role of PTs or other microbial epigenetic modifications in the human microbiome. Here we optimized and applied fecal DNA extraction, mass spectrometric, and metagenomics technologies to characterize the landscape and temporal dynamics of gut microbes possessing PT modifications.
RESULTS: Exploiting the nuclease-resistance of PTs, mass spectrometric analysis of limit digests of PT-containing DNA reveals PT dinucleotides as part of genomic consensus sequences, with 16 possible dinucleotide combinations. Analysis of mouse fecal DNA revealed a highly uniform spectrum of 11 PT dinucleotides in all littermates, with PTs estimated to occur in 5-10% of gut microbes. Though at similar levels, PT dinucleotides in fecal DNA from 11 healthy humans possessed signature combinations and levels of individual PTs. Comparison with a widely distributed microbial epigenetic mark, m[6]dA, suggested temporal dynamics consistent with expectations for gut microbial communities based on Taylor's Power Law. Application of PT-seq for site-specific metagenomic analysis of PT-containing bacteria in one fecal donor revealed the larger consensus sequences for the PT dinucleotides in Bacteroidota, Bacillota (formerly Firmicutes), Actinomycetota (formerly Actinobacteria), and Pseudomonadota (formerly Proteobacteria), which differed from unbiased metagenomics and suggested that the abundance of PT-containing bacteria did not simply mirror the spectrum of gut bacteria. PT-seq further revealed low abundance PT sites not detected as dinucleotides by mass spectrometry, attesting to the complementarity of the technologies. Video Abstract CONCLUSIONS: The results of our studies provide a benchmark for understanding the behavior of an abundant and chemically reactive epigenetic mark in the human gut microbiome, with implications for inflammatory conditions of the gut.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/genetics
*Metagenomics/methods
*Feces/microbiology
*Bacteria/genetics/classification/metabolism
Mice
Animals
Epigenesis, Genetic
Epigenome
Female
Male
Phosphates/metabolism
RevDate: 2025-03-23
Dietary whey protein protects against Crohn's disease by orchestrating cross-kingdom interaction between the gut phageome and bacteriome.
Gut pii:gutjnl-2024-334516 [Epub ahead of print].
BACKGROUND: The gut microbiome and diet are important factors in the pathogenesis and management of Crohn's disease (CD). However, the role of the gut phageome under dietary influences is unknown.
OBJECTIVE: We aim to explore the effect of diet on the gut phageome-bacteriome interaction linking to CD protection.
DESIGN: We recruited CD patients and healthy subjects (n=140) and conducted a multiomics investigation, including paired ileal mucosa phageome and bacteriome profiling, dietary survey and phenome interrogation. We screened for the effect of diet on the gut phageome and bacteriome, as well as its epidemiological association with CD risks. The underlying mechanisms were explored in target phage-bacteria monocultures and cocultures in vitro and in two mouse models in vivo.
RESULTS: On dietary screening in humans, whey protein (WP) consumption was found to profoundly impact the gut phageome and bacteriome (more pronounced on the phageome) and was associated with a lower CD risk. Indeed, the WP reshaped gut phageome can causally attenuate intestinal inflammation, as shown by faecal phageome versus bacteriome transplantation from WP-consuming versus WP-non-consuming mice to recipient mice. Mechanistically, WP induced phage (a newly isolated phage AkkZT003P herein) lysis of the mucin-foraging bacterium Akkermansia muciniphila, which unleashed the symbiotic bacterium Streptococcus thermophilus to counteract intestinal inflammation.
CONCLUSION: Our study charted the importance of cross-kingdom interaction between gut phage and bacteria in mediating the dietary effect on CD protection. Importantly, we uncovered a beneficial dietary WP, a keystone phage AkkZT003P, and a probiotic S. thermophilus that can be used in CD management in the future.
Additional Links: PMID-40122597
Publisher:
PubMed:
Citation:
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@article {pmid40122597,
year = {2025},
author = {Su, R and Wen, W and Jin, Y and Cao, Z and Feng, Z and Chen, J and Lu, Y and Zhou, G and Dong, C and Gao, S and Li, X and Zhang, H and Chao, K and Lan, P and Wu, X and Philips, A and Li, K and Gao, X and Zhang, F and Zuo, T},
title = {Dietary whey protein protects against Crohn's disease by orchestrating cross-kingdom interaction between the gut phageome and bacteriome.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2024-334516},
pmid = {40122597},
issn = {1468-3288},
abstract = {BACKGROUND: The gut microbiome and diet are important factors in the pathogenesis and management of Crohn's disease (CD). However, the role of the gut phageome under dietary influences is unknown.
OBJECTIVE: We aim to explore the effect of diet on the gut phageome-bacteriome interaction linking to CD protection.
DESIGN: We recruited CD patients and healthy subjects (n=140) and conducted a multiomics investigation, including paired ileal mucosa phageome and bacteriome profiling, dietary survey and phenome interrogation. We screened for the effect of diet on the gut phageome and bacteriome, as well as its epidemiological association with CD risks. The underlying mechanisms were explored in target phage-bacteria monocultures and cocultures in vitro and in two mouse models in vivo.
RESULTS: On dietary screening in humans, whey protein (WP) consumption was found to profoundly impact the gut phageome and bacteriome (more pronounced on the phageome) and was associated with a lower CD risk. Indeed, the WP reshaped gut phageome can causally attenuate intestinal inflammation, as shown by faecal phageome versus bacteriome transplantation from WP-consuming versus WP-non-consuming mice to recipient mice. Mechanistically, WP induced phage (a newly isolated phage AkkZT003P herein) lysis of the mucin-foraging bacterium Akkermansia muciniphila, which unleashed the symbiotic bacterium Streptococcus thermophilus to counteract intestinal inflammation.
CONCLUSION: Our study charted the importance of cross-kingdom interaction between gut phage and bacteria in mediating the dietary effect on CD protection. Importantly, we uncovered a beneficial dietary WP, a keystone phage AkkZT003P, and a probiotic S. thermophilus that can be used in CD management in the future.},
}
RevDate: 2025-03-22
Berry supplementation in healthy volunteers modulates gut microbiota, increases fecal polyphenol metabolites and reduces viability of colon cancer cells exposed to fecal water- a randomized controlled trial.
The Journal of nutritional biochemistry pii:S0955-2863(25)00069-5 [Epub ahead of print].
SCOPE: Diets high in red and processed meat and low in plant-based foods are associated with an increased risk of colorectal cancer. We investigated whether berry supplementation can impact gut metabolism to counteract the presumably cancer promoting luminal environment sustained by high red and processed meat consumption.
METHODS AND RESULTS: Altogether 43 healthy adults were randomized either into Meat group (150 g/d red and processed pork meat) or Meat & Berries group (150 g/d red and processed meat and 200 g/d of mixed berries). Fecal samples and 3-day food records were collected at baseline and at the end of the four-week intervention. Intakes of vitamin C, vitamin E, manganese, insoluble fibre, and the polyphenols available in the database were significantly higher in the Meat & Berries than Meat group. While between-group comparisons found no significant differences in the gut microbiota, the within-group analyses showed that the relative abundances of beneficial Roseburia and Faecalibacterium were decreased and an unclassified group of Peptostreptococcaceae increased significantly in the Meat group. In comparison to the Meat group, berry consumption resulted in higher fecal concentrations of p-coumaric and protocatechuic acids and lower viability of fecal water (FW) -treated CV1-P fibroblastoma and human colon adenocarcinoma HCA-7 and Caco-2 cells (P<0.05 with 30% FW).
CONCLUSIONS: Berry consumption provided protective nutrients and mitigated potentially unfavourable gut microbiota changes seen in the Meat group, increased fecal polyphenol metabolites, and reduced viability of FW-treated colon adenocarcinoma cells, collectively suggesting that berries may protect against colorectal cancer development.
Additional Links: PMID-40120775
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PubMed:
Citation:
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@article {pmid40120775,
year = {2025},
author = {Onali, T and SlabÑ, H and Jian, C and KoivumÀki, T and PÀivÀrinta, E and Marttinen, M and MÀÀttÀnen, M and Salonen, A and Pajari, AM},
title = {Berry supplementation in healthy volunteers modulates gut microbiota, increases fecal polyphenol metabolites and reduces viability of colon cancer cells exposed to fecal water- a randomized controlled trial.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {109906},
doi = {10.1016/j.jnutbio.2025.109906},
pmid = {40120775},
issn = {1873-4847},
abstract = {SCOPE: Diets high in red and processed meat and low in plant-based foods are associated with an increased risk of colorectal cancer. We investigated whether berry supplementation can impact gut metabolism to counteract the presumably cancer promoting luminal environment sustained by high red and processed meat consumption.
METHODS AND RESULTS: Altogether 43 healthy adults were randomized either into Meat group (150 g/d red and processed pork meat) or Meat & Berries group (150 g/d red and processed meat and 200 g/d of mixed berries). Fecal samples and 3-day food records were collected at baseline and at the end of the four-week intervention. Intakes of vitamin C, vitamin E, manganese, insoluble fibre, and the polyphenols available in the database were significantly higher in the Meat & Berries than Meat group. While between-group comparisons found no significant differences in the gut microbiota, the within-group analyses showed that the relative abundances of beneficial Roseburia and Faecalibacterium were decreased and an unclassified group of Peptostreptococcaceae increased significantly in the Meat group. In comparison to the Meat group, berry consumption resulted in higher fecal concentrations of p-coumaric and protocatechuic acids and lower viability of fecal water (FW) -treated CV1-P fibroblastoma and human colon adenocarcinoma HCA-7 and Caco-2 cells (P<0.05 with 30% FW).
CONCLUSIONS: Berry consumption provided protective nutrients and mitigated potentially unfavourable gut microbiota changes seen in the Meat group, increased fecal polyphenol metabolites, and reduced viability of FW-treated colon adenocarcinoma cells, collectively suggesting that berries may protect against colorectal cancer development.},
}
RevDate: 2025-03-22
Unpacking food fermentation: Clinically relevant tools for fermented food identification and consumption.
Advances in nutrition (Bethesda, Md.) pii:S2161-8313(25)00048-1 [Epub ahead of print].
Fermented foods have been consumed for millennia, valued for their extended shelf life, distinctive sensory properties, and potential health benefits. Emerging research suggests that fermented food consumption may contribute to gut microbiome diversity, immune modulation, and metabolic regulation; however, mechanistic insights and clinical validation remain limited. This review synthesizes current scientific evidence on the microbial and metabolite composition of fermented foods, their proposed health effects, and safety considerations for vulnerable populations. Additionally, we highlight the need for standardized definitions, serving sizes, and regulatory frameworks to enhance consumer transparency and research reproducibility. By providing a structured overview of existing data and knowledge gaps, this review establishes a foundation for integrating fermented foods into dietary recommendations and guiding future research directions. STATEMENT OF SIGNIFICANCE: While fermented foods have demonstrated benefits to human health, the gap between scientific research and marketing claims, including lack of regulatory standards in labeling can be disorienting to consumers seeking these potential benefits. This review provides an updated perspective on the role of fermented foods in health, emphasizing clinically relevant tools, research opportunities, and labeling recommendations to guide their identification and use.
Additional Links: PMID-40120687
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PubMed:
Citation:
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@article {pmid40120687,
year = {2025},
author = {Caffrey, EB and Perelman, D and Ward, CP and Sonnenburg, ED and Gardner, CD and Sonnenburg, JL},
title = {Unpacking food fermentation: Clinically relevant tools for fermented food identification and consumption.},
journal = {Advances in nutrition (Bethesda, Md.)},
volume = {},
number = {},
pages = {100412},
doi = {10.1016/j.advnut.2025.100412},
pmid = {40120687},
issn = {2156-5376},
abstract = {Fermented foods have been consumed for millennia, valued for their extended shelf life, distinctive sensory properties, and potential health benefits. Emerging research suggests that fermented food consumption may contribute to gut microbiome diversity, immune modulation, and metabolic regulation; however, mechanistic insights and clinical validation remain limited. This review synthesizes current scientific evidence on the microbial and metabolite composition of fermented foods, their proposed health effects, and safety considerations for vulnerable populations. Additionally, we highlight the need for standardized definitions, serving sizes, and regulatory frameworks to enhance consumer transparency and research reproducibility. By providing a structured overview of existing data and knowledge gaps, this review establishes a foundation for integrating fermented foods into dietary recommendations and guiding future research directions. STATEMENT OF SIGNIFICANCE: While fermented foods have demonstrated benefits to human health, the gap between scientific research and marketing claims, including lack of regulatory standards in labeling can be disorienting to consumers seeking these potential benefits. This review provides an updated perspective on the role of fermented foods in health, emphasizing clinically relevant tools, research opportunities, and labeling recommendations to guide their identification and use.},
}
RevDate: 2025-03-22
CmpDate: 2025-03-22
Genomic and proteomic characterization of four novel Schitoviridae family phages targeting uropathogenic Escherichia coli strain.
Virology journal, 22(1):83.
BACKGROUND: Escherichia coli-associated urinary tract infections (UTIs) are among the most prevalent bacterial infections in humans. Typically, antibiotic medication is used to treat UTIs, but over the time, growth of multidrug resistance among these bacteria has created a global public health issue that necessitates other treatment modalities, such as phage therapy.
METHODS: The UPEC strain PSU-5266 (UE-17) was isolated from human urine samples, while phages were obtained from wastewater. These phages were characterized through host range analysis, stability studies, adsorption assays, and electron microscopy. Additionally, genomic, phylogenetic, and proteomic analyses were conducted to provide further insights.
RESULTS: The current study describes the isolation and characterization of four Escherichia coli phages designated as UE-S5a, UE-S5b, UE-M3 and UE-M6. Bactericidal assays depicted that all bacteriophages exhibited a strong lytic ability against uropathogenic E. coli (UPEC) strain PSU-5266 (UE-17). The phages displayed a broad host range (31-41%) among 104 tested isolates and adsorption rate of 15-20 min. They were stable within pH range of 5-11 and temperature range of 4 to 55 °C. Electron microscopy showed that all phages have icosahedral heads (70-74 nm) and short non-contractile tails, thus exhibiting a podovirus morphology. Sequencing results showed that they have linear double stranded DNA, genome of 73 to 76 kb in length, with GC content of 42% and short direct terminal repeats. Their genomes contain 84-88 predicted genes with putative functions predicted to 42-48% of gene products. The phylogenetic and comparative genomic analysis results depicted that these phages, sharing > 98% sequence similarity, are new members of genus Gamaleyavirus of subfamily Enquatrovirinae, in the Schitoviridae family. Mass spectrometric analysis of purified phage particles identified 44-56 phage particle-associated proteins (PPAPs) belonging to various functional groups such as lysis proteins, structural proteins, DNA packaging related proteins, and proteins involved in replication, metabolism and regulation. In addition, no genes encoding virulence factors, antibiotic resistance or lysogeny factors were identified.
CONCLUSION: The overall findings suggest that these bacteriophages are potential candidates for phage therapy in treating UTIs caused by UPEC strains.
Additional Links: PMID-40119445
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Citation:
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@article {pmid40119445,
year = {2025},
author = {Niaz, H and Skurnik, M and Adnan, F},
title = {Genomic and proteomic characterization of four novel Schitoviridae family phages targeting uropathogenic Escherichia coli strain.},
journal = {Virology journal},
volume = {22},
number = {1},
pages = {83},
pmid = {40119445},
issn = {1743-422X},
mesh = {Humans ; *Genome, Viral ; *Uropathogenic Escherichia coli/virology/genetics ; *Host Specificity ; *Phylogeny ; *Proteomics ; Genomics ; Phage Therapy ; Urinary Tract Infections/microbiology/virology ; Escherichia coli Infections/microbiology ; Coliphages/genetics/isolation & purification/ultrastructure/classification/physiology ; Wastewater/virology/microbiology ; Proteome ; Bacteriophages/genetics/isolation & purification/classification/ultrastructure/physiology ; },
abstract = {BACKGROUND: Escherichia coli-associated urinary tract infections (UTIs) are among the most prevalent bacterial infections in humans. Typically, antibiotic medication is used to treat UTIs, but over the time, growth of multidrug resistance among these bacteria has created a global public health issue that necessitates other treatment modalities, such as phage therapy.
METHODS: The UPEC strain PSU-5266 (UE-17) was isolated from human urine samples, while phages were obtained from wastewater. These phages were characterized through host range analysis, stability studies, adsorption assays, and electron microscopy. Additionally, genomic, phylogenetic, and proteomic analyses were conducted to provide further insights.
RESULTS: The current study describes the isolation and characterization of four Escherichia coli phages designated as UE-S5a, UE-S5b, UE-M3 and UE-M6. Bactericidal assays depicted that all bacteriophages exhibited a strong lytic ability against uropathogenic E. coli (UPEC) strain PSU-5266 (UE-17). The phages displayed a broad host range (31-41%) among 104 tested isolates and adsorption rate of 15-20 min. They were stable within pH range of 5-11 and temperature range of 4 to 55 °C. Electron microscopy showed that all phages have icosahedral heads (70-74 nm) and short non-contractile tails, thus exhibiting a podovirus morphology. Sequencing results showed that they have linear double stranded DNA, genome of 73 to 76 kb in length, with GC content of 42% and short direct terminal repeats. Their genomes contain 84-88 predicted genes with putative functions predicted to 42-48% of gene products. The phylogenetic and comparative genomic analysis results depicted that these phages, sharing > 98% sequence similarity, are new members of genus Gamaleyavirus of subfamily Enquatrovirinae, in the Schitoviridae family. Mass spectrometric analysis of purified phage particles identified 44-56 phage particle-associated proteins (PPAPs) belonging to various functional groups such as lysis proteins, structural proteins, DNA packaging related proteins, and proteins involved in replication, metabolism and regulation. In addition, no genes encoding virulence factors, antibiotic resistance or lysogeny factors were identified.
CONCLUSION: The overall findings suggest that these bacteriophages are potential candidates for phage therapy in treating UTIs caused by UPEC strains.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Genome, Viral
*Uropathogenic Escherichia coli/virology/genetics
*Host Specificity
*Phylogeny
*Proteomics
Genomics
Phage Therapy
Urinary Tract Infections/microbiology/virology
Escherichia coli Infections/microbiology
Coliphages/genetics/isolation & purification/ultrastructure/classification/physiology
Wastewater/virology/microbiology
Proteome
Bacteriophages/genetics/isolation & purification/classification/ultrastructure/physiology
RevDate: 2025-03-22
Human microbiome acquisition and transmission.
Nature reviews. Microbiology [Epub ahead of print].
As humans, we host personal microbiomes intricately connected to our biology and health. Far from being isolated entities, our microbiomes are dynamically shaped by microbial exchange with the surroundings, in lifelong microbiome acquisition and transmission processes. In this Review, we explore recent studies on how our microbiomes are transmitted, beginning at birth and during interactions with other humans and the environment. We also describe the key methodological aspects of transmission inference, based on the uniqueness of the building blocks of the microbiome - single microbial strains. A better understanding of human microbiome transmission will have implications for studies of microbial host regulation, of microbiome-associated diseases, and for effective microbiome-targeting strategies. Besides exchanging strains with other humans, there is also preliminary evidence we acquire microorganisms from animals and food, and thus a complete understanding of microbiome acquisition and transmission can only be attained by adopting a One Health perspective.
Additional Links: PMID-40119155
PubMed:
Citation:
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@article {pmid40119155,
year = {2025},
author = {Heidrich, V and Valles-Colomer, M and Segata, N},
title = {Human microbiome acquisition and transmission.},
journal = {Nature reviews. Microbiology},
volume = {},
number = {},
pages = {},
pmid = {40119155},
issn = {1740-1534},
abstract = {As humans, we host personal microbiomes intricately connected to our biology and health. Far from being isolated entities, our microbiomes are dynamically shaped by microbial exchange with the surroundings, in lifelong microbiome acquisition and transmission processes. In this Review, we explore recent studies on how our microbiomes are transmitted, beginning at birth and during interactions with other humans and the environment. We also describe the key methodological aspects of transmission inference, based on the uniqueness of the building blocks of the microbiome - single microbial strains. A better understanding of human microbiome transmission will have implications for studies of microbial host regulation, of microbiome-associated diseases, and for effective microbiome-targeting strategies. Besides exchanging strains with other humans, there is also preliminary evidence we acquire microorganisms from animals and food, and thus a complete understanding of microbiome acquisition and transmission can only be attained by adopting a One Health perspective.},
}
RevDate: 2025-03-21
Complete genome sequence of Trueperella bernardiae strain UMB8254, isolated from the bladder of a female with metabolic syndrome and nephrolithiasis.
Microbiology resource announcements [Epub ahead of print].
Trueperella bernardiae is infrequently isolated, usually in polymicrobial communities, from human hosts with a wide variety of symptoms and diseases. Here, we report a complete genome sequence of Trueperella bernardiae (UMB8254), isolated from the bladder of a human female with metabolic syndrome and nephrolithiasis.
Additional Links: PMID-40116497
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PubMed:
Citation:
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@article {pmid40116497,
year = {2025},
author = {Moreland, RB and Choi, BI and Fontes Noronha, M and Baker, J and Kaindl, J and Wolfe, AJ},
title = {Complete genome sequence of Trueperella bernardiae strain UMB8254, isolated from the bladder of a female with metabolic syndrome and nephrolithiasis.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0126524},
doi = {10.1128/mra.01265-24},
pmid = {40116497},
issn = {2576-098X},
abstract = {Trueperella bernardiae is infrequently isolated, usually in polymicrobial communities, from human hosts with a wide variety of symptoms and diseases. Here, we report a complete genome sequence of Trueperella bernardiae (UMB8254), isolated from the bladder of a human female with metabolic syndrome and nephrolithiasis.},
}
RevDate: 2025-03-20
CmpDate: 2025-03-20
Modulation of the Human Microbiome: Probiotics, Prebiotics, and Microbial Transplants.
Advances in experimental medicine and biology, 1472:277-294.
The balance between health and disease is intrinsically linked to the interactions between microbial communities and the host. This complex environment of antagonism and synergy involves both prokaryotic and eukaryotic cells, whose collaborative metabolic pathways and immunomodulatory elements influence system homeostasis. As with the gut and other niches, the oral microbiome has the capacity to affect distal host sites. The ability to manipulate this environment holds the potential to impact local and systemic disease.With the increasing threat of antimicrobial resistance, novel approaches to reduce the burden of disease are essential. The use of probiotics and prebiotics is one such strategy. Probiotics introduce non-pathogenic bacteria into the environment to compete with pathogens for nutrients and attachment sites, or to produce metabolites that counteract disease aetiologies. Prebiotic compounds enhance the growth of health-associated organisms, offering additional benefits, whilst a conjunctive approach with probiotics potentially holds even greater promise. Though widely studied in the gastrointestinal context, their potential for treating oral diseases, such as dental caries and periodontitis, is less understood. Additionally, the use of microbial transplantations has demonstrated efficacy in other areas, reducing systemic inflammation and recolonising with commensal bacteria. Here we evaluate their use in the oral context and their modulatory impact on overall health.In this chapter, we discuss how pro- and prebiotic strategies seek to modulate both the oral and gut environments to promote oral health and prevent disease. We assess novel approaches for utilising health-associated microorganisms to combat oral disorders, either administered locally in the mouth or imparting influence through immune modulation via the oral-gut axis. By examining available clinical trial data, we aim to further understand the intricacies involved in this discipline. Furthermore, we consider the challenges facing the research community, including optimal candidate organism/compound selection and colonisation retention, as well as considerations for future research.
Additional Links: PMID-40111698
PubMed:
Citation:
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@article {pmid40111698,
year = {2025},
author = {Vernon, JJ},
title = {Modulation of the Human Microbiome: Probiotics, Prebiotics, and Microbial Transplants.},
journal = {Advances in experimental medicine and biology},
volume = {1472},
number = {},
pages = {277-294},
pmid = {40111698},
issn = {0065-2598},
mesh = {Humans ; *Prebiotics/administration & dosage ; *Probiotics/therapeutic use ; *Microbiota/physiology ; Mouth/microbiology ; Gastrointestinal Microbiome/physiology ; Fecal Microbiota Transplantation/methods ; },
abstract = {The balance between health and disease is intrinsically linked to the interactions between microbial communities and the host. This complex environment of antagonism and synergy involves both prokaryotic and eukaryotic cells, whose collaborative metabolic pathways and immunomodulatory elements influence system homeostasis. As with the gut and other niches, the oral microbiome has the capacity to affect distal host sites. The ability to manipulate this environment holds the potential to impact local and systemic disease.With the increasing threat of antimicrobial resistance, novel approaches to reduce the burden of disease are essential. The use of probiotics and prebiotics is one such strategy. Probiotics introduce non-pathogenic bacteria into the environment to compete with pathogens for nutrients and attachment sites, or to produce metabolites that counteract disease aetiologies. Prebiotic compounds enhance the growth of health-associated organisms, offering additional benefits, whilst a conjunctive approach with probiotics potentially holds even greater promise. Though widely studied in the gastrointestinal context, their potential for treating oral diseases, such as dental caries and periodontitis, is less understood. Additionally, the use of microbial transplantations has demonstrated efficacy in other areas, reducing systemic inflammation and recolonising with commensal bacteria. Here we evaluate their use in the oral context and their modulatory impact on overall health.In this chapter, we discuss how pro- and prebiotic strategies seek to modulate both the oral and gut environments to promote oral health and prevent disease. We assess novel approaches for utilising health-associated microorganisms to combat oral disorders, either administered locally in the mouth or imparting influence through immune modulation via the oral-gut axis. By examining available clinical trial data, we aim to further understand the intricacies involved in this discipline. Furthermore, we consider the challenges facing the research community, including optimal candidate organism/compound selection and colonisation retention, as well as considerations for future research.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Prebiotics/administration & dosage
*Probiotics/therapeutic use
*Microbiota/physiology
Mouth/microbiology
Gastrointestinal Microbiome/physiology
Fecal Microbiota Transplantation/methods
RevDate: 2025-03-20
CmpDate: 2025-03-20
Link Between Oral and Gut Microbiomes: The Oral-Gut Axis.
Advances in experimental medicine and biology, 1472:71-87.
In the last decades, groundbreaking research on the human microbiome has changed our reductionist conception of the etiology and pathogenesis of several chronic diseases. As a result, we have come to appreciate the significance of a balanced microbiome in maintaining human health. In this context, the upper and lower gastrointestinal tracts (GITs) comprise the most abundant and diverse microbiotas of the human body. In addition to its diversity, functional redundancy, and temporal stability, a healthy GIT microbiome is characterized by its body site specificity. In fact, current evidence has indicated that the translocation of oral species to the gut environment through the oral-gut axis is increased in an array of illnesses, including chronic inflammatory and metabolic diseases, neurological disorders, and cancer. Oral pathogens have also been shown to promote gut dysbiosis and systemic inflammation in animal models. Yet, some level of overlapping between oral and gut microbiomes may occur without disruption of these microbial communities and loss of site specificity. The uniqueness of each host-microbiome entity may hinder our ability to define a "universal" normal GIT microbiome. Despite that, this chapter summarizes the predominant health-related taxa along the human GIT, as well as their role in the physiology and immunity of the digestive system. Some mechanisms that may lead to disturbances and relevant shifts in the oral and gut microbiomes of major inflammatory chronic diseases are also pointed out. Lastly, oral-fecal microbial signatures are presented as potential biomarkers for several oral and systemic disorders. The recognition of such symbiotic/dysbiotic microbial profiles may provide insights into the development of more accurate early diagnosis and therapeutic ecological approaches to restore the balance of the GIT microbiome.
Additional Links: PMID-40111686
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Citation:
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@article {pmid40111686,
year = {2025},
author = {Colombo, APV and LourenΓ§o, TGB and de Oliveira, AM and da Costa, ALA},
title = {Link Between Oral and Gut Microbiomes: The Oral-Gut Axis.},
journal = {Advances in experimental medicine and biology},
volume = {1472},
number = {},
pages = {71-87},
pmid = {40111686},
issn = {0065-2598},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Mouth/microbiology ; *Dysbiosis/microbiology ; Animals ; Gastrointestinal Tract/microbiology ; },
abstract = {In the last decades, groundbreaking research on the human microbiome has changed our reductionist conception of the etiology and pathogenesis of several chronic diseases. As a result, we have come to appreciate the significance of a balanced microbiome in maintaining human health. In this context, the upper and lower gastrointestinal tracts (GITs) comprise the most abundant and diverse microbiotas of the human body. In addition to its diversity, functional redundancy, and temporal stability, a healthy GIT microbiome is characterized by its body site specificity. In fact, current evidence has indicated that the translocation of oral species to the gut environment through the oral-gut axis is increased in an array of illnesses, including chronic inflammatory and metabolic diseases, neurological disorders, and cancer. Oral pathogens have also been shown to promote gut dysbiosis and systemic inflammation in animal models. Yet, some level of overlapping between oral and gut microbiomes may occur without disruption of these microbial communities and loss of site specificity. The uniqueness of each host-microbiome entity may hinder our ability to define a "universal" normal GIT microbiome. Despite that, this chapter summarizes the predominant health-related taxa along the human GIT, as well as their role in the physiology and immunity of the digestive system. Some mechanisms that may lead to disturbances and relevant shifts in the oral and gut microbiomes of major inflammatory chronic diseases are also pointed out. Lastly, oral-fecal microbial signatures are presented as potential biomarkers for several oral and systemic disorders. The recognition of such symbiotic/dysbiotic microbial profiles may provide insights into the development of more accurate early diagnosis and therapeutic ecological approaches to restore the balance of the GIT microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Mouth/microbiology
*Dysbiosis/microbiology
Animals
Gastrointestinal Tract/microbiology
RevDate: 2025-03-20
CmpDate: 2025-03-20
The Oral Microbiome and Us.
Advances in experimental medicine and biology, 1472:3-9.
Oral and systemic human health depend on the symbiotic relationship between the human host and its microbiome. As the second most diverse site of the human microbiome, the oral cavity is instrumental in symbiotic relationships, transforming nutrients and acting as the human body's initial barrier against pathogens. However, under certain conditions, the typically beneficial oral microbiome can become harmful. Systemic inflammatory diseases can send signals through the oral-gut axis, such as cytokines and host defensins, altering gene expression and, consequently, the composition of the oral microbiome. These changes can be responsible for causing oral diseases, such as periodontitis and candidiasis. Evidence of metabolic syndrome, including obesity, hypertension, hyperglycemia, and dyslipidemia, exacerbates oral microbiome dysbiosis. On the other hand, the oral microbiota can also influence systemic health. Inflammatory processes in the gingival structures caused by a dysbiotic oral microbiome are linked to worsen glycemic levels in diabetics, premature birth, and rheumatoid arthritis, among others. The idea for this book emerged from the need to explore the multifaceted nature of this relationship in its various dimensions. We discuss multispecies characteristics from an ecological perspective, focusing on how the host affects the microbiome and vice versa. Understanding how the oral microbiome influences human health will guide tailored strategies for disease prevention and treatment, which is discussed in the last section of the book. Looking ahead, predictive health and disease models will enable personalized therapies centered on restoring the healthy human microbiome.
Additional Links: PMID-40111682
PubMed:
Citation:
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@article {pmid40111682,
year = {2025},
author = {Dame-Teixeira, N and Do, T and Deng, D},
title = {The Oral Microbiome and Us.},
journal = {Advances in experimental medicine and biology},
volume = {1472},
number = {},
pages = {3-9},
pmid = {40111682},
issn = {0065-2598},
mesh = {Humans ; *Mouth/microbiology ; *Microbiota/physiology ; *Dysbiosis/microbiology ; Periodontitis/microbiology ; Animals ; Oral Health ; },
abstract = {Oral and systemic human health depend on the symbiotic relationship between the human host and its microbiome. As the second most diverse site of the human microbiome, the oral cavity is instrumental in symbiotic relationships, transforming nutrients and acting as the human body's initial barrier against pathogens. However, under certain conditions, the typically beneficial oral microbiome can become harmful. Systemic inflammatory diseases can send signals through the oral-gut axis, such as cytokines and host defensins, altering gene expression and, consequently, the composition of the oral microbiome. These changes can be responsible for causing oral diseases, such as periodontitis and candidiasis. Evidence of metabolic syndrome, including obesity, hypertension, hyperglycemia, and dyslipidemia, exacerbates oral microbiome dysbiosis. On the other hand, the oral microbiota can also influence systemic health. Inflammatory processes in the gingival structures caused by a dysbiotic oral microbiome are linked to worsen glycemic levels in diabetics, premature birth, and rheumatoid arthritis, among others. The idea for this book emerged from the need to explore the multifaceted nature of this relationship in its various dimensions. We discuss multispecies characteristics from an ecological perspective, focusing on how the host affects the microbiome and vice versa. Understanding how the oral microbiome influences human health will guide tailored strategies for disease prevention and treatment, which is discussed in the last section of the book. Looking ahead, predictive health and disease models will enable personalized therapies centered on restoring the healthy human microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mouth/microbiology
*Microbiota/physiology
*Dysbiosis/microbiology
Periodontitis/microbiology
Animals
Oral Health
RevDate: 2025-03-20
Backtracking identification techniques for predicting unclear bacterial taxonomy at species level: molecular diagnosis-based bacterial classification.
Genes & genomics [Epub ahead of print].
Bacterial 16S rRNA genes are widely used to classify bacterial communities within interesting environments (e.g., plants, water, human body) because they contain nine hyper-variable regions (V1-V9) reflecting a large number of sequence variation sites between species. Short-read sequencing platform (targeting partial region of 16S rRNA gene; approximately 150-500 bp) commonly used in the 16S-based microbiome study is favored by many researchers because it is economical and can generate highthroughput sequencing data faster than long-read sequencing platforms. However, this sequencing platform has technical limitations in that it cannot clarify bacterial classification at the species level compared to long-read sequencing technology, which can cover the unclassification issue due to sequence similarity between species by targeting the 16S full-length region. In recent microbiome research-related industries, species-level high-resolution microbial classification is considered a key challenge to secure microbial resources among institutions in the field. However, the long-read sequencing platforms currently offered are still under price adjustment (demanding higher cost than short-read sequencing platforms) and have the disadvantage of low base-calling accuracy compared to short-read sequencing platforms. Therefore, this brief communication introduces the'Molecular diagnosis-based bacterial classification' technology to predict candidate species by backtracking for unclassified bacterial taxonomy at the species level in the NGS-based 16S microbiome study.
Additional Links: PMID-40111647
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Citation:
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@article {pmid40111647,
year = {2025},
author = {Choi, Y and Jeong, J and Kim, M and Cha, S and Han, K},
title = {Backtracking identification techniques for predicting unclear bacterial taxonomy at species level: molecular diagnosis-based bacterial classification.},
journal = {Genes & genomics},
volume = {},
number = {},
pages = {},
pmid = {40111647},
issn = {2092-9293},
support = {RS-2024-00355393//National Institute for International Education/ ; },
abstract = {Bacterial 16S rRNA genes are widely used to classify bacterial communities within interesting environments (e.g., plants, water, human body) because they contain nine hyper-variable regions (V1-V9) reflecting a large number of sequence variation sites between species. Short-read sequencing platform (targeting partial region of 16S rRNA gene; approximately 150-500 bp) commonly used in the 16S-based microbiome study is favored by many researchers because it is economical and can generate highthroughput sequencing data faster than long-read sequencing platforms. However, this sequencing platform has technical limitations in that it cannot clarify bacterial classification at the species level compared to long-read sequencing technology, which can cover the unclassification issue due to sequence similarity between species by targeting the 16S full-length region. In recent microbiome research-related industries, species-level high-resolution microbial classification is considered a key challenge to secure microbial resources among institutions in the field. However, the long-read sequencing platforms currently offered are still under price adjustment (demanding higher cost than short-read sequencing platforms) and have the disadvantage of low base-calling accuracy compared to short-read sequencing platforms. Therefore, this brief communication introduces the'Molecular diagnosis-based bacterial classification' technology to predict candidate species by backtracking for unclassified bacterial taxonomy at the species level in the NGS-based 16S microbiome study.},
}
RevDate: 2025-03-20
Quantifying uncertainty in microbiome-based prediction using Gaussian processes with microbial community dissimilarities.
Bioinformatics advances, 5(1):vbaf045.
SUMMARY: The human microbiome is closely associated with the health and disease of the human host. Machine learning models have recently utilized the human microbiome to predict health conditions and disease status. Quantifying predictive uncertainty is essential for the reliable application of these microbiome-based prediction models in clinical settings. However, uncertainty quantification in such prediction models remains unexplored. In this study, we have developed a probabilistic prediction model using a Gaussian process (GP) with a kernel function that incorporates microbial community dissimilarities. We evaluated the performance of probabilistic prediction across three regression tasks: chronological age, body mass index, and disease severity, using publicly available human gut microbiome datasets. The results demonstrated that our model outperformed existing methods in terms of probabilistic prediction accuracy. Furthermore, we found that the confidence levels closely matched the empirical coverage and that data points predicted with lower uncertainty corresponded to lower prediction errors. These findings suggest that GP regression models incorporating community dissimilarities effectively capture the characteristics of phylogenetic, high-dimensional, and sparse microbial abundance data. Our study provides a more reliable framework for microbiome-based prediction, potentially advancing the application of microbiome data in health monitoring and disease diagnosis in clinical settings.
The code is available at https://github.com/asahiadachi/gp4microbiome.
Additional Links: PMID-40110560
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Citation:
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@article {pmid40110560,
year = {2025},
author = {Adachi, A and Zhang, F and Kanaya, S and Ono, N},
title = {Quantifying uncertainty in microbiome-based prediction using Gaussian processes with microbial community dissimilarities.},
journal = {Bioinformatics advances},
volume = {5},
number = {1},
pages = {vbaf045},
pmid = {40110560},
issn = {2635-0041},
abstract = {SUMMARY: The human microbiome is closely associated with the health and disease of the human host. Machine learning models have recently utilized the human microbiome to predict health conditions and disease status. Quantifying predictive uncertainty is essential for the reliable application of these microbiome-based prediction models in clinical settings. However, uncertainty quantification in such prediction models remains unexplored. In this study, we have developed a probabilistic prediction model using a Gaussian process (GP) with a kernel function that incorporates microbial community dissimilarities. We evaluated the performance of probabilistic prediction across three regression tasks: chronological age, body mass index, and disease severity, using publicly available human gut microbiome datasets. The results demonstrated that our model outperformed existing methods in terms of probabilistic prediction accuracy. Furthermore, we found that the confidence levels closely matched the empirical coverage and that data points predicted with lower uncertainty corresponded to lower prediction errors. These findings suggest that GP regression models incorporating community dissimilarities effectively capture the characteristics of phylogenetic, high-dimensional, and sparse microbial abundance data. Our study provides a more reliable framework for microbiome-based prediction, potentially advancing the application of microbiome data in health monitoring and disease diagnosis in clinical settings.
The code is available at https://github.com/asahiadachi/gp4microbiome.},
}
RevDate: 2025-03-20
CmpDate: 2025-03-20
Extracellular Vesicle-Associated miR-ERIA Exerts the Antiangiogenic Effect of Macrophages in Diabetic Wound Healing.
Diabetes, 74(4):596-610.
An understanding of cell interactions is needed to identify therapeutic targets for diabetic cutaneous ulcers. We explored extracellular vesicles after treatment with advanced glycation end products (AGEs-EVs) derived from macrophages that can suppress diabetic cutaneous wound healing. We found that a novel miRNA enriched in AGEs-EVs (miR-ERIA) suppresses the migration and tube formation of vascular endothelial cells by targeting helicase with zinc finger 2. miR-ERIA offers a potential therapeutic target for diabetic cutaneous ulcers.
Additional Links: PMID-39854218
Publisher:
PubMed:
Citation:
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@article {pmid39854218,
year = {2025},
author = {Zeng, T and Sun, K and Mai, L and Hong, X and He, X and Lin, W and Chen, S and Yan, L},
title = {Extracellular Vesicle-Associated miR-ERIA Exerts the Antiangiogenic Effect of Macrophages in Diabetic Wound Healing.},
journal = {Diabetes},
volume = {74},
number = {4},
pages = {596-610},
doi = {10.2337/db24-0701},
pmid = {39854218},
issn = {1939-327X},
support = {82222014//The National Natural Science Foundation of China Excellent Young Scientists Fund/ ; 2023A03J0706//Ministry of Education, China; Guangzhou Science and Technology Program/ ; 2020B1111170009//Guangdong Clinical Research Center for Metabolic Diseases/ ; 202102100004//Guangzhou Key Laboratory for Metabolic Diseases/ ; 32271185//The National Natural Science Foundation of China/ ; Sun Yat-sen University//Key Laboratory of Human Microbiome and Chronic Diseases/ ; 82200902//National Natural Science Foundation of China/ ; },
mesh = {*Wound Healing/drug effects/physiology ; *Extracellular Vesicles/metabolism ; *MicroRNAs/metabolism/genetics ; *Macrophages/metabolism/drug effects ; Animals ; Humans ; Mice ; Glycation End Products, Advanced/metabolism ; Cell Movement/drug effects ; Human Umbilical Vein Endothelial Cells/metabolism ; Endothelial Cells/metabolism/drug effects ; Angiogenesis Inhibitors/pharmacology/therapeutic use ; Skin Ulcer/metabolism/genetics ; Diabetes Mellitus, Experimental/metabolism ; },
abstract = {An understanding of cell interactions is needed to identify therapeutic targets for diabetic cutaneous ulcers. We explored extracellular vesicles after treatment with advanced glycation end products (AGEs-EVs) derived from macrophages that can suppress diabetic cutaneous wound healing. We found that a novel miRNA enriched in AGEs-EVs (miR-ERIA) suppresses the migration and tube formation of vascular endothelial cells by targeting helicase with zinc finger 2. miR-ERIA offers a potential therapeutic target for diabetic cutaneous ulcers.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Wound Healing/drug effects/physiology
*Extracellular Vesicles/metabolism
*MicroRNAs/metabolism/genetics
*Macrophages/metabolism/drug effects
Animals
Humans
Mice
Glycation End Products, Advanced/metabolism
Cell Movement/drug effects
Human Umbilical Vein Endothelial Cells/metabolism
Endothelial Cells/metabolism/drug effects
Angiogenesis Inhibitors/pharmacology/therapeutic use
Skin Ulcer/metabolism/genetics
Diabetes Mellitus, Experimental/metabolism
RevDate: 2025-03-19
CmpDate: 2025-03-19
Maternal balanced energy-protein supplementation reshapes the maternal gut microbiome and enhances carbohydrate metabolism in infants: a randomized controlled trial.
Nature communications, 16(1):2683.
Balanced energy-protein (BEP) supplementation during pregnancy and lactation can improve birth outcomes and infant growth, with the gut microbiome as a potential mediator. The MISAME-III randomized controlled trial (ClinicalTrial.gov: NCT03533712) assessed the effect of BEP supplementation, provided during pregnancy and the first six months of lactation, on small-for-gestational age prevalence and length-for-age Z-scores at six months in rural Burkina Faso. Nested within MISAME-III, this sub-study examines the impact of BEP supplementation on maternal and infant gut microbiomes and their mediating role in birth outcomes and infant growth. A total of 152 mother-infant dyads (n = 71 intervention, n = 81 control) were included for metagenomic sequencing, with stool samples collected at the second and third trimesters, and at 1-2 and 5-6 months postpartum. BEP supplementation significantly altered maternal gut microbiome diversity, composition, and function, particularly those with immune-modulatory properties. Pathways linked to lipopolysaccharide biosynthesis were depleted and the species Bacteroides fragilis was enriched in BEP-supplemented mothers. Maternal BEP supplementation also accelerated infant microbiome changes and enhanced carbohydrate metabolism. Causal mediation analyses identified specific taxa mediating the effect of BEP on birth outcomes and infant growth. These findings suggest that maternal supplementation modulates gut microbiome composition and influences early-life development in resource-limited settings.
Additional Links: PMID-40102379
PubMed:
Citation:
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@article {pmid40102379,
year = {2025},
author = {Deng, L and Taelman, S and Olm, MR and Toe, LC and Balini, E and OuΓ©draogo, LO and Bastos-Moreira, Y and Argaw, A and Tesfamariam, K and Sonnenburg, ED and Hanley-Cook, GT and OuΓ©draogo, M and Ganaba, R and Van Criekinge, W and Huybregts, L and Stock, M and Kolsteren, P and Sonnenburg, JL and Lachat, C and Dailey-ChwalibΓ³g, T},
title = {Maternal balanced energy-protein supplementation reshapes the maternal gut microbiome and enhances carbohydrate metabolism in infants: a randomized controlled trial.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {2683},
pmid = {40102379},
issn = {2041-1723},
support = {OPP1175213//Bill and Melinda Gates Foundation (Bill & Melinda Gates Foundation)/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Female ; *Dietary Supplements ; Infant ; Pregnancy ; Adult ; Burkina Faso ; *Carbohydrate Metabolism ; Infant, Newborn ; Feces/microbiology ; Dietary Proteins/metabolism ; Male ; Lactation ; },
abstract = {Balanced energy-protein (BEP) supplementation during pregnancy and lactation can improve birth outcomes and infant growth, with the gut microbiome as a potential mediator. The MISAME-III randomized controlled trial (ClinicalTrial.gov: NCT03533712) assessed the effect of BEP supplementation, provided during pregnancy and the first six months of lactation, on small-for-gestational age prevalence and length-for-age Z-scores at six months in rural Burkina Faso. Nested within MISAME-III, this sub-study examines the impact of BEP supplementation on maternal and infant gut microbiomes and their mediating role in birth outcomes and infant growth. A total of 152 mother-infant dyads (n = 71 intervention, n = 81 control) were included for metagenomic sequencing, with stool samples collected at the second and third trimesters, and at 1-2 and 5-6 months postpartum. BEP supplementation significantly altered maternal gut microbiome diversity, composition, and function, particularly those with immune-modulatory properties. Pathways linked to lipopolysaccharide biosynthesis were depleted and the species Bacteroides fragilis was enriched in BEP-supplemented mothers. Maternal BEP supplementation also accelerated infant microbiome changes and enhanced carbohydrate metabolism. Causal mediation analyses identified specific taxa mediating the effect of BEP on birth outcomes and infant growth. These findings suggest that maternal supplementation modulates gut microbiome composition and influences early-life development in resource-limited settings.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/drug effects
Female
*Dietary Supplements
Infant
Pregnancy
Adult
Burkina Faso
*Carbohydrate Metabolism
Infant, Newborn
Feces/microbiology
Dietary Proteins/metabolism
Male
Lactation
RevDate: 2025-03-18
The human microbiome-derived antimicrobial lugdunin self-regulates its biosynthesis by a feed-forward mechanism.
mBio [Epub ahead of print].
Many human microbiome members inhibit bacterial competitors by production of antimicrobial compounds whose expression needs to be tightly controlled to balance the costs and benefits of compound biosynthesis. The nasal commensal Staphylococcus lugdunensis outcompetes Staphylococcus aureus using the antimicrobial lugdunin. The lugdunin biosynthetic gene cluster (BGC) encodes two potential regulators whose roles have remained unknown. Deletion of the regulator genes lugR or lugJ led to increased lugdunin production and/or immunity. While LugR was found to repress the transcription of the biosynthetic lugRABCTDZ operon, LugJ repressed the lugIEFGH export and immunity genes. Both regulators bound to different inverted repeats in the controlled promoter regions. Notably, both repressors were released from cognate promoters to allow transcription upon addition of exogenous lugdunin. Even minor structural changes disabled lugdunin derivatives to induce expression of its BGC, which is consistent with inferior binding to the predicted LugR and LugJ binding pockets. Thus, lugdunin controls its own biosynthesis through a feed-forward mechanism probably to avoid futile production.IMPORTANCEBiosynthetic gene clusters (BGCs) are usually tightly controlled to avoid production of costly goods at inappropriate time points or unfavorable conditions. However, in most cases, the regulatory signals of these clusters have remained unknown. Frequently, quorum sensing or two-component regulatory systems are involved in BGC expression control. This study elucidates the sophisticated regulation of lugdunin biosynthesis and secretion via two independent regulators, LugR and LugJ. Although belonging to different families of repressors, both directly interact with the antimicrobial lugdunin and thereby enhance biosynthesis and secretion in a feed forward-like mechanism.
Additional Links: PMID-40099907
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@article {pmid40099907,
year = {2025},
author = {Reetz, L and Schulze, L and Kronenberger, T and Selim, KA and Schaefle, T and Dema, T and Zipperer, A and MΓΆΓner, J and Poso, A and Grond, S and Peschel, A and Krismer, B},
title = {The human microbiome-derived antimicrobial lugdunin self-regulates its biosynthesis by a feed-forward mechanism.},
journal = {mBio},
volume = {},
number = {},
pages = {e0357124},
doi = {10.1128/mbio.03571-24},
pmid = {40099907},
issn = {2150-7511},
abstract = {Many human microbiome members inhibit bacterial competitors by production of antimicrobial compounds whose expression needs to be tightly controlled to balance the costs and benefits of compound biosynthesis. The nasal commensal Staphylococcus lugdunensis outcompetes Staphylococcus aureus using the antimicrobial lugdunin. The lugdunin biosynthetic gene cluster (BGC) encodes two potential regulators whose roles have remained unknown. Deletion of the regulator genes lugR or lugJ led to increased lugdunin production and/or immunity. While LugR was found to repress the transcription of the biosynthetic lugRABCTDZ operon, LugJ repressed the lugIEFGH export and immunity genes. Both regulators bound to different inverted repeats in the controlled promoter regions. Notably, both repressors were released from cognate promoters to allow transcription upon addition of exogenous lugdunin. Even minor structural changes disabled lugdunin derivatives to induce expression of its BGC, which is consistent with inferior binding to the predicted LugR and LugJ binding pockets. Thus, lugdunin controls its own biosynthesis through a feed-forward mechanism probably to avoid futile production.IMPORTANCEBiosynthetic gene clusters (BGCs) are usually tightly controlled to avoid production of costly goods at inappropriate time points or unfavorable conditions. However, in most cases, the regulatory signals of these clusters have remained unknown. Frequently, quorum sensing or two-component regulatory systems are involved in BGC expression control. This study elucidates the sophisticated regulation of lugdunin biosynthesis and secretion via two independent regulators, LugR and LugJ. Although belonging to different families of repressors, both directly interact with the antimicrobial lugdunin and thereby enhance biosynthesis and secretion in a feed forward-like mechanism.},
}
RevDate: 2025-03-14
Modelling international travel as risk of acquiring Dientamoeba fragilis: comparison to Giardia duodenalis data.
Travel medicine and infectious disease pii:S1477-8939(25)00042-0 [Epub ahead of print].
BACKGROUND: The intestinal parasite Dientamoeba fragilis (DF) is spread worldwide and can cause prolonged gastrointestinal symptoms, yet its link to international travel has been scarcely studied. To explore this connection, we examined the association between DF cases and international travel history by destination, comparing the findings to data on Giardia duodenalis (GD), a common travel-acquired intestinal parasite.
METHODS: We analysed clinical data from patients with DF or GD infection in the Helsinki Metropolitan Area, categorizing the patients as travellers and non-travellers on the basis of their travel history. To assess acquisition risk by destination, we devised a DF/GD risk score (RS) relating case numbers to travel volumes as denominators in each destination, with travel data retrieved from the Official Statistics of Finland (OSF).
RESULTS: Travel history was reported less frequently by patients with DF (30%) than GD (60%). DF had the highest RSs for Africa (41.3), followed by Asia and Oceania (17.9) and the Americas (11.5). The respective GD RSs were 32.8, 25.4, and 11.9. The lowest RSs for both parasites were recorded for Eastern and Western Europe, Russia and the Baltic countries, and Scandinavia. For Asia and Oceania, the GD RS exceeded that of DF; for the other sites, DF had higher RSs than GD.
CONCLUSIONS: Dientamoeba fragilis appears to be transmitted both domestically and internationally. Although the overall acquisition risk appears low, for both Dientamoeba fragilis and Giardia duodenalis, the highest RSs are linked to visits to (sub)tropical regions, with subregional differences between the two parasites.
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@article {pmid40086654,
year = {2025},
author = {PietilΓ€, JP and HΓ€kkinen, T and Ollgren, J and Kantele, A},
title = {Modelling international travel as risk of acquiring Dientamoeba fragilis: comparison to Giardia duodenalis data.},
journal = {Travel medicine and infectious disease},
volume = {},
number = {},
pages = {102836},
doi = {10.1016/j.tmaid.2025.102836},
pmid = {40086654},
issn = {1873-0442},
abstract = {BACKGROUND: The intestinal parasite Dientamoeba fragilis (DF) is spread worldwide and can cause prolonged gastrointestinal symptoms, yet its link to international travel has been scarcely studied. To explore this connection, we examined the association between DF cases and international travel history by destination, comparing the findings to data on Giardia duodenalis (GD), a common travel-acquired intestinal parasite.
METHODS: We analysed clinical data from patients with DF or GD infection in the Helsinki Metropolitan Area, categorizing the patients as travellers and non-travellers on the basis of their travel history. To assess acquisition risk by destination, we devised a DF/GD risk score (RS) relating case numbers to travel volumes as denominators in each destination, with travel data retrieved from the Official Statistics of Finland (OSF).
RESULTS: Travel history was reported less frequently by patients with DF (30%) than GD (60%). DF had the highest RSs for Africa (41.3), followed by Asia and Oceania (17.9) and the Americas (11.5). The respective GD RSs were 32.8, 25.4, and 11.9. The lowest RSs for both parasites were recorded for Eastern and Western Europe, Russia and the Baltic countries, and Scandinavia. For Asia and Oceania, the GD RS exceeded that of DF; for the other sites, DF had higher RSs than GD.
CONCLUSIONS: Dientamoeba fragilis appears to be transmitted both domestically and internationally. Although the overall acquisition risk appears low, for both Dientamoeba fragilis and Giardia duodenalis, the highest RSs are linked to visits to (sub)tropical regions, with subregional differences between the two parasites.},
}
RevDate: 2025-03-14
Mycobiome: an underexplored kingdom in cancer.
Microbiology and molecular biology reviews : MMBR [Epub ahead of print].
SUMMARYThe human microbiome, including bacteria, fungi, archaea, and viruses, is intimately linked to both health and disease. The relationship between bacteria and disease has received much attention and intensive investigation, while that of the fungal microbiome, also known as mycobiome, has lagged far behind bacteria. There is growing evidence showing mycobiome dysbiosis in cancer patients, and certain cancer-specific fungi may contribute to cancer progression by interacting with both host and bacteria. It was also demonstrated that the role of fungi-derived products in cancer should also not be underestimated. Therefore, investigating how fungal pathogenesis contributes to the onset and spread of cancer would yield crucial information for cancer diagnosis, prevention, and anti-cancer therapy.
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@article {pmid40084887,
year = {2025},
author = {Sun, Y-Y and Liu, N-N},
title = {Mycobiome: an underexplored kingdom in cancer.},
journal = {Microbiology and molecular biology reviews : MMBR},
volume = {},
number = {},
pages = {e0026124},
doi = {10.1128/mmbr.00261-24},
pmid = {40084887},
issn = {1098-5557},
abstract = {SUMMARYThe human microbiome, including bacteria, fungi, archaea, and viruses, is intimately linked to both health and disease. The relationship between bacteria and disease has received much attention and intensive investigation, while that of the fungal microbiome, also known as mycobiome, has lagged far behind bacteria. There is growing evidence showing mycobiome dysbiosis in cancer patients, and certain cancer-specific fungi may contribute to cancer progression by interacting with both host and bacteria. It was also demonstrated that the role of fungi-derived products in cancer should also not be underestimated. Therefore, investigating how fungal pathogenesis contributes to the onset and spread of cancer would yield crucial information for cancer diagnosis, prevention, and anti-cancer therapy.},
}
RevDate: 2025-03-14
Engineering mucus to study and influence the microbiome.
Nature reviews. Materials, 4(2):134-145.
Mucus is a 3D hydrogel that houses the majority of the human microbiome. The mucous environment plays an important role in the differentiation and behaviour of microbial phenotypes and enables the creation of spatial distributions. Dysregulation of mucus is further associated with various diseases. Therefore, mucus is the key ingredient to study the behaviour of commensal and pathogenic microbiota in vitro. Indeed, microorganisms cultured in mucus exhibit phenotypes substantially different from those exhibited in standard laboratory media. In this Review, we discuss the impact of mucus on the microbiome and examine the structure and glycosylation of mucins - the main building blocks of mucus. We investigate the impact of glycans on mucin function and highlight different approaches for the engineering of synthetic mucins, including synthesis of the backbone, the design of mucin-mimetic hydrogels and the engineering of glycans. Finally, mucin mimetics for 3D in vitro cell culture and for modulating microbial community structure and function are discussed.
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@article {pmid40084234,
year = {2019},
author = {Werlang, C and CΓ‘rcarmo-Oyarce, G and Ribbeck, K},
title = {Engineering mucus to study and influence the microbiome.},
journal = {Nature reviews. Materials},
volume = {4},
number = {2},
pages = {134-145},
pmid = {40084234},
issn = {2058-8437},
abstract = {Mucus is a 3D hydrogel that houses the majority of the human microbiome. The mucous environment plays an important role in the differentiation and behaviour of microbial phenotypes and enables the creation of spatial distributions. Dysregulation of mucus is further associated with various diseases. Therefore, mucus is the key ingredient to study the behaviour of commensal and pathogenic microbiota in vitro. Indeed, microorganisms cultured in mucus exhibit phenotypes substantially different from those exhibited in standard laboratory media. In this Review, we discuss the impact of mucus on the microbiome and examine the structure and glycosylation of mucins - the main building blocks of mucus. We investigate the impact of glycans on mucin function and highlight different approaches for the engineering of synthetic mucins, including synthesis of the backbone, the design of mucin-mimetic hydrogels and the engineering of glycans. Finally, mucin mimetics for 3D in vitro cell culture and for modulating microbial community structure and function are discussed.},
}
RevDate: 2025-03-13
CmpDate: 2025-03-13
Host Transcriptome and Microbial Variation in Relation to Visceral Hyperalgesia.
Nutrients, 17(5): pii:nu17050921.
BACKGROUND: Chronic visceral hypersensitivity is associated with an overstressed pain response to noxious stimuli (hyperalgesia). Microbiota are active modulators of host biology and are implicated in the etiology of visceral hypersensitivity.
OBJECTIVES: we studied the association between the circulating mRNA transcriptome, the intensity of induced visceral pain (IVP), and variation in the oral microbiome among participants with and without baseline visceral hypersensitivity.
METHODS: Transcriptomic profiles and microbial abundance were correlated with IVP intensity. Host mRNA and microbes associated with IVP were explored, linking variation in the microbiome to host RNA biology.
RESULTS: 259 OTUs were found to be associated with IVP through correlation to differential expression of 471 genes in molecular pathways related to inflammation and neural mechanisms, including Rho and PI3K/AKT pathways. The bacterial families Lachnospiraceae, Prevotellaceae, and Veillonellaceae showed the highest degree of association. Oral microbial profiles with reduced diversity were characteristic of participants with visceral hypersensitivity.
CONCLUSIONS: Our results suggest that the oral microbiome may be involved in systemic immune and inflammatory effects and play a role in nervous system and stem cell pathways. The interactions between visceral hypersensitivity, differentially expressed molecular pathways, and microbiota described here provide a framework for further work exploring the relationship between host and microbiome.
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@article {pmid40077792,
year = {2025},
author = {Costa, CJ and Prescott, S and Fourie, NH and Abey, SK and Sherwin, LB and Rahim-Williams, B and Joseph, PV and Posada-Quintero, H and Hoffman, RK and Henderson, WA},
title = {Host Transcriptome and Microbial Variation in Relation to Visceral Hyperalgesia.},
journal = {Nutrients},
volume = {17},
number = {5},
pages = {},
doi = {10.3390/nu17050921},
pmid = {40077792},
issn = {2072-6643},
support = {1ZIANR000018-01-09; K22MD006143-01/GF/NIH HHS/United States ; },
mesh = {Humans ; *Hyperalgesia/microbiology ; *Transcriptome ; Male ; Female ; Adult ; Visceral Pain/microbiology ; Microbiota ; RNA, Messenger/metabolism ; Middle Aged ; Mouth/microbiology ; Gastrointestinal Microbiome ; Bacteria/genetics/classification ; Young Adult ; },
abstract = {BACKGROUND: Chronic visceral hypersensitivity is associated with an overstressed pain response to noxious stimuli (hyperalgesia). Microbiota are active modulators of host biology and are implicated in the etiology of visceral hypersensitivity.
OBJECTIVES: we studied the association between the circulating mRNA transcriptome, the intensity of induced visceral pain (IVP), and variation in the oral microbiome among participants with and without baseline visceral hypersensitivity.
METHODS: Transcriptomic profiles and microbial abundance were correlated with IVP intensity. Host mRNA and microbes associated with IVP were explored, linking variation in the microbiome to host RNA biology.
RESULTS: 259 OTUs were found to be associated with IVP through correlation to differential expression of 471 genes in molecular pathways related to inflammation and neural mechanisms, including Rho and PI3K/AKT pathways. The bacterial families Lachnospiraceae, Prevotellaceae, and Veillonellaceae showed the highest degree of association. Oral microbial profiles with reduced diversity were characteristic of participants with visceral hypersensitivity.
CONCLUSIONS: Our results suggest that the oral microbiome may be involved in systemic immune and inflammatory effects and play a role in nervous system and stem cell pathways. The interactions between visceral hypersensitivity, differentially expressed molecular pathways, and microbiota described here provide a framework for further work exploring the relationship between host and microbiome.},
}
MeSH Terms:
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Humans
*Hyperalgesia/microbiology
*Transcriptome
Male
Female
Adult
Visceral Pain/microbiology
Microbiota
RNA, Messenger/metabolism
Middle Aged
Mouth/microbiology
Gastrointestinal Microbiome
Bacteria/genetics/classification
Young Adult
RevDate: 2025-03-13
CmpDate: 2025-03-13
Mediation CNN (Med-CNN) Model for High-Dimensional Mediation Data.
International journal of molecular sciences, 26(5): pii:ijms26051819.
Complex biological features such as the human microbiome and gene expressions play a crucial role in human health by mediating various biomedical processes that influence disease progression, such as immune responses and metabolic processes. Understanding these mediation roles is essential for gaining insights into disease pathogenesis and improving treatment outcomes. However, analyzing such high-dimensional mediation features presents challenges due to their inherent structural and correlations, such as the hierarchical taxonomic structures in microbial operational taxonomic units (OTUs), gene-pathway relationships, and the high dimensionality of the datasets, which complicates mediation analysis. We propose the Med-CNN model, an iterative approach using Convolutional Neural Networks (CNNs) to incorporate the complex biological network of the mediation features. The output values from network-specific CNN models are condensed into an integrative mediation metric (IMM), which captures essential biological information for estimating mediation effects. Our approach is designed to handle high-dimensional data and accommodate their unique structures and non-linear interactive mediation effects. Through comprehensive simulation studies, we evaluated the performance of our algorithm across different scenarios, including various mediation effects, effect sizes, and sample sizes, and we compared it to conventional methods. Our simulations demonstrated consistently lower biases in mediation effect estimates, with values ranging from 0.17 to 0.56, which were lower than other established methods ranging from 0.24 to 13.27. In a real data application, our method identified a mediation effect of 0.06 between ethnicity and vaginal pH levels.
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@article {pmid40076446,
year = {2025},
author = {Li, Y and Zhang, ZJ and Saarela, O and Sharma, D and Xu, W},
title = {Mediation CNN (Med-CNN) Model for High-Dimensional Mediation Data.},
journal = {International journal of molecular sciences},
volume = {26},
number = {5},
pages = {},
doi = {10.3390/ijms26051819},
pmid = {40076446},
issn = {1422-0067},
support = {RGPIN-2024-06081//Natural Sciences and Engineering Research Council/ ; },
mesh = {Humans ; *Algorithms ; *Neural Networks, Computer ; *Microbiota ; Female ; Computer Simulation ; },
abstract = {Complex biological features such as the human microbiome and gene expressions play a crucial role in human health by mediating various biomedical processes that influence disease progression, such as immune responses and metabolic processes. Understanding these mediation roles is essential for gaining insights into disease pathogenesis and improving treatment outcomes. However, analyzing such high-dimensional mediation features presents challenges due to their inherent structural and correlations, such as the hierarchical taxonomic structures in microbial operational taxonomic units (OTUs), gene-pathway relationships, and the high dimensionality of the datasets, which complicates mediation analysis. We propose the Med-CNN model, an iterative approach using Convolutional Neural Networks (CNNs) to incorporate the complex biological network of the mediation features. The output values from network-specific CNN models are condensed into an integrative mediation metric (IMM), which captures essential biological information for estimating mediation effects. Our approach is designed to handle high-dimensional data and accommodate their unique structures and non-linear interactive mediation effects. Through comprehensive simulation studies, we evaluated the performance of our algorithm across different scenarios, including various mediation effects, effect sizes, and sample sizes, and we compared it to conventional methods. Our simulations demonstrated consistently lower biases in mediation effect estimates, with values ranging from 0.17 to 0.56, which were lower than other established methods ranging from 0.24 to 13.27. In a real data application, our method identified a mediation effect of 0.06 between ethnicity and vaginal pH levels.},
}
MeSH Terms:
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Humans
*Algorithms
*Neural Networks, Computer
*Microbiota
Female
Computer Simulation
RevDate: 2025-03-12
CmpDate: 2025-03-12
Dietary risk factors in Crohn's disease and ulcerative colitis: a cohort study with paired healthy relatives as controls.
European journal of nutrition, 64(3):123.
PURPOSE: Conflicting results have been reported on dietary factors in inflammatory bowel diseases (IBDs). Here, we compared the dietary intakes of IBD patients with those of paired healthy relatives (HRs), aiming to minimize the impact of genetic and environmental confounders.
METHODS: Patients with Crohn's disease (CD, N = 45) and ulcerative colitis (UC, N = 20), their paired HRs (NCD-HR = 45, NUC-HR = 20) and healthy non-relative (HNR, NCD-HNR = 25, NUC-HNR = 55) controls were recruited. Participants have kept dietary habits since the onset of IBDs and report no other recent digestive diseases or surgeries. Pre-illness dietary factors were assessed through 24-hour recall interviews. Statistical analyses included Analysis of Variance, Fisher's exact tests, Wilcoxon rank sum tests, logistic regressions, Area Under the Receiver-Operator Curve (AUROC) analysis, and Least Absolute Shrinkage and Selection Operator (LASSO) regression.
RESULTS: Dietary features identified in IBD patients using the HR controls differed from those identified using the HNR controls. For CD, lower intakes of vitamin C, dietary fiber, calcium, vegetables, decanoic acid (10:0), milk, dairy foods, and β-carotene were identified as risk factors when compared to HRs. LASSO regression highlighted milk, vegetables, and vitamin C as the most significant risk factors for CD. In UC patients, lower intakes of phosphorus, docosapentaenoic acid (DPA, 22:5, n-3), vitamins B-2 and B-12, and choline, along with a higher intake of α-carotene, were identified as risk factors compared to HRs. LASSO regression emphasized DPA, vitamins B-2 and B-12, and α-carotene as the most significant risk factors for UC.
CONCLUSION: Monitoring dietary intake patterns is crucial for the prevention and personalized treatment of CD and UC.
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@article {pmid40072660,
year = {2025},
author = {Hu, J and Chen, W and Zhu, R and Yang, F and Xu, J and Xiang, B and Li, Y and Wang, W and Zhu, L and Chen, G and Zhi, M},
title = {Dietary risk factors in Crohn's disease and ulcerative colitis: a cohort study with paired healthy relatives as controls.},
journal = {European journal of nutrition},
volume = {64},
number = {3},
pages = {123},
pmid = {40072660},
issn = {1436-6215},
support = {2014008//Sun Yat-sen University Clinical Research 5010 Program/ ; 82170542//National Natural Science Foundation of China/ ; 92251307//National Natural Science Foundation of China/ ; 82270544//National Natural Science Foundation of China/ ; 2019ZT08Y464//Guangdong Province "Pearl River Talent Plan" Innovation and Entrepreneurship Team Project/ ; 2021YFF0703702//National Key Research and Development Program of China/ ; 2023YFF1104404//National Key Research and Development Program of China/ ; 2023AFD124//Hubei Provincial Natural Science Foundation of China/ ; },
mesh = {Humans ; *Crohn Disease/epidemiology ; *Colitis, Ulcerative/epidemiology ; Female ; Male ; Risk Factors ; Adult ; *Diet/methods/statistics & numerical data ; Cohort Studies ; Middle Aged ; Case-Control Studies ; Family ; Feeding Behavior ; },
abstract = {PURPOSE: Conflicting results have been reported on dietary factors in inflammatory bowel diseases (IBDs). Here, we compared the dietary intakes of IBD patients with those of paired healthy relatives (HRs), aiming to minimize the impact of genetic and environmental confounders.
METHODS: Patients with Crohn's disease (CD, N = 45) and ulcerative colitis (UC, N = 20), their paired HRs (NCD-HR = 45, NUC-HR = 20) and healthy non-relative (HNR, NCD-HNR = 25, NUC-HNR = 55) controls were recruited. Participants have kept dietary habits since the onset of IBDs and report no other recent digestive diseases or surgeries. Pre-illness dietary factors were assessed through 24-hour recall interviews. Statistical analyses included Analysis of Variance, Fisher's exact tests, Wilcoxon rank sum tests, logistic regressions, Area Under the Receiver-Operator Curve (AUROC) analysis, and Least Absolute Shrinkage and Selection Operator (LASSO) regression.
RESULTS: Dietary features identified in IBD patients using the HR controls differed from those identified using the HNR controls. For CD, lower intakes of vitamin C, dietary fiber, calcium, vegetables, decanoic acid (10:0), milk, dairy foods, and β-carotene were identified as risk factors when compared to HRs. LASSO regression highlighted milk, vegetables, and vitamin C as the most significant risk factors for CD. In UC patients, lower intakes of phosphorus, docosapentaenoic acid (DPA, 22:5, n-3), vitamins B-2 and B-12, and choline, along with a higher intake of α-carotene, were identified as risk factors compared to HRs. LASSO regression emphasized DPA, vitamins B-2 and B-12, and α-carotene as the most significant risk factors for UC.
CONCLUSION: Monitoring dietary intake patterns is crucial for the prevention and personalized treatment of CD and UC.},
}
MeSH Terms:
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Humans
*Crohn Disease/epidemiology
*Colitis, Ulcerative/epidemiology
Female
Male
Risk Factors
Adult
*Diet/methods/statistics & numerical data
Cohort Studies
Middle Aged
Case-Control Studies
Family
Feeding Behavior
RevDate: 2025-03-12
Role of human microbiota in facilitating the metastatic journey of cancer cells.
Naunyn-Schmiedeberg's archives of pharmacology [Epub ahead of print].
Cancer continues to be the leading cause of mortality worldwide, with metastasis being the primary contributor to cancer-related deaths. Despite significant advancements in cancer therapies, metastasis remains a major challenge in effective cancer management. Metastasis, the process by which cancer cells spread from the primary tumor to distant organs, is a complex phenomenon influenced by multiple factors, including the human microbiota. The human body encompasses various microorganisms, comprising bacteria, viruses, fungi, and protozoa, collectively known as microbiota. In fact, the microbiota is more abundant than human cells, and its disruption, leading to an imbalance in host-microbiota interactions (dysbiosis), has been linked to various diseases, including cancer. Among all microbiota, bacteria are one of the key contributors to cancer progression. Bacteria and bacteria-derived components such as secondary metabolites, QSPs, and toxins play a pivotal role in the metastatic progression of cancers. This review explores the intricate relationship between the human microbiota and cancer progression, focusing on different bacterial species which have been implicated in tumorigenesis, immune evasion, and metastasis. The present review explores the role of the human microbiome, specifically of bacteria in promoting metastasis in different types of cancers, demonstrating its ability to impact both the spread of tumors and their underlying mechanisms. This review also highlights the therapeutic potential and challenges of microbiome-based interventions in combating metastatic cancers. By addressing these challenges and by integrating microbiome-targeted strategies into clinical cancer treatment could represent a transformative approach in the fight against metastasis.
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@article {pmid40072555,
year = {2025},
author = {Shah, H and Patel, P and Nath, A and Shah, U and Sarkar, R},
title = {Role of human microbiota in facilitating the metastatic journey of cancer cells.},
journal = {Naunyn-Schmiedeberg's archives of pharmacology},
volume = {},
number = {},
pages = {},
pmid = {40072555},
issn = {1432-1912},
abstract = {Cancer continues to be the leading cause of mortality worldwide, with metastasis being the primary contributor to cancer-related deaths. Despite significant advancements in cancer therapies, metastasis remains a major challenge in effective cancer management. Metastasis, the process by which cancer cells spread from the primary tumor to distant organs, is a complex phenomenon influenced by multiple factors, including the human microbiota. The human body encompasses various microorganisms, comprising bacteria, viruses, fungi, and protozoa, collectively known as microbiota. In fact, the microbiota is more abundant than human cells, and its disruption, leading to an imbalance in host-microbiota interactions (dysbiosis), has been linked to various diseases, including cancer. Among all microbiota, bacteria are one of the key contributors to cancer progression. Bacteria and bacteria-derived components such as secondary metabolites, QSPs, and toxins play a pivotal role in the metastatic progression of cancers. This review explores the intricate relationship between the human microbiota and cancer progression, focusing on different bacterial species which have been implicated in tumorigenesis, immune evasion, and metastasis. The present review explores the role of the human microbiome, specifically of bacteria in promoting metastasis in different types of cancers, demonstrating its ability to impact both the spread of tumors and their underlying mechanisms. This review also highlights the therapeutic potential and challenges of microbiome-based interventions in combating metastatic cancers. By addressing these challenges and by integrating microbiome-targeted strategies into clinical cancer treatment could represent a transformative approach in the fight against metastasis.},
}
RevDate: 2025-03-12
Leveraging microbiome signatures to predict tumor immune microenvironment and prognosis of patients with endometrial carcinoma.
Discover oncology, 16(1):299.
Recent studies suggest that the human microbiome influence tumor development. Endometrial carcinoma (EC) is the sixth most common malignancy in women. Recent research has demonstrated the microbes play a critical role in the development and metastasis of EC. However, it remains unclear whether intratumoral microbes are associated with tumor microenvironment (TME) and prognosis of EC. In this study, we collected the EC microbiome data from cBioPortal and constructed a prognostic model based on Resident Microbiome of Endometrium (RME). We then examined the relationship between the RME score, immune cell infiltration, immunotherapy-related signature, and prognosis. The findings demonstrated the independent prognostic value of the RME score for EC. The group with low RME scores had higher enrichment of immune cells. Drug sensitivity analysis revealed that the RME score may serve as a potential predictor of chemotherapy efficacy. In conclusion, our research offers new perspectives on the relationships between tumor immunity and microbes.
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@article {pmid40069468,
year = {2025},
author = {Yang, Y and Meng, Y and Xu, Z and Zhang, Q and Li, M and Kong, F and Zhang, S and Li, X and Zhu, Y},
title = {Leveraging microbiome signatures to predict tumor immune microenvironment and prognosis of patients with endometrial carcinoma.},
journal = {Discover oncology},
volume = {16},
number = {1},
pages = {299},
pmid = {40069468},
issn = {2730-6011},
support = {20214Y0226//Shanghai Municipal Health Commission/ ; 2024CRTS045//Sunshine Clinical Research Incubator Program/ ; 2024CRTS017//Sunshine Clinical Research Incubator Program/ ; 2024CRTS015//Sunshine Clinical Research Incubator Program/ ; },
abstract = {Recent studies suggest that the human microbiome influence tumor development. Endometrial carcinoma (EC) is the sixth most common malignancy in women. Recent research has demonstrated the microbes play a critical role in the development and metastasis of EC. However, it remains unclear whether intratumoral microbes are associated with tumor microenvironment (TME) and prognosis of EC. In this study, we collected the EC microbiome data from cBioPortal and constructed a prognostic model based on Resident Microbiome of Endometrium (RME). We then examined the relationship between the RME score, immune cell infiltration, immunotherapy-related signature, and prognosis. The findings demonstrated the independent prognostic value of the RME score for EC. The group with low RME scores had higher enrichment of immune cells. Drug sensitivity analysis revealed that the RME score may serve as a potential predictor of chemotherapy efficacy. In conclusion, our research offers new perspectives on the relationships between tumor immunity and microbes.},
}
RevDate: 2025-03-12
CmpDate: 2025-03-12
Gut microbiota analysis in cirrhosis and non-cirrhotic portal hypertension suggests that portal hypertension can be main factor of cirrhosis-specific dysbiosis.
Scientific reports, 15(1):8394.
Gut dysbiosis plays an important role in cirrhosis, but the mechanism of its development was not established. The aim of the study was to test the hypothesis that portal hypertension can be the main factor in the development of gut dysbiosis in cirrhosis. This cross-sectional study included 25 patients with chronic non-cirrhotic portal hypertension due to extrahepatic portal vein obstruction after portal vein thrombosis (PVT) (NCPVT group), 29 cirrhotic patients without PVT (CirNoPVT), 15 cirrhotic patients with chronic PVT (CPVT), and 22 healthy controls. The fecal microbiota was assessed using 16S rRNA gene sequencing. The CirNoPVT and CPVT groups had largely similar differences in gut microbiota composition from the control group. Patients with NCPVT, as well as patients with cirrhosis, had a higher abundance of Streptococcus, Escherichia, Enterococcus, Enterobacteriaceae, Enterococcaceae, Streptococcaceae, Bacilli, Gammaproteobacteria, Proteobacteria, and a lower abundance of Roseburia, Faecalibacterium, Methanobrevibacter, Ruminococcaceae, Methanobacteriaceae, Clostridia, Methanobacteria, and Euryarchaeota as they were compared with healthy individuals. Patients with NCPVT had a higher abundance of Bifidobacterium, Bifidobacteriaceae, Actinobacteria, and a lower abundance of Gemmiger and Catenibacterium compared to healthy individuals, which was not observed in the cirrhosis groups. The abundance of Porphyromonadaceae with the genus Parabacteroides was reduced in both groups with PVT, but not in CirNoPVT. There were no significant differences in gut microbiota beta-diversity among the CirNoPVT, CPVT and NCPVT groups. All these groups had significant differences in beta-diversity from the control group. Portal hypertension seems be the main factor in the development of gut dysbiosis in cirrhosis.
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@article {pmid40069378,
year = {2025},
author = {Gulyaeva, K and Nadinskaia, M and Maslennikov, R and Aleshina, Y and Goptar, I and Lukashev, A and Poluektova, E and Ivashkin, V},
title = {Gut microbiota analysis in cirrhosis and non-cirrhotic portal hypertension suggests that portal hypertension can be main factor of cirrhosis-specific dysbiosis.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {8394},
pmid = {40069378},
issn = {2045-2322},
support = {123021000156-7//Ministry of Health/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Dysbiosis/microbiology ; Male ; Female ; *Hypertension, Portal/microbiology ; *Liver Cirrhosis/microbiology/complications ; Middle Aged ; Cross-Sectional Studies ; *RNA, Ribosomal, 16S/genetics ; Adult ; Aged ; Feces/microbiology ; Bacteria/classification/genetics/isolation & purification ; Case-Control Studies ; },
abstract = {Gut dysbiosis plays an important role in cirrhosis, but the mechanism of its development was not established. The aim of the study was to test the hypothesis that portal hypertension can be the main factor in the development of gut dysbiosis in cirrhosis. This cross-sectional study included 25 patients with chronic non-cirrhotic portal hypertension due to extrahepatic portal vein obstruction after portal vein thrombosis (PVT) (NCPVT group), 29 cirrhotic patients without PVT (CirNoPVT), 15 cirrhotic patients with chronic PVT (CPVT), and 22 healthy controls. The fecal microbiota was assessed using 16S rRNA gene sequencing. The CirNoPVT and CPVT groups had largely similar differences in gut microbiota composition from the control group. Patients with NCPVT, as well as patients with cirrhosis, had a higher abundance of Streptococcus, Escherichia, Enterococcus, Enterobacteriaceae, Enterococcaceae, Streptococcaceae, Bacilli, Gammaproteobacteria, Proteobacteria, and a lower abundance of Roseburia, Faecalibacterium, Methanobrevibacter, Ruminococcaceae, Methanobacteriaceae, Clostridia, Methanobacteria, and Euryarchaeota as they were compared with healthy individuals. Patients with NCPVT had a higher abundance of Bifidobacterium, Bifidobacteriaceae, Actinobacteria, and a lower abundance of Gemmiger and Catenibacterium compared to healthy individuals, which was not observed in the cirrhosis groups. The abundance of Porphyromonadaceae with the genus Parabacteroides was reduced in both groups with PVT, but not in CirNoPVT. There were no significant differences in gut microbiota beta-diversity among the CirNoPVT, CPVT and NCPVT groups. All these groups had significant differences in beta-diversity from the control group. Portal hypertension seems be the main factor in the development of gut dysbiosis in cirrhosis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Dysbiosis/microbiology
Male
Female
*Hypertension, Portal/microbiology
*Liver Cirrhosis/microbiology/complications
Middle Aged
Cross-Sectional Studies
*RNA, Ribosomal, 16S/genetics
Adult
Aged
Feces/microbiology
Bacteria/classification/genetics/isolation & purification
Case-Control Studies
RevDate: 2025-03-10
All Properties of Infertility Microbiome in a Review Article.
Journal of clinical laboratory analysis [Epub ahead of print].
BACKGROUND: The microbiome is crucial for many physiological processes, including immunity, metabolism, and reproduction.
AIMS: This review aims to contribute to a detailed understanding of the microbiome of the genital tract, which can lead to better management of dysbiosis and reproductive disorders.
METHODS: Data from the four international information databases Medline, Scopus, Embase, and Google Scholar. The search strategy was based on the combination of the following terms: "microbiota," "microbiome," "microfilm," "microflora," "fertility," or "infertility."
RESULT: The advent of next-generation sequencing-based technologies during the last decade has revealed the presence of microbial communities in nearly every part of the human body, including the reproductive system. Several studies have shown significant differences between the microbiota of the vagina and endometrium, as well as other parts of the upper genital tract.
DISCUSSION: The human microbiome plays a critical role in determining a person's health state, and the microbiome of the genital tract may impact fertility potential before and after assisted reproductive treatments (ARTs).
CONCLUSION: To completely understand the role of the microbiome, future research should focus not only on the description of microbiota but also on the interaction between bacteria, the production of biofilms, and the interaction of microorganisms with human cells.
Additional Links: PMID-40059472
Publisher:
PubMed:
Citation:
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@article {pmid40059472,
year = {2025},
author = {Elahi, Z and Mokhtaryan, M and Mahmoodi, S and Shahroodian, S and Darbandi, T and Ghasemi, F and Ghanavati, R and Darbandi, A},
title = {All Properties of Infertility Microbiome in a Review Article.},
journal = {Journal of clinical laboratory analysis},
volume = {},
number = {},
pages = {e25158},
doi = {10.1002/jcla.25158},
pmid = {40059472},
issn = {1098-2825},
support = {4150//Behbahan Faculty of Medical Sciences/ ; },
abstract = {BACKGROUND: The microbiome is crucial for many physiological processes, including immunity, metabolism, and reproduction.
AIMS: This review aims to contribute to a detailed understanding of the microbiome of the genital tract, which can lead to better management of dysbiosis and reproductive disorders.
METHODS: Data from the four international information databases Medline, Scopus, Embase, and Google Scholar. The search strategy was based on the combination of the following terms: "microbiota," "microbiome," "microfilm," "microflora," "fertility," or "infertility."
RESULT: The advent of next-generation sequencing-based technologies during the last decade has revealed the presence of microbial communities in nearly every part of the human body, including the reproductive system. Several studies have shown significant differences between the microbiota of the vagina and endometrium, as well as other parts of the upper genital tract.
DISCUSSION: The human microbiome plays a critical role in determining a person's health state, and the microbiome of the genital tract may impact fertility potential before and after assisted reproductive treatments (ARTs).
CONCLUSION: To completely understand the role of the microbiome, future research should focus not only on the description of microbiota but also on the interaction between bacteria, the production of biofilms, and the interaction of microorganisms with human cells.},
}
RevDate: 2025-03-07
CmpDate: 2025-03-07
Parvimonas micra promotes oral squamous cell carcinoma metastasis through TmpC-CKAP4 axis.
Nature communications, 16(1):2305.
Parvimonas micra (P. micra), an opportunistic oral pathogen associated with multiple cancers, has limited research on its role in oral squamous cell carcinoma (OSCC). This study shows that P. micra is enriched in OSCC tissues and positively correlated with tumor metastasis and stages. P. micra infection promotes OSCC metastasis by inducing hypoxia/HIF-1Ξ±, glycolysis, and autophagy. Mechanistically, P. micra surface protein TmpC binds to CKAP4, a receptor overexpressed in OSCC, facilitating bacterial attachment and invasion. This interaction activates HIF-1Ξ± and autophagy via CKAP4-RanBP2 and CKAP4-NBR1 pathways, driving metastasis. Targeting CKAP4 with masitinib or antibodies impairs P. micra attachment and abolishes P. micra-promoted OSCC metastasis in vitro and in vivo. Together, our findings identify P. micra as a pathogen that promotes OSCC metastasis and highlight that TmpC-CKAP4 interaction could be a potential therapeutic target for OSCC.
Additional Links: PMID-40055343
PubMed:
Citation:
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@article {pmid40055343,
year = {2025},
author = {Qi, H and Gao, H and Li, M and Sun, T and Gu, X and Wei, L and Zhi, M and Li, Z and Fu, D and Liu, Y and Wei, Z and Dou, Y and Feng, Q},
title = {Parvimonas micra promotes oral squamous cell carcinoma metastasis through TmpC-CKAP4 axis.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {2305},
pmid = {40055343},
issn = {2041-1723},
support = {82270980//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Humans ; *Mouth Neoplasms/pathology/metabolism/microbiology ; Animals ; Cell Line, Tumor ; Mice ; *Membrane Proteins/metabolism/genetics ; Carcinoma, Squamous Cell/metabolism/pathology/microbiology ; Neoplasm Metastasis ; Female ; Male ; Mice, Nude ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Mice, Inbred BALB C ; Bacterial Proteins/metabolism/genetics ; Middle Aged ; Glycolysis ; },
abstract = {Parvimonas micra (P. micra), an opportunistic oral pathogen associated with multiple cancers, has limited research on its role in oral squamous cell carcinoma (OSCC). This study shows that P. micra is enriched in OSCC tissues and positively correlated with tumor metastasis and stages. P. micra infection promotes OSCC metastasis by inducing hypoxia/HIF-1Ξ±, glycolysis, and autophagy. Mechanistically, P. micra surface protein TmpC binds to CKAP4, a receptor overexpressed in OSCC, facilitating bacterial attachment and invasion. This interaction activates HIF-1Ξ± and autophagy via CKAP4-RanBP2 and CKAP4-NBR1 pathways, driving metastasis. Targeting CKAP4 with masitinib or antibodies impairs P. micra attachment and abolishes P. micra-promoted OSCC metastasis in vitro and in vivo. Together, our findings identify P. micra as a pathogen that promotes OSCC metastasis and highlight that TmpC-CKAP4 interaction could be a potential therapeutic target for OSCC.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mouth Neoplasms/pathology/metabolism/microbiology
Animals
Cell Line, Tumor
Mice
*Membrane Proteins/metabolism/genetics
Carcinoma, Squamous Cell/metabolism/pathology/microbiology
Neoplasm Metastasis
Female
Male
Mice, Nude
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
Mice, Inbred BALB C
Bacterial Proteins/metabolism/genetics
Middle Aged
Glycolysis
RevDate: 2025-03-07
Endotypes of Atopic Dermatitis.
The Journal of allergy and clinical immunology pii:S0091-6749(25)00260-X [Epub ahead of print].
Atopic dermatitis (AD) is a chronic, heterogeneous skin condition driven by a combination of genetic, immune, and environmental factors. The original classification into extrinsic and intrinsic endotypes has proven overly simplistic. Recent research into the varied immune profiles and molecular signatures of AD has revealed distinct endotypes - subtypes defined by specific biological processes rather than visible symptoms alone. These endotypes encompass classifications based on immune pathways, including Th2-dominant, Th1, Th17/Th22-driven responses, genetic factors, and microbial interactions. Recognizing these endotypes has become essential for advancing personalized treatments, as each subtype responds differently to immune-modulating therapies. Current treatment options, such as moisturizers, immunosuppressants, and biologics, show varied efficacy across AD endotypes, underscoring the need for more precise, endotype-specific approaches. Emerging molecular profiling technologies offer promising avenues to identify distinct biomarkers, refining AD classification and paving the way for more targeted treatments and improved patient outcomes.
Additional Links: PMID-40054744
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PubMed:
Citation:
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@article {pmid40054744,
year = {2025},
author = {Fyhrquist, N and Yang, Y and Karisola, P and Alenius, H},
title = {Endotypes of Atopic Dermatitis.},
journal = {The Journal of allergy and clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaci.2025.02.029},
pmid = {40054744},
issn = {1097-6825},
abstract = {Atopic dermatitis (AD) is a chronic, heterogeneous skin condition driven by a combination of genetic, immune, and environmental factors. The original classification into extrinsic and intrinsic endotypes has proven overly simplistic. Recent research into the varied immune profiles and molecular signatures of AD has revealed distinct endotypes - subtypes defined by specific biological processes rather than visible symptoms alone. These endotypes encompass classifications based on immune pathways, including Th2-dominant, Th1, Th17/Th22-driven responses, genetic factors, and microbial interactions. Recognizing these endotypes has become essential for advancing personalized treatments, as each subtype responds differently to immune-modulating therapies. Current treatment options, such as moisturizers, immunosuppressants, and biologics, show varied efficacy across AD endotypes, underscoring the need for more precise, endotype-specific approaches. Emerging molecular profiling technologies offer promising avenues to identify distinct biomarkers, refining AD classification and paving the way for more targeted treatments and improved patient outcomes.},
}
RevDate: 2025-03-07
CmpDate: 2025-03-07
Applying 3D cultures and high-throughput technologies to study host-pathogen interactions.
Frontiers in immunology, 16:1488699.
Recent advances in cell culturing and DNA sequencing have dramatically altered the field of human microbiome research. Three-dimensional (3D) cell culture is an important tool in cell biology, in cancer research, and for studying host-microbe interactions, as it mimics the in vivo characteristics of the host environment in an in vitro system, providing reliable and reproducible models. This work provides an overview of the main 3D culture techniques applied to study interactions between host cells and pathogenic microorganisms, how these systems can be integrated with high-throughput molecular methods, and how multi-species model systems may pave the way forward to pinpoint interactions among host, beneficial microbes and pathogens.
Additional Links: PMID-40051624
PubMed:
Citation:
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@article {pmid40051624,
year = {2025},
author = {De Martinis, ECP and Alves, VF and Pereira, MG and Andrade, LN and Abichabki, N and Abramova, A and Dannborg, M and Bengtsson-Palme, J},
title = {Applying 3D cultures and high-throughput technologies to study host-pathogen interactions.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1488699},
pmid = {40051624},
issn = {1664-3224},
mesh = {Humans ; *Host-Pathogen Interactions ; *Cell Culture Techniques, Three Dimensional/methods ; Animals ; High-Throughput Screening Assays/methods ; Microbiota ; High-Throughput Nucleotide Sequencing ; },
abstract = {Recent advances in cell culturing and DNA sequencing have dramatically altered the field of human microbiome research. Three-dimensional (3D) cell culture is an important tool in cell biology, in cancer research, and for studying host-microbe interactions, as it mimics the in vivo characteristics of the host environment in an in vitro system, providing reliable and reproducible models. This work provides an overview of the main 3D culture techniques applied to study interactions between host cells and pathogenic microorganisms, how these systems can be integrated with high-throughput molecular methods, and how multi-species model systems may pave the way forward to pinpoint interactions among host, beneficial microbes and pathogens.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Host-Pathogen Interactions
*Cell Culture Techniques, Three Dimensional/methods
Animals
High-Throughput Screening Assays/methods
Microbiota
High-Throughput Nucleotide Sequencing
RevDate: 2025-03-06
Dynamics of gut resistome and mobilome in early life: a meta-analysis.
EBioMedicine, 114:105630 pii:S2352-3964(25)00074-X [Epub ahead of print].
BACKGROUND: The gut microbiota of infants harbours a higher proportion of antibiotic resistance genes (ARGs) compared to adults, even in infants never exposed to antibiotics. Our study aims to elucidate this phenomenon by analysing how different perinatal factors influence the presence of ARGs, mobile genetic elements (MGEs), and their bacterial hosts in the infant gut.
METHODS: We searched MEDLINE and Embase up to April 3rd, 2023, for studies reporting infant cohorts with shotgun metagenomic sequencing of stool samples. The systematic search identified 14 longitudinal infant cohorts from 10 countries across three continents, featuring publicly available sequencing data with corresponding metadata. For subsequent integrative bioinformatic analyses, we used 3981 high-quality metagenomic samples from 1270 infants and 415 mothers.
FINDINGS: We identified distinct trajectories of the resistome and mobilome associated with birth mode, gestational age, antibiotic use, and geographical location. Geographical variation was exemplified by differences between cohorts from Europe, Southern Africa, and Northern America, which showed variation in both diversity and abundance of ARGs. On the other hand, we did not detect a significant impact of breastfeeding on the infants' gut resistome. More than half of detected ARGs co-localised with plasmids in key bacterial hosts, such as Escherichia coli and Enterococcus faecalis. These ARG-associated plasmids were gradually lost during infancy. We also demonstrate that E. coli role as a primary modulator of the infant gut resistome and mobilome is facilitated by its increased abundance and strain diversity compared to adults.
INTERPRETATION: Birth mode, gestational age, antibiotic exposure, and geographical location significantly influence the development of the infant gut resistome and mobilome. A reduction in E. coli relative abundance over time appears as a key factor driving the decrease in both resistome and plasmid relative abundance as infants grow.
FUNDING: Centre for Advanced Study in Oslo, Norway. Centre for New Antibacterial Strategies through the Tromsø Research Foundation, Norway.
Additional Links: PMID-40048849
Publisher:
PubMed:
Citation:
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@article {pmid40048849,
year = {2025},
author = {Bargheet, A and Noordzij, HT and Ponsero, AJ and Jian, C and Korpela, K and Valles-Colomer, M and Debelius, J and Kurilshikov, A and Pettersen, VK},
title = {Dynamics of gut resistome and mobilome in early life: a meta-analysis.},
journal = {EBioMedicine},
volume = {114},
number = {},
pages = {105630},
doi = {10.1016/j.ebiom.2025.105630},
pmid = {40048849},
issn = {2352-3964},
abstract = {BACKGROUND: The gut microbiota of infants harbours a higher proportion of antibiotic resistance genes (ARGs) compared to adults, even in infants never exposed to antibiotics. Our study aims to elucidate this phenomenon by analysing how different perinatal factors influence the presence of ARGs, mobile genetic elements (MGEs), and their bacterial hosts in the infant gut.
METHODS: We searched MEDLINE and Embase up to April 3rd, 2023, for studies reporting infant cohorts with shotgun metagenomic sequencing of stool samples. The systematic search identified 14 longitudinal infant cohorts from 10 countries across three continents, featuring publicly available sequencing data with corresponding metadata. For subsequent integrative bioinformatic analyses, we used 3981 high-quality metagenomic samples from 1270 infants and 415 mothers.
FINDINGS: We identified distinct trajectories of the resistome and mobilome associated with birth mode, gestational age, antibiotic use, and geographical location. Geographical variation was exemplified by differences between cohorts from Europe, Southern Africa, and Northern America, which showed variation in both diversity and abundance of ARGs. On the other hand, we did not detect a significant impact of breastfeeding on the infants' gut resistome. More than half of detected ARGs co-localised with plasmids in key bacterial hosts, such as Escherichia coli and Enterococcus faecalis. These ARG-associated plasmids were gradually lost during infancy. We also demonstrate that E. coli role as a primary modulator of the infant gut resistome and mobilome is facilitated by its increased abundance and strain diversity compared to adults.
INTERPRETATION: Birth mode, gestational age, antibiotic exposure, and geographical location significantly influence the development of the infant gut resistome and mobilome. A reduction in E. coli relative abundance over time appears as a key factor driving the decrease in both resistome and plasmid relative abundance as infants grow.
FUNDING: Centre for Advanced Study in Oslo, Norway. Centre for New Antibacterial Strategies through the Tromsø Research Foundation, Norway.},
}
RevDate: 2025-03-05
CmpDate: 2025-03-05
Oxidative stress-induced changes in wooden breast and mitigation strategies: A review.
Comprehensive reviews in food science and food safety, 24(2):e70148.
Wooden breast (WB) is a multifactorial muscular abnormality resulting from the interplay between genetic predispositions for rapid growth, physiological stress, and anatomical impairments. This myopathy has been a persistent challenge in the poultry industry since its initial identification a decade ago. WB negatively impacts meat quality, leading to increased toughness and reduced nutritional value. Building on foundational research utilizing multiomics technologies, hypoxia-induced oxidative stress has been identified as a key early event driving the pathological processes of WB. This review provides a comprehensive overview and the state-of-the-art evidence on the pivotal role of oxidative stress in WB myopathy. It begins by examining the generation of reactive intermediates that induce oxidative damage and the host's defense mechanisms aimed at mitigating these threats. The discussion then focuses on the consequences of oxidative damage for mitochondria, protein and lipid oxidation, connective tissue remodeling, and inflammation-pathological hallmarks of WB-affected muscles. Additionally, the review highlights how oxidative stress influences satellite cell behavior, impairing the repair and regeneration of muscle tissues, a process implicated in WB. Finally, efforts to prevent or mitigate WB myopathy are summarized, with particular attention to potential intervention strategies targeting oxidative stress. These include innovative feed formulations and gut microbiota modulation, which show promise in alleviating the severity of the condition.
Additional Links: PMID-40040485
Publisher:
PubMed:
Citation:
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@article {pmid40040485,
year = {2025},
author = {Wang, Y and Li, B and Jian, C and Gagaoua, M and EstΓ©vez, M and Puolanne, E and Ertbjerg, P},
title = {Oxidative stress-induced changes in wooden breast and mitigation strategies: A review.},
journal = {Comprehensive reviews in food science and food safety},
volume = {24},
number = {2},
pages = {e70148},
doi = {10.1111/1541-4337.70148},
pmid = {40040485},
issn = {1541-4337},
support = {348385//Research Council of Finland/ ; },
mesh = {*Oxidative Stress ; Animals ; Poultry Diseases/microbiology/prevention & control ; Meat ; Chickens ; Muscular Diseases ; },
abstract = {Wooden breast (WB) is a multifactorial muscular abnormality resulting from the interplay between genetic predispositions for rapid growth, physiological stress, and anatomical impairments. This myopathy has been a persistent challenge in the poultry industry since its initial identification a decade ago. WB negatively impacts meat quality, leading to increased toughness and reduced nutritional value. Building on foundational research utilizing multiomics technologies, hypoxia-induced oxidative stress has been identified as a key early event driving the pathological processes of WB. This review provides a comprehensive overview and the state-of-the-art evidence on the pivotal role of oxidative stress in WB myopathy. It begins by examining the generation of reactive intermediates that induce oxidative damage and the host's defense mechanisms aimed at mitigating these threats. The discussion then focuses on the consequences of oxidative damage for mitochondria, protein and lipid oxidation, connective tissue remodeling, and inflammation-pathological hallmarks of WB-affected muscles. Additionally, the review highlights how oxidative stress influences satellite cell behavior, impairing the repair and regeneration of muscle tissues, a process implicated in WB. Finally, efforts to prevent or mitigate WB myopathy are summarized, with particular attention to potential intervention strategies targeting oxidative stress. These include innovative feed formulations and gut microbiota modulation, which show promise in alleviating the severity of the condition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Oxidative Stress
Animals
Poultry Diseases/microbiology/prevention & control
Meat
Chickens
Muscular Diseases
RevDate: 2025-03-03
CmpDate: 2025-03-04
Isolation and characterization of fMGyn-Pae01, a phiKZ-like jumbo phage infecting Pseudomonas aeruginosa.
Virology journal, 22(1):55.
BACKGROUND: Pseudomonas aeruginosa is an opportunistic pathogen that causes a wide variety of infections, and belongs to the group of ESKAPE pathogens that are the leading cause of healthcare-associated infections and have high level of antibiotic resistance. The treatment of infections caused by antibiotic-resistant P. aeruginosa is challenging, which makes it a common target for phage therapy. The successful utilization of phage therapy requires a collection of well characterized phages.
METHODS: Phage fMGyn-Pae01 was isolated from a commercial phage therapy cocktail. The phage morphology was studied by transmission electron microscopy and the host range was analyzed with a liquid culture method. The phage genome was sequenced and characterized, and the genome was compared to closest phage genomes. Phage resistant bacterial mutants were isolated and whole genome sequencing and motility, phage adsorption and biofilm formation assays were performed to the mutants and host bacterium.
RESULTS: The genomic analysis revealed that fMGyn-Pae01 is a lytic, phiKZ-like jumbo phage with genome size of 277.8 kb. No genes associated with lysogeny, bacterial virulence, or antibiotic resistance were identified. Phage fMGyn-Pae01 did not reduce biofilm formation of P. aeruginosa, suggesting that it may not be an optimal phage to be used in monophage therapy in conditions where biofilm formation is expected. Host range screening revealed that fMGyn-Pae01 has a wide host range among P. aeruginosa strains and its infection was not dependent on O-serotype. Whole genome sequencing of the host bacterium and phage resistant mutants revealed that the mutations had inactivated either a flagellar or rpoN gene, thereby preventing the biosynthesis of a functional flagellum. The lack of functional flagella was confirmed in motility assays. Additionally, fMGyn-Pae01 failed to adsorb on non-motile mutants indicating that the bacterial flagellum is the phage-binding receptor.
CONCLUSION: fMGyn-Pae01 is a phiKZ-like jumbo phage infecting P. aeruginosa. fMGyn-Pae01 uses the flagellum as its phage-binding receptor, supporting earlier suggestions that flagellum might be utilized by phiKZ but differs from some other previous findings showing that phiKZ-like phages use the type-IV pili as the phage-binding receptor.
Additional Links: PMID-40033410
PubMed:
Citation:
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@article {pmid40033410,
year = {2025},
author = {Ranta, K and Skurnik, M and Kiljunen, S},
title = {Isolation and characterization of fMGyn-Pae01, a phiKZ-like jumbo phage infecting Pseudomonas aeruginosa.},
journal = {Virology journal},
volume = {22},
number = {1},
pages = {55},
pmid = {40033410},
issn = {1743-422X},
mesh = {*Pseudomonas aeruginosa/virology/drug effects ; *Host Specificity ; *Genome, Viral ; *Pseudomonas Phages/genetics/isolation & purification/physiology/classification ; Biofilms/growth & development ; Whole Genome Sequencing ; Phage Therapy ; Microscopy, Electron, Transmission ; },
abstract = {BACKGROUND: Pseudomonas aeruginosa is an opportunistic pathogen that causes a wide variety of infections, and belongs to the group of ESKAPE pathogens that are the leading cause of healthcare-associated infections and have high level of antibiotic resistance. The treatment of infections caused by antibiotic-resistant P. aeruginosa is challenging, which makes it a common target for phage therapy. The successful utilization of phage therapy requires a collection of well characterized phages.
METHODS: Phage fMGyn-Pae01 was isolated from a commercial phage therapy cocktail. The phage morphology was studied by transmission electron microscopy and the host range was analyzed with a liquid culture method. The phage genome was sequenced and characterized, and the genome was compared to closest phage genomes. Phage resistant bacterial mutants were isolated and whole genome sequencing and motility, phage adsorption and biofilm formation assays were performed to the mutants and host bacterium.
RESULTS: The genomic analysis revealed that fMGyn-Pae01 is a lytic, phiKZ-like jumbo phage with genome size of 277.8 kb. No genes associated with lysogeny, bacterial virulence, or antibiotic resistance were identified. Phage fMGyn-Pae01 did not reduce biofilm formation of P. aeruginosa, suggesting that it may not be an optimal phage to be used in monophage therapy in conditions where biofilm formation is expected. Host range screening revealed that fMGyn-Pae01 has a wide host range among P. aeruginosa strains and its infection was not dependent on O-serotype. Whole genome sequencing of the host bacterium and phage resistant mutants revealed that the mutations had inactivated either a flagellar or rpoN gene, thereby preventing the biosynthesis of a functional flagellum. The lack of functional flagella was confirmed in motility assays. Additionally, fMGyn-Pae01 failed to adsorb on non-motile mutants indicating that the bacterial flagellum is the phage-binding receptor.
CONCLUSION: fMGyn-Pae01 is a phiKZ-like jumbo phage infecting P. aeruginosa. fMGyn-Pae01 uses the flagellum as its phage-binding receptor, supporting earlier suggestions that flagellum might be utilized by phiKZ but differs from some other previous findings showing that phiKZ-like phages use the type-IV pili as the phage-binding receptor.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Pseudomonas aeruginosa/virology/drug effects
*Host Specificity
*Genome, Viral
*Pseudomonas Phages/genetics/isolation & purification/physiology/classification
Biofilms/growth & development
Whole Genome Sequencing
Phage Therapy
Microscopy, Electron, Transmission
RevDate: 2025-03-03
A Consensus Statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research.
Nature reviews. Gastroenterology & hepatology [Epub ahead of print].
The gut microbiome comprises trillions of microorganisms and profoundly influences human health by modulating metabolism, immune responses and neuronal functions. Disruption in gut microbiome composition is implicated in various inflammatory conditions, metabolic disorders and neurodegenerative diseases. However, determining the underlying mechanisms and establishing cause and effect is extremely difficult. Preclinical models offer crucial insights into the role of the gut microbiome in diseases and help identify potential therapeutic interventions. The Human Microbiome Action Consortium initiated a Delphi survey to assess the utility of preclinical models, including animal and cell-based models, in elucidating the causal role of the gut microbiome in these diseases. The Delphi survey aimed to address the complexity of selecting appropriate preclinical models to investigate disease causality and to study host-microbiome interactions effectively. We adopted a structured approach encompassing a literature review, expert workshops and the Delphi questionnaire to gather insights from a diverse range of stakeholders. Experts were requested to evaluate the strengths, limitations, and suitability of these models in addressing the causal relationship between the gut microbiome and disease pathogenesis. The resulting consensus statements and recommendations provide valuable insights for selecting preclinical models in future studies of gut microbiome-related diseases.
Additional Links: PMID-40033063
PubMed:
Citation:
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@article {pmid40033063,
year = {2025},
author = {Metwaly, A and Kriaa, A and Hassani, Z and Carraturo, F and Druart, C and , and Arnauts, K and Wilmes, P and Walter, J and Rosshart, S and Desai, MS and Dore, J and Blottiere, HM and Maguin, E and Haller, D},
title = {A Consensus Statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {40033063},
issn = {1759-5053},
abstract = {The gut microbiome comprises trillions of microorganisms and profoundly influences human health by modulating metabolism, immune responses and neuronal functions. Disruption in gut microbiome composition is implicated in various inflammatory conditions, metabolic disorders and neurodegenerative diseases. However, determining the underlying mechanisms and establishing cause and effect is extremely difficult. Preclinical models offer crucial insights into the role of the gut microbiome in diseases and help identify potential therapeutic interventions. The Human Microbiome Action Consortium initiated a Delphi survey to assess the utility of preclinical models, including animal and cell-based models, in elucidating the causal role of the gut microbiome in these diseases. The Delphi survey aimed to address the complexity of selecting appropriate preclinical models to investigate disease causality and to study host-microbiome interactions effectively. We adopted a structured approach encompassing a literature review, expert workshops and the Delphi questionnaire to gather insights from a diverse range of stakeholders. Experts were requested to evaluate the strengths, limitations, and suitability of these models in addressing the causal relationship between the gut microbiome and disease pathogenesis. The resulting consensus statements and recommendations provide valuable insights for selecting preclinical models in future studies of gut microbiome-related diseases.},
}
RevDate: 2025-03-03
Antibiotic Use: Impact on the Microbiome and Cellular Therapy Outcomes.
Blood advances pii:535817 [Epub ahead of print].
Antibiotics disrupt the delicate balance of bacteria, fungi, and viruses in the human microbiome. Growing evidence indicates a significant relationship between the intestinal microbiome and cellular therapy, which aligns with the established influence of the microbiome on immune responses. When examining the link between cellular therapy and the microbiome, it is essential to understand how disruptions in the microbiome-especially those caused by antibiotics-affect these therapies. Here, we discuss the impact of antibiotics on the intestinal microbiome, cellular therapy outcomes, and associated toxicities, particularly in the context of hematopoietic cell transplantation and chimeric antigen receptor T-cell therapy. Furthermore, we examine the mechanisms through which antibiotics affect cellular therapy, the future implications of this knowledge, and the areas that warrant further investigation.
Additional Links: PMID-40030005
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@article {pmid40030005,
year = {2025},
author = {Darwin, A and Xie, J and Smith, M},
title = {Antibiotic Use: Impact on the Microbiome and Cellular Therapy Outcomes.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2024013809},
pmid = {40030005},
issn = {2473-9537},
abstract = {Antibiotics disrupt the delicate balance of bacteria, fungi, and viruses in the human microbiome. Growing evidence indicates a significant relationship between the intestinal microbiome and cellular therapy, which aligns with the established influence of the microbiome on immune responses. When examining the link between cellular therapy and the microbiome, it is essential to understand how disruptions in the microbiome-especially those caused by antibiotics-affect these therapies. Here, we discuss the impact of antibiotics on the intestinal microbiome, cellular therapy outcomes, and associated toxicities, particularly in the context of hematopoietic cell transplantation and chimeric antigen receptor T-cell therapy. Furthermore, we examine the mechanisms through which antibiotics affect cellular therapy, the future implications of this knowledge, and the areas that warrant further investigation.},
}
RevDate: 2025-03-03
Intestinal Microbiota Contributes to the Development of Cardiovascular Inflammation and Vasculitis in Mice.
Circulation research [Epub ahead of print].
BACKGROUND: Alterations in the intestinal microbiota contribute to the pathogenesis of various cardiovascular disorders, but how they affect the development of Kawasaki disease, an acute pediatric vasculitis, remains unclear. Here, using a murine model mimicking Kawasaki disease vasculitis, we assessed the contribution of the intestinal microbiota to the development of vascular inflammation.
METHODS AND RESULTS: We report that depleting the gut microbiota reduces the development of cardiovascular inflammation in a murine model mimicking Kawasaki disease vasculitis. The development of cardiovascular lesions was associated with alterations in the intestinal microbiota composition and, notably, a decreased abundance of Akkermansia muciniphila and Faecalibacterium prausnitzii. Oral supplementation with either of these live or pasteurized individual bacteria or with short-chain fatty acids produced by them attenuated cardiovascular inflammation, as reflected by decreased local immune cell infiltrations. Treatment with Amuc_1100, the TLR-2 signaling outer membrane protein from Akkermansia muciniphila, also reduced the severity of vascular inflammation.
CONCLUSIONS: This study reveals an underappreciated gut microbiota-cardiovascular inflammation axis in Kawasaki disease vasculitis pathogenesis and identifies specific intestinal commensals that regulate vasculitis in mice by producing metabolites or via extracellular proteins capable of enhancing and supporting gut barrier function.
Additional Links: PMID-40026151
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@article {pmid40026151,
year = {2025},
author = {Jena, PK and Wakita, D and Gomez, AC and Carvalho, TT and Atici, AE and Aubuchon, E and Narayanan, M and Lee, Y and Fishbein, MC and Takasato, Y and Kurashima, Y and Kiyono, H and Cani, PD and de Vos, WM and Underhill, DM and Devkota, S and Chen, S and Shimada, K and Crother, TR and Arditi, M and Noval Rivas, M},
title = {Intestinal Microbiota Contributes to the Development of Cardiovascular Inflammation and Vasculitis in Mice.},
journal = {Circulation research},
volume = {},
number = {},
pages = {},
doi = {10.1161/CIRCRESAHA.124.325079},
pmid = {40026151},
issn = {1524-4571},
abstract = {BACKGROUND: Alterations in the intestinal microbiota contribute to the pathogenesis of various cardiovascular disorders, but how they affect the development of Kawasaki disease, an acute pediatric vasculitis, remains unclear. Here, using a murine model mimicking Kawasaki disease vasculitis, we assessed the contribution of the intestinal microbiota to the development of vascular inflammation.
METHODS AND RESULTS: We report that depleting the gut microbiota reduces the development of cardiovascular inflammation in a murine model mimicking Kawasaki disease vasculitis. The development of cardiovascular lesions was associated with alterations in the intestinal microbiota composition and, notably, a decreased abundance of Akkermansia muciniphila and Faecalibacterium prausnitzii. Oral supplementation with either of these live or pasteurized individual bacteria or with short-chain fatty acids produced by them attenuated cardiovascular inflammation, as reflected by decreased local immune cell infiltrations. Treatment with Amuc_1100, the TLR-2 signaling outer membrane protein from Akkermansia muciniphila, also reduced the severity of vascular inflammation.
CONCLUSIONS: This study reveals an underappreciated gut microbiota-cardiovascular inflammation axis in Kawasaki disease vasculitis pathogenesis and identifies specific intestinal commensals that regulate vasculitis in mice by producing metabolites or via extracellular proteins capable of enhancing and supporting gut barrier function.},
}
RevDate: 2025-03-02
De-coding the complex role of microbial metabolites in cancer.
Cell reports, 44(3):115358 pii:S2211-1247(25)00129-9 [Epub ahead of print].
The human microbiome, an intricate ecosystem of trillions of microbes residing across various body sites, significantly influences cancer, a leading cause of morbidity and mortality worldwide. Recent studies have illuminated the microbiome's pivotal role in cancer development, either through direct cellular interactions or by secreting bioactive compounds such as metabolites. Microbial metabolites contribute to cancer initiation through mechanisms such as DNA damage, epithelial barrier dysfunction, and chronic inflammation. Furthermore, microbial metabolites exert dual roles on cancer progression and response to therapy by modulating cellular metabolism, gene expression, and signaling pathways. Understanding these complex interactions is vital for devising new therapeutic strategies. This review highlights microbial metabolites as promising targets for cancer prevention and treatment, emphasizing their impact on therapy responses and underscoring the need for further research into their roles in metastasis and therapy resistance.
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@article {pmid40023841,
year = {2025},
author = {PΓ©rez Escriva, P and Correia Tavares Bernardino, C and Letellier, E},
title = {De-coding the complex role of microbial metabolites in cancer.},
journal = {Cell reports},
volume = {44},
number = {3},
pages = {115358},
doi = {10.1016/j.celrep.2025.115358},
pmid = {40023841},
issn = {2211-1247},
abstract = {The human microbiome, an intricate ecosystem of trillions of microbes residing across various body sites, significantly influences cancer, a leading cause of morbidity and mortality worldwide. Recent studies have illuminated the microbiome's pivotal role in cancer development, either through direct cellular interactions or by secreting bioactive compounds such as metabolites. Microbial metabolites contribute to cancer initiation through mechanisms such as DNA damage, epithelial barrier dysfunction, and chronic inflammation. Furthermore, microbial metabolites exert dual roles on cancer progression and response to therapy by modulating cellular metabolism, gene expression, and signaling pathways. Understanding these complex interactions is vital for devising new therapeutic strategies. This review highlights microbial metabolites as promising targets for cancer prevention and treatment, emphasizing their impact on therapy responses and underscoring the need for further research into their roles in metastasis and therapy resistance.},
}
RevDate: 2025-03-01
Harnessing the Human Microbiome and its Impact on Immuno-Oncology and Nanotechnology for Next-Generation Cancer Therapies.
European journal of pharmacology pii:S0014-2999(25)00190-6 [Epub ahead of print].
The integration of microbiome research and nanotechnology represents a significant advancement in immuno-oncology, potentially improving the effectiveness of cancer immunotherapies. Recent studies highlight the influential role of the human microbiome in modulating immune responses, presenting new opportunities to enhance immune checkpoint inhibitors (ICIs) and other cancer therapies. Nanotechnology offers precise drug delivery and immune modulation capabilities, minimizing off-target effects while maximizing therapeutic outcomes. This review consolidates current knowledge on the interactions between the microbiome and the immune system, emphasizing the microbiome's impact on ICIs, and explores the incorporation of nanotechnology in cancer treatment strategies. Additionally, it provides a forward-looking perspective on the synergistic potential of microbiome modulation and nanotechnology to overcome existing challenges in immuno-oncology. This integrated approach may enhance the personalization and effectiveness of next-generation cancer treatments, paving the way for transformative patient care.
Additional Links: PMID-40023356
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@article {pmid40023356,
year = {2025},
author = {Das, M and Kiruthiga, C and Shafreen, RB and Nachammai, KT and Selvaraj, C and Langeswaran, K},
title = {Harnessing the Human Microbiome and its Impact on Immuno-Oncology and Nanotechnology for Next-Generation Cancer Therapies.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {177436},
doi = {10.1016/j.ejphar.2025.177436},
pmid = {40023356},
issn = {1879-0712},
abstract = {The integration of microbiome research and nanotechnology represents a significant advancement in immuno-oncology, potentially improving the effectiveness of cancer immunotherapies. Recent studies highlight the influential role of the human microbiome in modulating immune responses, presenting new opportunities to enhance immune checkpoint inhibitors (ICIs) and other cancer therapies. Nanotechnology offers precise drug delivery and immune modulation capabilities, minimizing off-target effects while maximizing therapeutic outcomes. This review consolidates current knowledge on the interactions between the microbiome and the immune system, emphasizing the microbiome's impact on ICIs, and explores the incorporation of nanotechnology in cancer treatment strategies. Additionally, it provides a forward-looking perspective on the synergistic potential of microbiome modulation and nanotechnology to overcome existing challenges in immuno-oncology. This integrated approach may enhance the personalization and effectiveness of next-generation cancer treatments, paving the way for transformative patient care.},
}
RevDate: 2025-02-28
CmpDate: 2025-02-28
The impact of perinatal maternal stress on the maternal and infant gut and human milk microbiomes: A scoping review.
PloS one, 20(2):e0318237 pii:PONE-D-24-25079.
BACKGROUND: Perinatal maternal stress, which includes both psychological and physiological stress experienced by healthy women during pregnancy and the postpartum period, is becoming increasingly prevalent. Infant early exposure to adverse environments such as perinatal stress has been shown to increase the long-term risk to metabolic, immunologic and neurobehavioral disorders. Evidence suggests that the human microbiome facilitates the transmission of maternal factors to infants via the vaginal, gut, and human milk microbiomes. The colonization of aberrant microorganisms in the mother's microbiome, influenced by the microbiome-brain-gut axis, may be transferred to infants during a critical early developmental period. This transfer may predispose infants to a more inflammatory-prone microbiome which is associated with dysregulated metabolic process leading to adverse health outcomes. Given the prevalence and potential impact of perinatal stress on maternal and infant health, with no systematic mapping or review of the data to date, the aim of this scoping review is to gather evidence on the relationship between perinatal maternal stress, and the human milk, maternal, and infant gut microbiomes.
METHODS: This is an exploratory mapping scoping review, guided by the Joanna Briggs Institute's methodology along with use of the Prisma Scr reporting guideline. A comprehensive search was conducted using the following databases, CINAHL Complete; MEDLINE; PsycINFO, Web of Science and Scopus with a protocol registered with Open Science Framework DOI 10.17605/OSF.IO/5SRMV.
RESULTS: After screening 1145 papers there were 7 paper that met the inclusion criteria. Statistically significant associations were found in five of the studies which identify higher abundance of potentially pathogenic bacteria such as Erwinia, Serratia, T mayombie, Bacteroides with higher maternal stress, and lower levels of stress linked to potentially beneficial bacteria such Lactococcus, Lactobacillus, Akkermansia. However, one study presents conflicting results where it was reported that higher maternal stress was linked to the prevalence of more beneficial bacteria.
CONCLUSION: This review suggests that maternal stress does have an impact on the alteration of abundance and diversity of influential bacteria in the gut microbiome, however, it can affect colonisation in different ways. These bacterial changes have the capacity to influence long term health and disease. The review analyses data collection tools and methods, offers potential reasons for these findings as well as suggestions for future research.
Additional Links: PMID-40019912
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PubMed:
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@article {pmid40019912,
year = {2025},
author = {Ryan, N and O'Mahony, S and Leahy-Warren, P and Philpott, L and Mulcahy, H},
title = {The impact of perinatal maternal stress on the maternal and infant gut and human milk microbiomes: A scoping review.},
journal = {PloS one},
volume = {20},
number = {2},
pages = {e0318237},
doi = {10.1371/journal.pone.0318237},
pmid = {40019912},
issn = {1932-6203},
mesh = {Humans ; *Milk, Human/microbiology ; Female ; Pregnancy ; *Gastrointestinal Microbiome ; *Stress, Psychological/microbiology ; Infant ; Infant, Newborn ; },
abstract = {BACKGROUND: Perinatal maternal stress, which includes both psychological and physiological stress experienced by healthy women during pregnancy and the postpartum period, is becoming increasingly prevalent. Infant early exposure to adverse environments such as perinatal stress has been shown to increase the long-term risk to metabolic, immunologic and neurobehavioral disorders. Evidence suggests that the human microbiome facilitates the transmission of maternal factors to infants via the vaginal, gut, and human milk microbiomes. The colonization of aberrant microorganisms in the mother's microbiome, influenced by the microbiome-brain-gut axis, may be transferred to infants during a critical early developmental period. This transfer may predispose infants to a more inflammatory-prone microbiome which is associated with dysregulated metabolic process leading to adverse health outcomes. Given the prevalence and potential impact of perinatal stress on maternal and infant health, with no systematic mapping or review of the data to date, the aim of this scoping review is to gather evidence on the relationship between perinatal maternal stress, and the human milk, maternal, and infant gut microbiomes.
METHODS: This is an exploratory mapping scoping review, guided by the Joanna Briggs Institute's methodology along with use of the Prisma Scr reporting guideline. A comprehensive search was conducted using the following databases, CINAHL Complete; MEDLINE; PsycINFO, Web of Science and Scopus with a protocol registered with Open Science Framework DOI 10.17605/OSF.IO/5SRMV.
RESULTS: After screening 1145 papers there were 7 paper that met the inclusion criteria. Statistically significant associations were found in five of the studies which identify higher abundance of potentially pathogenic bacteria such as Erwinia, Serratia, T mayombie, Bacteroides with higher maternal stress, and lower levels of stress linked to potentially beneficial bacteria such Lactococcus, Lactobacillus, Akkermansia. However, one study presents conflicting results where it was reported that higher maternal stress was linked to the prevalence of more beneficial bacteria.
CONCLUSION: This review suggests that maternal stress does have an impact on the alteration of abundance and diversity of influential bacteria in the gut microbiome, however, it can affect colonisation in different ways. These bacterial changes have the capacity to influence long term health and disease. The review analyses data collection tools and methods, offers potential reasons for these findings as well as suggestions for future research.},
}
MeSH Terms:
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Humans
*Milk, Human/microbiology
Female
Pregnancy
*Gastrointestinal Microbiome
*Stress, Psychological/microbiology
Infant
Infant, Newborn
RevDate: 2025-02-27
Transcriptomic profile of RNA pseudouridine modification as a biomarker for cellular senescence associated with survival outcomes in colorectal cancer.
BMC biology, 23(1):61.
BACKGROUND: Colorectal cancer (CRC) is considered as an age-related disease, and cellular senescence (CS) plays a crucial role in cancer development and progression. Previous studies have shown the role of epigenetic changes in aging and cancer development, but the role of RNA pseudouridine (Ξ¨) modification in aging and cancer remains to be explored.
RESULTS: Using bulk RNA sequencing, CRC cells with low Ψ writers expression levels have higher CS levels. We developed the Psi Score for assessing the transcriptomic profile of RNA Ψ modification regulation and found that the Psi Score correlates with CS. Furthermore, Psi-related senescence may be mediated by mTOR, TGF-β, TNF-α, and inflammatory response signaling pathways. Meanwhile, Psi Score could predict the anti-cancer treatment outcomes of anti-aging interventions and could be used to predict the response to immunotherapy.
CONCLUSIONS: Overall, these findings reveal that RNA Ψ modification connected aging and cancer and provided novel insights into biomarker-guided cancer regimens.
Additional Links: PMID-40016751
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Citation:
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@article {pmid40016751,
year = {2025},
author = {Gan, Y and Yuan, Z and Weng, J and Huang, M and Li, T and Wu, Y and Lin, K and Han, J and Li, X and Liu, H and Wan, Z and Li, Z and Chen, Z and Cui, J and Luo, Y and Huang, M and Yu, H and Lin, J},
title = {Transcriptomic profile of RNA pseudouridine modification as a biomarker for cellular senescence associated with survival outcomes in colorectal cancer.},
journal = {BMC biology},
volume = {23},
number = {1},
pages = {61},
pmid = {40016751},
issn = {1741-7007},
abstract = {BACKGROUND: Colorectal cancer (CRC) is considered as an age-related disease, and cellular senescence (CS) plays a crucial role in cancer development and progression. Previous studies have shown the role of epigenetic changes in aging and cancer development, but the role of RNA pseudouridine (Ξ¨) modification in aging and cancer remains to be explored.
RESULTS: Using bulk RNA sequencing, CRC cells with low Ψ writers expression levels have higher CS levels. We developed the Psi Score for assessing the transcriptomic profile of RNA Ψ modification regulation and found that the Psi Score correlates with CS. Furthermore, Psi-related senescence may be mediated by mTOR, TGF-β, TNF-α, and inflammatory response signaling pathways. Meanwhile, Psi Score could predict the anti-cancer treatment outcomes of anti-aging interventions and could be used to predict the response to immunotherapy.
CONCLUSIONS: Overall, these findings reveal that RNA Ψ modification connected aging and cancer and provided novel insights into biomarker-guided cancer regimens.},
}
RevDate: 2025-02-27
Analyzing microbiome data with taxonomic misclassification using a zero-inflated Dirichlet-multinomial model.
BMC bioinformatics, 26(1):69.
The human microbiome is the collection of microorganisms living on and inside of our bodies. A major aim of microbiome research is understanding the role microbial communities play in human health with the goal of designing personalized interventions that modulate the microbiome to treat or prevent disease. Microbiome data are challenging to analyze due to their high-dimensionality, overdispersion, and zero-inflation. Analysis is further complicated by the steps taken to collect and process microbiome samples. For example, sequencing instruments have a fixed capacity for the total number of reads delivered. It is therefore essential to treat microbial samples as compositional. Another complicating factor of modeling microbiome data is that taxa counts are subject to measurement error introduced at various stages of the measurement protocol. Advances in sequencing technology and preprocessing pipelines coupled with our growing knowledge of the human microbiome have reduced, but not eliminated, measurement error. Ignoring measurement error during analysis, though common in practice, can then lead to biased inference and curb reproducibility. We propose a Dirichlet-multinomial modeling framework for microbiome data with excess zeros and potential taxonomic misclassification. We demonstrate how accommodating taxonomic misclassification improves estimation performance and investigate differences in gut microbial composition between healthy and obese children.
Additional Links: PMID-40016656
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@article {pmid40016656,
year = {2025},
author = {Koslovsky, MD},
title = {Analyzing microbiome data with taxonomic misclassification using a zero-inflated Dirichlet-multinomial model.},
journal = {BMC bioinformatics},
volume = {26},
number = {1},
pages = {69},
pmid = {40016656},
issn = {1471-2105},
support = {DMS-2245492//National Science Foundation/ ; },
abstract = {The human microbiome is the collection of microorganisms living on and inside of our bodies. A major aim of microbiome research is understanding the role microbial communities play in human health with the goal of designing personalized interventions that modulate the microbiome to treat or prevent disease. Microbiome data are challenging to analyze due to their high-dimensionality, overdispersion, and zero-inflation. Analysis is further complicated by the steps taken to collect and process microbiome samples. For example, sequencing instruments have a fixed capacity for the total number of reads delivered. It is therefore essential to treat microbial samples as compositional. Another complicating factor of modeling microbiome data is that taxa counts are subject to measurement error introduced at various stages of the measurement protocol. Advances in sequencing technology and preprocessing pipelines coupled with our growing knowledge of the human microbiome have reduced, but not eliminated, measurement error. Ignoring measurement error during analysis, though common in practice, can then lead to biased inference and curb reproducibility. We propose a Dirichlet-multinomial modeling framework for microbiome data with excess zeros and potential taxonomic misclassification. We demonstrate how accommodating taxonomic misclassification improves estimation performance and investigate differences in gut microbial composition between healthy and obese children.},
}
RevDate: 2025-02-26
Exploring the role of oral bacteria in oral cancer: a narrative review.
Discover oncology, 16(1):242.
A growing body of research indicates that a wide range of cancer types may correlate with human microbiome components. On the other hand, little is known about the potential contribution of the oral microbiota to oral cancer. However, some oral microbiome components can stimulate different tumorigenic processes associated with the development of cancer. In this line, two prevalent oral infections, Porphyromonas gingivalis, and Fusobacterium nucleatum can increase tumor growth. The microbiome can impact the course of the illness through direct interactions with the human body and major modifications to the toxicity and responsiveness to different kinds of cancer therapy. Recent research has demonstrated a relationship between specific phylogenetic groupings and the results of immunotherapy treatment for particular tumor types. Conversely, there has been a recent upsurge in interest in the possibility of using microbes to treat cancer. At the moment, some species, such as Salmonella typhimurium and Clostridium spp., are being explored as possible cancer treatment vectors. Thus, understanding these microbial interactions highlights the importance of maintaining a healthy oral microbiome in preventing oral cancers. From this perspective, this review will discuss the role of the microbiome on oral cancers and their possible application in oral cancer treatment/improvement.
Additional Links: PMID-40009328
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Citation:
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@article {pmid40009328,
year = {2025},
author = {Mivehchi, H and Eskandari-Yaghbastlo, A and Pour Bahrami, P and Elhami, A and Faghihinia, F and Nejati, ST and Kazemi, KS and Nabi Afjadi, M},
title = {Exploring the role of oral bacteria in oral cancer: a narrative review.},
journal = {Discover oncology},
volume = {16},
number = {1},
pages = {242},
pmid = {40009328},
issn = {2730-6011},
abstract = {A growing body of research indicates that a wide range of cancer types may correlate with human microbiome components. On the other hand, little is known about the potential contribution of the oral microbiota to oral cancer. However, some oral microbiome components can stimulate different tumorigenic processes associated with the development of cancer. In this line, two prevalent oral infections, Porphyromonas gingivalis, and Fusobacterium nucleatum can increase tumor growth. The microbiome can impact the course of the illness through direct interactions with the human body and major modifications to the toxicity and responsiveness to different kinds of cancer therapy. Recent research has demonstrated a relationship between specific phylogenetic groupings and the results of immunotherapy treatment for particular tumor types. Conversely, there has been a recent upsurge in interest in the possibility of using microbes to treat cancer. At the moment, some species, such as Salmonella typhimurium and Clostridium spp., are being explored as possible cancer treatment vectors. Thus, understanding these microbial interactions highlights the importance of maintaining a healthy oral microbiome in preventing oral cancers. From this perspective, this review will discuss the role of the microbiome on oral cancers and their possible application in oral cancer treatment/improvement.},
}
RevDate: 2025-02-26
The Urogenital System Microbiota: Is It a New Gamechanger in Urogenital Cancers?.
Microorganisms, 13(2): pii:microorganisms13020315.
The human microbiome, which encompasses microbial communities and their genetic material, significantly influences health and disease, including cancer. The urogenital microbiota, naturally present in the urinary and genital tracts, interact with factors such as age, lifestyle, and health conditions to affect homeostasis and carcinogenesis. Studies suggest that alterations in this microbiota contribute to the development and progression of genitourinary cancers, emphasizing the concept of oncobiome, which refers to microbial genetic contributions to cancer. Similarly, gut microbiota can influence hormone levels and systemic inflammation, impacting cancers such as cervical and prostate cancer. Advanced studies indicate that microbial communities in genitourinary cancers have distinct profiles that may serve as diagnostic biomarkers or therapeutic targets. Dysbiosis of the urinary microbiota correlates with bladder and kidney cancer. Additionally, gut microbiota influence the effectiveness of cancer treatments. However, further research is necessary to clarify causality, the role of microbial metabolites, and hormonal regulation. The aim of this review is to understand that these dynamics present opportunities for innovative cancer diagnostics and therapies, highlighting the need for integration of microbiology, oncology, and genomics to explore the role of microbiota in genitourinary cancers. For this, a comprehensive search of relevant databases was conducted, applying specific inclusion and exclusion criteria to identify studies examining the association between microbiota and urogenital cancers. Research into the mechanisms by which microbiota influence urogenital cancers may pave the way for new diagnostic and therapeutic approaches, ultimately improving patient outcomes.
Additional Links: PMID-40005682
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PubMed:
Citation:
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@article {pmid40005682,
year = {2025},
author = {Ece, G and AktaΕ, A and Caner, A and SaΔlΔ±k, İ and Kula Atik, T and Ulusan BaΔcΔ±, Ö and BayΔ±ndΔ±r Bilman, F and Demirbakan, H and GΓΌdΓΌl Havuz, S and Kaya, E and Koyuncu Γzyurt, Ö and Yetkin, G and Zorbozan, O},
title = {The Urogenital System Microbiota: Is It a New Gamechanger in Urogenital Cancers?.},
journal = {Microorganisms},
volume = {13},
number = {2},
pages = {},
doi = {10.3390/microorganisms13020315},
pmid = {40005682},
issn = {2076-2607},
abstract = {The human microbiome, which encompasses microbial communities and their genetic material, significantly influences health and disease, including cancer. The urogenital microbiota, naturally present in the urinary and genital tracts, interact with factors such as age, lifestyle, and health conditions to affect homeostasis and carcinogenesis. Studies suggest that alterations in this microbiota contribute to the development and progression of genitourinary cancers, emphasizing the concept of oncobiome, which refers to microbial genetic contributions to cancer. Similarly, gut microbiota can influence hormone levels and systemic inflammation, impacting cancers such as cervical and prostate cancer. Advanced studies indicate that microbial communities in genitourinary cancers have distinct profiles that may serve as diagnostic biomarkers or therapeutic targets. Dysbiosis of the urinary microbiota correlates with bladder and kidney cancer. Additionally, gut microbiota influence the effectiveness of cancer treatments. However, further research is necessary to clarify causality, the role of microbial metabolites, and hormonal regulation. The aim of this review is to understand that these dynamics present opportunities for innovative cancer diagnostics and therapies, highlighting the need for integration of microbiology, oncology, and genomics to explore the role of microbiota in genitourinary cancers. For this, a comprehensive search of relevant databases was conducted, applying specific inclusion and exclusion criteria to identify studies examining the association between microbiota and urogenital cancers. Research into the mechanisms by which microbiota influence urogenital cancers may pave the way for new diagnostic and therapeutic approaches, ultimately improving patient outcomes.},
}
RevDate: 2025-02-26
Exploring Competitive Relationship Between Haemophilus parainfluenzae and Mitis Streptococci via Co-Culture-Based Molecular Diagnosis and Metabolomic Assay.
Microorganisms, 13(2): pii:microorganisms13020279.
Various bacterial strains with nitrate-reducing capacity (NRC), such as Haemophilus, Actinomyces, and Neisseria, are known to promote NH3 production, control pH in the oral cavity, and inhibit the growth of aciduric bacteria. However, experimental evidence on various estimated bacterial networks within the salivary microbiome is insufficient. This study aims to explore potential bacterial compositional competition observed within saliva samples from dental caries patients through a co-culture assay of mitis Streptococci, which is a primary colonizer in the salivary microbiome, and nitrate-reducing bacteria Haemophilus parainfluenzae. We investigated bacterial growth efficiency change by co-culture time using the qRT-PCR method. In addition, we applied LC/Q-TOF-based metabolites screening to confirm metabolic interactions between oral bacterial species and their association with dental caries from a metabolomics perspective. As a result, we first found that the nitrate reduction ability of H. parainfluenzae is maintained even in a co-culture environment with the mitis Streptococci group through a nitrate reduction test. However, nitrate reduction efficiency was hindered when compared with monoculture-based nitrate reduction test results. Next, we designed species-specific primers, and we confirmed by qRT-PCR that there is an obvious competitive relationship in growth efficiency between H. parainfluenzae and two mitis Streptococci (S. australis and S. sanguinis). Furthermore, although direct effects of nitrate reduction on competition have not been identified, we have potentially confirmed through LC/Q-TOF-based metabolite screening analysis that the interaction of various metabolic compounds synthesized from mitis Streptococci is driving inter-strain competition. In particular, we constructed a basic reference core-metabolites list to understand the metabolic network between each target bacterial species (H. parainfluenzae and mitis Streptococci) within the salivary microbiome, which still lacks accumulated research data. Ultimately, we suggest that our data have potential value to be referenced in further metagenomics and metabolomics-based studies related to oral health care.
Additional Links: PMID-40005646
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PubMed:
Citation:
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@article {pmid40005646,
year = {2025},
author = {Choi, Y and Jeong, J and Han, Y and Han, M and Yu, B and Han, K},
title = {Exploring Competitive Relationship Between Haemophilus parainfluenzae and Mitis Streptococci via Co-Culture-Based Molecular Diagnosis and Metabolomic Assay.},
journal = {Microorganisms},
volume = {13},
number = {2},
pages = {},
doi = {10.3390/microorganisms13020279},
pmid = {40005646},
issn = {2076-2607},
support = {RS-2024-00355393//the Ministry of Education of the Republic of Korea and the National Research Foundation of Korea/ ; },
abstract = {Various bacterial strains with nitrate-reducing capacity (NRC), such as Haemophilus, Actinomyces, and Neisseria, are known to promote NH3 production, control pH in the oral cavity, and inhibit the growth of aciduric bacteria. However, experimental evidence on various estimated bacterial networks within the salivary microbiome is insufficient. This study aims to explore potential bacterial compositional competition observed within saliva samples from dental caries patients through a co-culture assay of mitis Streptococci, which is a primary colonizer in the salivary microbiome, and nitrate-reducing bacteria Haemophilus parainfluenzae. We investigated bacterial growth efficiency change by co-culture time using the qRT-PCR method. In addition, we applied LC/Q-TOF-based metabolites screening to confirm metabolic interactions between oral bacterial species and their association with dental caries from a metabolomics perspective. As a result, we first found that the nitrate reduction ability of H. parainfluenzae is maintained even in a co-culture environment with the mitis Streptococci group through a nitrate reduction test. However, nitrate reduction efficiency was hindered when compared with monoculture-based nitrate reduction test results. Next, we designed species-specific primers, and we confirmed by qRT-PCR that there is an obvious competitive relationship in growth efficiency between H. parainfluenzae and two mitis Streptococci (S. australis and S. sanguinis). Furthermore, although direct effects of nitrate reduction on competition have not been identified, we have potentially confirmed through LC/Q-TOF-based metabolite screening analysis that the interaction of various metabolic compounds synthesized from mitis Streptococci is driving inter-strain competition. In particular, we constructed a basic reference core-metabolites list to understand the metabolic network between each target bacterial species (H. parainfluenzae and mitis Streptococci) within the salivary microbiome, which still lacks accumulated research data. Ultimately, we suggest that our data have potential value to be referenced in further metagenomics and metabolomics-based studies related to oral health care.},
}
RevDate: 2025-02-25
Heterologous Expression of a Cryptic BGC from Bilophila sp. Provides Access to a Novel Family of Antibacterial Thiazoles.
ACS synthetic biology [Epub ahead of print].
Human health is greatly influenced by the gut microbiota and microbiota imbalance can lead to the development of diseases. It is widely acknowledged that the interaction of bacteria within competitive ecosystems is influenced by their specialized metabolites, which act, e.g., as antibacterials or siderophores. However, our understanding of the occurrence and impact of such natural products in the human gut microbiome remains very limited. As arylthiazole siderophores are an emerging family of growth-promoting molecules in pathogenic bacteria, we analyzed a metagenomic data set from the human microbiome and thereby identified the bil-BGC, which originates from an uncultured Bilophila strain. Through gene synthesis and BGC assembly, heterologous expression and mutasynthetic experiments, we discovered the arylthiazole natural products bilothiazoles A-F. While established activities of related molecules indicate their involvement in metal-binding and -uptake, which could promote the growth of pathogenic strains, we also found antibiotic activity for some bilothiazoles. This is supported by biosensor-experiments, where bilothiazoles C and E show PrecA-suppressing activity, while bilothiazole F induces PblaZ, a biosensor characteristic for Ξ²-lactam antibiotics. These findings serve as a starting point for investigating the role of bilothiazoles in the pathogenicity of Bilophila species in the gut.
Additional Links: PMID-39999339
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PubMed:
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@article {pmid39999339,
year = {2025},
author = {Hohmann, M and Iliasov, D and Larralde, M and Johannes, W and JanΓen, KP and Zeller, G and Mascher, T and Gulder, TAM},
title = {Heterologous Expression of a Cryptic BGC from Bilophila sp. Provides Access to a Novel Family of Antibacterial Thiazoles.},
journal = {ACS synthetic biology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acssynbio.5c00042},
pmid = {39999339},
issn = {2161-5063},
abstract = {Human health is greatly influenced by the gut microbiota and microbiota imbalance can lead to the development of diseases. It is widely acknowledged that the interaction of bacteria within competitive ecosystems is influenced by their specialized metabolites, which act, e.g., as antibacterials or siderophores. However, our understanding of the occurrence and impact of such natural products in the human gut microbiome remains very limited. As arylthiazole siderophores are an emerging family of growth-promoting molecules in pathogenic bacteria, we analyzed a metagenomic data set from the human microbiome and thereby identified the bil-BGC, which originates from an uncultured Bilophila strain. Through gene synthesis and BGC assembly, heterologous expression and mutasynthetic experiments, we discovered the arylthiazole natural products bilothiazoles A-F. While established activities of related molecules indicate their involvement in metal-binding and -uptake, which could promote the growth of pathogenic strains, we also found antibiotic activity for some bilothiazoles. This is supported by biosensor-experiments, where bilothiazoles C and E show PrecA-suppressing activity, while bilothiazole F induces PblaZ, a biosensor characteristic for Ξ²-lactam antibiotics. These findings serve as a starting point for investigating the role of bilothiazoles in the pathogenicity of Bilophila species in the gut.},
}
RevDate: 2025-02-25
Reevaluation of the gastrointestinal methanogenic archaeome in multiple sclerosis and its association with treatment.
Microbiology spectrum [Epub ahead of print].
The role of the gut archaeal microbiome (archaeome) in health and disease remains poorly understood. Methanogenic archaea have been linked to multiple sclerosis (MS), but prior studies were limited by small cohorts and inconsistent methodologies. To address this, we re-evaluated the association between methanogenic archaea and MS using metagenomic data from the International Multiple Sclerosis Microbiome Study. We analyzed gut microbiome profiles from 115 MS patients and 115 healthy household controls across Buenos Aires (27.8%), Edinburgh (33.9%), New York (10.4%), and San Francisco (27.8%). Metagenomic sequences were taxonomically classified using kraken2/bracken and a curated profiling database to detect archaea, specifically Methanobrevibacter species. Most MS patients were female (80/115), aged 25-72 years (median: 44.5), and 70% were undergoing treatment, including dimethyl fumarate (n = 21), fingolimod (n = 20), glatiramer acetate (n = 14), interferon (n = 18), natalizumab (n = 6), or ocrelizumab/rituximab (n = 1). We found no significant differences in overall archaeome profiles between MS patients and controls. However, treated MS patients exhibited higher abundances of Methanobrevibacter smithii and M. sp900766745 compared to untreated patients. Notably, M. sp900766745 abundance correlated with lower disease severity scores in treated patients. Our results suggest that gut methanogens are not directly associated with MS onset or progression but may reflect microbiome health during treatment. These findings highlight potential roles for M. smithii and M. sp900766745 in modulating treatment outcomes, warranting further investigation into their relevance to gut microbiome function and MS management.IMPORTANCEMultiple sclerosis (MS) is a chronic neuroinflammatory disease affecting the central nervous system, with approximately 2.8 million people diagnosed worldwide, mainly young adults aged 20-30 years. While recent studies have focused on bacterial changes in the MS microbiome, the role of gut archaea has been less explored. Previous research suggested a potential link between methanogenic archaea and MS disease status, but these findings remained inconclusive. Our study addresses this gap by investigating the gut archaeal composition in MS patients and examining how it changes in response to treatment. By focusing on methanogens, we aim to uncover novel insights into their role in MS, potentially revealing new biomarkers or therapeutic targets. This research is crucial for enhancing our understanding of the gut microbiome's impact on MS and improving patient management.
Additional Links: PMID-39998261
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PubMed:
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@article {pmid39998261,
year = {2025},
author = {Woh, PY and Chen, Y and Kumpitsch, C and Mohammadzadeh, R and Schmidt, L and Moissl-Eichinger, C},
title = {Reevaluation of the gastrointestinal methanogenic archaeome in multiple sclerosis and its association with treatment.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0218324},
doi = {10.1128/spectrum.02183-24},
pmid = {39998261},
issn = {2165-0497},
abstract = {The role of the gut archaeal microbiome (archaeome) in health and disease remains poorly understood. Methanogenic archaea have been linked to multiple sclerosis (MS), but prior studies were limited by small cohorts and inconsistent methodologies. To address this, we re-evaluated the association between methanogenic archaea and MS using metagenomic data from the International Multiple Sclerosis Microbiome Study. We analyzed gut microbiome profiles from 115 MS patients and 115 healthy household controls across Buenos Aires (27.8%), Edinburgh (33.9%), New York (10.4%), and San Francisco (27.8%). Metagenomic sequences were taxonomically classified using kraken2/bracken and a curated profiling database to detect archaea, specifically Methanobrevibacter species. Most MS patients were female (80/115), aged 25-72 years (median: 44.5), and 70% were undergoing treatment, including dimethyl fumarate (n = 21), fingolimod (n = 20), glatiramer acetate (n = 14), interferon (n = 18), natalizumab (n = 6), or ocrelizumab/rituximab (n = 1). We found no significant differences in overall archaeome profiles between MS patients and controls. However, treated MS patients exhibited higher abundances of Methanobrevibacter smithii and M. sp900766745 compared to untreated patients. Notably, M. sp900766745 abundance correlated with lower disease severity scores in treated patients. Our results suggest that gut methanogens are not directly associated with MS onset or progression but may reflect microbiome health during treatment. These findings highlight potential roles for M. smithii and M. sp900766745 in modulating treatment outcomes, warranting further investigation into their relevance to gut microbiome function and MS management.IMPORTANCEMultiple sclerosis (MS) is a chronic neuroinflammatory disease affecting the central nervous system, with approximately 2.8 million people diagnosed worldwide, mainly young adults aged 20-30 years. While recent studies have focused on bacterial changes in the MS microbiome, the role of gut archaea has been less explored. Previous research suggested a potential link between methanogenic archaea and MS disease status, but these findings remained inconclusive. Our study addresses this gap by investigating the gut archaeal composition in MS patients and examining how it changes in response to treatment. By focusing on methanogens, we aim to uncover novel insights into their role in MS, potentially revealing new biomarkers or therapeutic targets. This research is crucial for enhancing our understanding of the gut microbiome's impact on MS and improving patient management.},
}
RevDate: 2025-02-25
SARS-CoV-2 infectivity can be modulated through bacterial grooming of the glycocalyx.
mBio [Epub ahead of print].
The gastrointestinal (GI) tract is a site of replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and GI symptoms are often reported by patients. SARS-CoV-2 cell entry depends upon heparan sulfate (HS) proteoglycans, which commensal bacteria that bathe the human mucosa are known to modify. To explore human gut HS-modifying bacterial abundances and how their presence may impact SARS-CoV-2 infection, we developed a task-based analysis of proteoglycan degradation on large-scale shotgun metagenomic data. We observed that gut bacteria with high predicted catabolic capacity for HS differ by age and sex, factors associated with coronavirus disease 2019 (COVID-19) severity, and directly by disease severity during/after infection, but do not vary between subjects with COVID-19 comorbidities or by diet. Gut commensal bacterial HS-modifying enzymes reduce spike protein binding and infection of authentic SARS-CoV-2, suggesting that bacterial grooming of the GI mucosa may impact viral susceptibility.IMPORTANCESevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019, can infect the gastrointestinal (GI) tract, and individuals who exhibit GI symptoms often have more severe disease. The GI tract's glycocalyx, a component of the mucosa covering the large intestine, plays a key role in viral entry by binding SARS-CoV-2's spike protein via heparan sulfate (HS). Here, using metabolic task analysis of multiple large microbiome sequencing data sets of the human gut microbiome, we identify a key commensal human intestinal bacteria capable of grooming glycocalyx HS and modulating SARS-CoV-2 infectivity in vitro. Moreover, we engineered the common probiotic Escherichia coli Nissle 1917 (EcN) to effectively block SARS-CoV-2 binding and infection of human cell cultures. Understanding these microbial interactions could lead to better risk assessments and novel therapies targeting viral entry mechanisms.
Additional Links: PMID-39998226
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@article {pmid39998226,
year = {2025},
author = {Martino, C and Kellman, BP and Sandoval, DR and Clausen, TM and Cooper, R and Benjdia, A and Soualmia, F and Clark, AE and Garretson, AF and Marotz, CA and Song, SJ and Wandro, S and Zaramela, LS and Salido, RA and Zhu, Q and Armingol, E and VΓ‘zquez-Baeza, Y and McDonald, D and Sorrentino, JT and Taylor, B and Belda-Ferre, P and Das, P and Ali, F and Liang, C and Zhang, Y and Schifanella, L and Covizzi, A and Lai, A and Riva, A and Basting, C and Broedlow, CA and Havulinna, AS and Jousilahti, P and Estaki, M and Kosciolek, T and Kuplicki, R and Victor, TA and Paulus, MP and Savage, KE and Benbow, JL and Spielfogel, ES and Anderson, CAM and Martinez, ME and Lacey, JV and Huang, S and Haiminen, N and Parida, L and Kim, H-C and Gilbert, JA and Sweeney, DA and Allard, SM and Swafford, AD and Cheng, S and Inoyue, M and Niiranen, T and Jain, M and Salomaa, V and Zengler, K and Klatt, NR and Hasty, J and Berteau, O and Carlin, AF and Esko, JD and Lewis, NE and Knight, R},
title = {SARS-CoV-2 infectivity can be modulated through bacterial grooming of the glycocalyx.},
journal = {mBio},
volume = {},
number = {},
pages = {e0401524},
doi = {10.1128/mbio.04015-24},
pmid = {39998226},
issn = {2150-7511},
abstract = {The gastrointestinal (GI) tract is a site of replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and GI symptoms are often reported by patients. SARS-CoV-2 cell entry depends upon heparan sulfate (HS) proteoglycans, which commensal bacteria that bathe the human mucosa are known to modify. To explore human gut HS-modifying bacterial abundances and how their presence may impact SARS-CoV-2 infection, we developed a task-based analysis of proteoglycan degradation on large-scale shotgun metagenomic data. We observed that gut bacteria with high predicted catabolic capacity for HS differ by age and sex, factors associated with coronavirus disease 2019 (COVID-19) severity, and directly by disease severity during/after infection, but do not vary between subjects with COVID-19 comorbidities or by diet. Gut commensal bacterial HS-modifying enzymes reduce spike protein binding and infection of authentic SARS-CoV-2, suggesting that bacterial grooming of the GI mucosa may impact viral susceptibility.IMPORTANCESevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019, can infect the gastrointestinal (GI) tract, and individuals who exhibit GI symptoms often have more severe disease. The GI tract's glycocalyx, a component of the mucosa covering the large intestine, plays a key role in viral entry by binding SARS-CoV-2's spike protein via heparan sulfate (HS). Here, using metabolic task analysis of multiple large microbiome sequencing data sets of the human gut microbiome, we identify a key commensal human intestinal bacteria capable of grooming glycocalyx HS and modulating SARS-CoV-2 infectivity in vitro. Moreover, we engineered the common probiotic Escherichia coli Nissle 1917 (EcN) to effectively block SARS-CoV-2 binding and infection of human cell cultures. Understanding these microbial interactions could lead to better risk assessments and novel therapies targeting viral entry mechanisms.},
}
RevDate: 2025-02-24
CmpDate: 2025-02-24
Isolation and characterization of new lytic bacteriophage PSA-KC1 against Pseudomonas aeruginosa isolates from cystic fibrosis patients.
Scientific reports, 15(1):6551.
A novel lytic bacteriophage, PSA-KC1, was isolated from wastewater. In this study, the whole genome of the bacteriophage PSA-KC1 was analyzed, and its lytic properties were assessed. PSA-KC1 has a linear double-stranded DNA genome with a total length of 43,237 base pairs and a GC content of 53.6%. In total, 65 genes were predicted, 46 of which were assigned functions as structural proteins involved in genome replication, packaging or phage lysis. PSA-KC1 belongs to the genus Septimatrevirus under the Caudoviricetes class. The aim of this study was to investigate the efficacy of the lytic bacteriophage PSA-KC1 and compare it with that of the Pyophage phage cocktail on 25 multi drug resistant (MDR) Pseudomonas aeruginosa strains isolated from sputum samples of cystic fibrosis patients. Seventeen of these strains were susceptible (68%) to the PSA-KC1 lytic phage we isolated, whereas eight clinical strains were resistant. However, 22 (88%) of the P. aeruginosa strains were susceptible to the Pyophage cocktail, and three (12%) were resistant to the Phage cocktail. At the end of our study, a new lytic phage active against multidrug-resistant P. aeruginosa strains from CF patients was isolated, and its genome was characterized. Since the PSA-KC1 phage does not contain virulence factors, toxins or integrase genes, it can be expected to be a therapeutic candidate with the potential to be used safely in phage therapy.
Additional Links: PMID-39994360
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@article {pmid39994360,
year = {2025},
author = {Kurt, KC and Kurt, H and TokuΓ§, E and Γzbey, D and ArabacΔ±, DN and AydΔ±n, S and GΓΆnΓΌllΓΌ, N and Skurnik, M and Tokman, HB},
title = {Isolation and characterization of new lytic bacteriophage PSA-KC1 against Pseudomonas aeruginosa isolates from cystic fibrosis patients.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {6551},
pmid = {39994360},
issn = {2045-2322},
support = {IUC-BAP 34517//Istanbul University-Cerrahpasa, BAP/ ; },
mesh = {*Pseudomonas aeruginosa/virology/isolation & purification/genetics ; Humans ; *Cystic Fibrosis/microbiology ; *Genome, Viral ; *Pseudomonas Infections/microbiology ; Pseudomonas Phages/genetics/isolation & purification ; Bacteriophages/isolation & purification/genetics/physiology ; Drug Resistance, Multiple, Bacterial/genetics ; },
abstract = {A novel lytic bacteriophage, PSA-KC1, was isolated from wastewater. In this study, the whole genome of the bacteriophage PSA-KC1 was analyzed, and its lytic properties were assessed. PSA-KC1 has a linear double-stranded DNA genome with a total length of 43,237 base pairs and a GC content of 53.6%. In total, 65 genes were predicted, 46 of which were assigned functions as structural proteins involved in genome replication, packaging or phage lysis. PSA-KC1 belongs to the genus Septimatrevirus under the Caudoviricetes class. The aim of this study was to investigate the efficacy of the lytic bacteriophage PSA-KC1 and compare it with that of the Pyophage phage cocktail on 25 multi drug resistant (MDR) Pseudomonas aeruginosa strains isolated from sputum samples of cystic fibrosis patients. Seventeen of these strains were susceptible (68%) to the PSA-KC1 lytic phage we isolated, whereas eight clinical strains were resistant. However, 22 (88%) of the P. aeruginosa strains were susceptible to the Pyophage cocktail, and three (12%) were resistant to the Phage cocktail. At the end of our study, a new lytic phage active against multidrug-resistant P. aeruginosa strains from CF patients was isolated, and its genome was characterized. Since the PSA-KC1 phage does not contain virulence factors, toxins or integrase genes, it can be expected to be a therapeutic candidate with the potential to be used safely in phage therapy.},
}
MeSH Terms:
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*Pseudomonas aeruginosa/virology/isolation & purification/genetics
Humans
*Cystic Fibrosis/microbiology
*Genome, Viral
*Pseudomonas Infections/microbiology
Pseudomonas Phages/genetics/isolation & purification
Bacteriophages/isolation & purification/genetics/physiology
Drug Resistance, Multiple, Bacterial/genetics
RevDate: 2025-02-24
CmpDate: 2025-02-24
Correlation between gut microbiota dysbiosis, metabolic syndrome and breast cancer.
Scientific reports, 15(1):6652.
Breast cancer is a widespread cancer with a high death rate globally. The incidence of breast cancer is expected to increase, particularly in low and middle-income countries due to environmental factors and lifestyle changes. Several risk factors, such as age, family history, hormonal and reproductive factors, have been identified to influence breast cancer development. Metabolic syndrome, is a metabolic disorder that has also been linked to breast cancer risk. The gut microbiome has been suggested as one of the environmental factors leading to breast cancer. The human microbiome is mainly colonized in the intestine by various bacterial species, including Lactobacillus, Bifidobacterium, and Streptococcus and protect the host against pathogenic microorganisms and regulate the immune system. This study included 50 female breast cancer patients and 50 healthy controls with matched ages. Stool fresh samples were taken from test and control groups and stored at - 20 Β°C until further investigations. DNA of the bacteria in stool samples was extracted using reverse transcription-quantitative polymerase chain reaction to check for the bacterial 16s rRNA gene. The exclusion criteria included other malignancies, recent intestinal surgery, infectious diarrhea, prolonged use of antibiotics, substance addiction, and pregnancy or lactation. Our findings exhibited that breast cancer patients had a higher incidence of metabolic syndrome (60%) compared to cancer-free controls (40%). Furthermore, breast cancer patients had significantly lower Bifidobacterium and Lactobacillus counts than the controls. No significant difference was found in Streptococcus counts between groups. These findings support the relationship between breast cancer and metabolic syndrome and suggest the potential involvement of Lactobacillus and Bifidobacterium in breast cancer pathophysiology. Our study supports the relation between breast cancer and disorder of metabolic syndrome and suggests the potential involvement of Lactobacillus and Bifidobacterium in breast cancer pathophysiology. Further research is necessary to investigate the complex interactions between genes, the environment, and the gut microbiome in breast cancer development. Understanding these interactions could lead to the progress of novel strategies for breast cancer prevention and treatment.
Additional Links: PMID-39994329
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@article {pmid39994329,
year = {2025},
author = {Abdelqader, EM and Mahmoud, WS and Gebreel, HM and Kamel, MM and Abu-Elghait, M},
title = {Correlation between gut microbiota dysbiosis, metabolic syndrome and breast cancer.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {6652},
pmid = {39994329},
issn = {2045-2322},
mesh = {Humans ; Female ; *Metabolic Syndrome/microbiology ; *Gastrointestinal Microbiome ; *Breast Neoplasms/microbiology/epidemiology ; *Dysbiosis/microbiology ; Middle Aged ; Adult ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Case-Control Studies ; Bifidobacterium/isolation & purification/genetics ; Lactobacillus/isolation & purification/genetics ; Risk Factors ; },
abstract = {Breast cancer is a widespread cancer with a high death rate globally. The incidence of breast cancer is expected to increase, particularly in low and middle-income countries due to environmental factors and lifestyle changes. Several risk factors, such as age, family history, hormonal and reproductive factors, have been identified to influence breast cancer development. Metabolic syndrome, is a metabolic disorder that has also been linked to breast cancer risk. The gut microbiome has been suggested as one of the environmental factors leading to breast cancer. The human microbiome is mainly colonized in the intestine by various bacterial species, including Lactobacillus, Bifidobacterium, and Streptococcus and protect the host against pathogenic microorganisms and regulate the immune system. This study included 50 female breast cancer patients and 50 healthy controls with matched ages. Stool fresh samples were taken from test and control groups and stored at - 20 Β°C until further investigations. DNA of the bacteria in stool samples was extracted using reverse transcription-quantitative polymerase chain reaction to check for the bacterial 16s rRNA gene. The exclusion criteria included other malignancies, recent intestinal surgery, infectious diarrhea, prolonged use of antibiotics, substance addiction, and pregnancy or lactation. Our findings exhibited that breast cancer patients had a higher incidence of metabolic syndrome (60%) compared to cancer-free controls (40%). Furthermore, breast cancer patients had significantly lower Bifidobacterium and Lactobacillus counts than the controls. No significant difference was found in Streptococcus counts between groups. These findings support the relationship between breast cancer and metabolic syndrome and suggest the potential involvement of Lactobacillus and Bifidobacterium in breast cancer pathophysiology. Our study supports the relation between breast cancer and disorder of metabolic syndrome and suggests the potential involvement of Lactobacillus and Bifidobacterium in breast cancer pathophysiology. Further research is necessary to investigate the complex interactions between genes, the environment, and the gut microbiome in breast cancer development. Understanding these interactions could lead to the progress of novel strategies for breast cancer prevention and treatment.},
}
MeSH Terms:
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hide MeSH Terms
Humans
Female
*Metabolic Syndrome/microbiology
*Gastrointestinal Microbiome
*Breast Neoplasms/microbiology/epidemiology
*Dysbiosis/microbiology
Middle Aged
Adult
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Case-Control Studies
Bifidobacterium/isolation & purification/genetics
Lactobacillus/isolation & purification/genetics
Risk Factors
RevDate: 2025-02-24
Disrupting the balance: how acne duration impacts skin microbiota assembly processes.
Microbiology spectrum [Epub ahead of print].
Growing interest in the impact of microbial balance on health has driven studies on the ecological processes shaping the skin microbiota. Skin diseases, which alter the skin's local environment, can disrupt the microbial structure and interact with the disease itself. However, research on microbial assembly in diseased skin remains limited. In this study, we applied ecological models to characterize the processes shaping the skin microbiota in acne patients, considering the impact of disease duration on both skin pores and surfaces using bacterial amplicon sequencing. Our results revealed a significant shift in microbial diversity on the skin surface of patients with long-term acne. Further microbial community analyses showed a transition in ecological processes from healthy to diseased skin. Microbial communities on the skin surfaces of healthy controls and individuals with short-duration acne were primarily driven by heterogeneous selection, whereas microbial drift dominated the assembly process in the long-duration groups. Using the Sloan neutral model, we classified amplicon sequence variants (ASVs) into high-effect and low-effect groups based on relative abundance and sample occurrence. High-effect ASVs, likely exerting a greater ecological influence, were predominantly represented by Cutibacterium across all acne-affected skin groups, while Staphylococcus became enriched among high-effect ASVs in patients with long-term acne. Functional profiling further demonstrated that high-effect ASVs were significantly enriched in motility-related pathways. Additionally, we observed a reduction in microbial network complexity on skin surfaces as disease duration increased. Overall, the ecological dynamics of skin microbial communities may offer valuable insights into the mechanisms underlying disease onset and persistence.IMPORTANCEThe skin microbiota plays a critical role in acne development, yet the processes governing microbial assembly during acne progression remain poorly understood. Previous studies predominantly focused on factors such as acne severity, location, and duration in relation to skin microbial structure, with little attention given to the ecological mechanisms shaping the communities. In this study, we applied ecological models to investigate the processes influencing microbial assembly of skin microbiota in acne patients with varying disease durations and examined functions of ecologically important non-neutral amplicon sequence variants (ASVs). Our findings reveal a transition in ecological processes from deterministic to neutral processes as acne duration increased, with non-neutral ASVs potentially contributing to acne pathogenicity and persistence. These insights contribute to a deeper understanding of the ecological dynamics underlying acne and indicate that targeting these non-neutral ASVs or their associated functions may serve as the basis for future therapeutic strategies.
Additional Links: PMID-39992142
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PubMed:
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@article {pmid39992142,
year = {2025},
author = {Sun, L and Wang, Q and Huang, J and Wang, H and Yu, Z},
title = {Disrupting the balance: how acne duration impacts skin microbiota assembly processes.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0260324},
doi = {10.1128/spectrum.02603-24},
pmid = {39992142},
issn = {2165-0497},
abstract = {Growing interest in the impact of microbial balance on health has driven studies on the ecological processes shaping the skin microbiota. Skin diseases, which alter the skin's local environment, can disrupt the microbial structure and interact with the disease itself. However, research on microbial assembly in diseased skin remains limited. In this study, we applied ecological models to characterize the processes shaping the skin microbiota in acne patients, considering the impact of disease duration on both skin pores and surfaces using bacterial amplicon sequencing. Our results revealed a significant shift in microbial diversity on the skin surface of patients with long-term acne. Further microbial community analyses showed a transition in ecological processes from healthy to diseased skin. Microbial communities on the skin surfaces of healthy controls and individuals with short-duration acne were primarily driven by heterogeneous selection, whereas microbial drift dominated the assembly process in the long-duration groups. Using the Sloan neutral model, we classified amplicon sequence variants (ASVs) into high-effect and low-effect groups based on relative abundance and sample occurrence. High-effect ASVs, likely exerting a greater ecological influence, were predominantly represented by Cutibacterium across all acne-affected skin groups, while Staphylococcus became enriched among high-effect ASVs in patients with long-term acne. Functional profiling further demonstrated that high-effect ASVs were significantly enriched in motility-related pathways. Additionally, we observed a reduction in microbial network complexity on skin surfaces as disease duration increased. Overall, the ecological dynamics of skin microbial communities may offer valuable insights into the mechanisms underlying disease onset and persistence.IMPORTANCEThe skin microbiota plays a critical role in acne development, yet the processes governing microbial assembly during acne progression remain poorly understood. Previous studies predominantly focused on factors such as acne severity, location, and duration in relation to skin microbial structure, with little attention given to the ecological mechanisms shaping the communities. In this study, we applied ecological models to investigate the processes influencing microbial assembly of skin microbiota in acne patients with varying disease durations and examined functions of ecologically important non-neutral amplicon sequence variants (ASVs). Our findings reveal a transition in ecological processes from deterministic to neutral processes as acne duration increased, with non-neutral ASVs potentially contributing to acne pathogenicity and persistence. These insights contribute to a deeper understanding of the ecological dynamics underlying acne and indicate that targeting these non-neutral ASVs or their associated functions may serve as the basis for future therapeutic strategies.},
}
RevDate: 2025-02-24
The MicroMap is a network visualisation resource for microbiome metabolism.
bioRxiv : the preprint server for biology pii:2025.02.13.637616.
The human microbiome plays a crucial role in metabolism and thereby influences health and disease. Constraint-based reconstruction and analysis (COBRA) has proven an attractive framework to generate mechanism-derived hypotheses along the nutrition-host-microbiome-disease axis within the computational systems biology community. Unlike for human, no large-scale visualisation resource for microbiome metabolism has been available to date. To address this gap, we created the MicroMap, a manually curated microbiome metabolic network visualisation, which captures the metabolic content of over a quarter million microbial genome-scale metabolic reconstructions. The MicroMap contains 5,064 unique reactions and 3,499 unique metabolites, including for 98 drugs. The MicroMap allows users to intuitively explore microbiome metabolism, inspect microbial metabolic capabilities, and visualise computational modelling results. Further, the MicroMap shall serve as an educational tool to make microbiome metabolism accessible to broader audiences beyond computational modellers. For example, we utilised the MicroMap to generate a comprehensive collection of 257,429 visualisations, corresponding to the entire scope of our current microbiome reconstruction resources, to enable users to visually compare and contrast the metabolic capabilities for different microbes. The MicroMap seamlessly integrates with the Virtual Metabolic Human (VMH, www.vmh.life) and the COBRA Toolbox (opencobra.github.io), and is freely accessible at the MicroMap dataverse (https://dataverse.harvard.edu/dataverse/micromap), in addition to all the generated reconstruction visualisations.
Additional Links: PMID-39990405
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@article {pmid39990405,
year = {2025},
author = {Thinnes, CC and Waschkowitz, R and Courtney, E and Culligan, E and Fahy, K and Ferrazza, RAM and Ferris, C and Lagali, A and Lane, R and Maye, C and Murphy, O and Noone, D and Ryan, S and Bet, M and Corr, MC and Cummins, H and Hackett, D and Healy, E and Kulczycka, N and Lang, N and Madden, L and McHugh, L and Pyne, I and Varley, C and Harkin, N and Meade, R and O'Donnell, G and Nap, B and Martinelli, F and Heinken, A and Thiele, I},
title = {The MicroMap is a network visualisation resource for microbiome metabolism.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.02.13.637616},
pmid = {39990405},
issn = {2692-8205},
abstract = {The human microbiome plays a crucial role in metabolism and thereby influences health and disease. Constraint-based reconstruction and analysis (COBRA) has proven an attractive framework to generate mechanism-derived hypotheses along the nutrition-host-microbiome-disease axis within the computational systems biology community. Unlike for human, no large-scale visualisation resource for microbiome metabolism has been available to date. To address this gap, we created the MicroMap, a manually curated microbiome metabolic network visualisation, which captures the metabolic content of over a quarter million microbial genome-scale metabolic reconstructions. The MicroMap contains 5,064 unique reactions and 3,499 unique metabolites, including for 98 drugs. The MicroMap allows users to intuitively explore microbiome metabolism, inspect microbial metabolic capabilities, and visualise computational modelling results. Further, the MicroMap shall serve as an educational tool to make microbiome metabolism accessible to broader audiences beyond computational modellers. For example, we utilised the MicroMap to generate a comprehensive collection of 257,429 visualisations, corresponding to the entire scope of our current microbiome reconstruction resources, to enable users to visually compare and contrast the metabolic capabilities for different microbes. The MicroMap seamlessly integrates with the Virtual Metabolic Human (VMH, www.vmh.life) and the COBRA Toolbox (opencobra.github.io), and is freely accessible at the MicroMap dataverse (https://dataverse.harvard.edu/dataverse/micromap), in addition to all the generated reconstruction visualisations.},
}
RevDate: 2025-02-21
Identification of body fluid sources based on microbiome antibiotic resistance genes using high-throughput qPCR.
Forensic science international. Genetics, 77:103241 pii:S1872-4973(25)00021-3 [Epub ahead of print].
Identifying the origin of body fluids is a critical step in forensic investigation. Recently, the development of high-throughput sequencing technology has led to the use of microbiomes for body fluid identification in forensic studies. However, high-throughput sequencing data are difficult to analyze, the sequencing protocol is complicated. An increasing number of studies have focused on antibiotic resistance genes (ARGs) in the human microbiome. The abundance and diversity of ARGs in different parts of the human body can be detected using quantitative polymerase chain reaction (qPCR). To date, no studies have inferred the sources of body fluids based on ARGs. Therefore, we attempted to use ARGs as a tool to infer the origin of body fluids. We assessed the abundance and diversity of 64 ARGs in blood, semen, saliva, vaginal secretions (VS), nasal secretions (NS), and fecal samples using high-throughput qPCR. The results showed that ARGs were more diverse in fecal samples, which was significantly higher than those of other sample types (P < 0.05). Principal coordinate analysis (PCoA) showed that the samples clustered mainly according to their type. We constructed a random forest classification model based on 64 ARGs with a prediction accuracy of 92.68 %. Next, we evaluated the importance of the features in the random forest model (mean decrease accuracy, MDA). Subsequently, we constructed prediction models for the top 40 and 20 ARGs after sorting genes with the highest MDA, and their prediction accuracies were both 92.68 %. The accuracy of the top 10 ARGs was 87.80 %. Notably, when only the top 10 characterized ARGs were used to construct models for saliva, semen, and VS samples, the prediction accuracy reached was 95.24 %. This shows that blood, semen, saliva, NS, VS, and fecal samples can be accurately identified using ARGs. Our results suggest that ARGs are promising markers for forensic body fluid identification.
Additional Links: PMID-39983320
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PubMed:
Citation:
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@article {pmid39983320,
year = {2025},
author = {Yu, D and Wang, T and Zhang, L and Gao, N and Huang, Y and Zhang, J and Yan, J},
title = {Identification of body fluid sources based on microbiome antibiotic resistance genes using high-throughput qPCR.},
journal = {Forensic science international. Genetics},
volume = {77},
number = {},
pages = {103241},
doi = {10.1016/j.fsigen.2025.103241},
pmid = {39983320},
issn = {1878-0326},
abstract = {Identifying the origin of body fluids is a critical step in forensic investigation. Recently, the development of high-throughput sequencing technology has led to the use of microbiomes for body fluid identification in forensic studies. However, high-throughput sequencing data are difficult to analyze, the sequencing protocol is complicated. An increasing number of studies have focused on antibiotic resistance genes (ARGs) in the human microbiome. The abundance and diversity of ARGs in different parts of the human body can be detected using quantitative polymerase chain reaction (qPCR). To date, no studies have inferred the sources of body fluids based on ARGs. Therefore, we attempted to use ARGs as a tool to infer the origin of body fluids. We assessed the abundance and diversity of 64 ARGs in blood, semen, saliva, vaginal secretions (VS), nasal secretions (NS), and fecal samples using high-throughput qPCR. The results showed that ARGs were more diverse in fecal samples, which was significantly higher than those of other sample types (P < 0.05). Principal coordinate analysis (PCoA) showed that the samples clustered mainly according to their type. We constructed a random forest classification model based on 64 ARGs with a prediction accuracy of 92.68 %. Next, we evaluated the importance of the features in the random forest model (mean decrease accuracy, MDA). Subsequently, we constructed prediction models for the top 40 and 20 ARGs after sorting genes with the highest MDA, and their prediction accuracies were both 92.68 %. The accuracy of the top 10 ARGs was 87.80 %. Notably, when only the top 10 characterized ARGs were used to construct models for saliva, semen, and VS samples, the prediction accuracy reached was 95.24 %. This shows that blood, semen, saliva, NS, VS, and fecal samples can be accurately identified using ARGs. Our results suggest that ARGs are promising markers for forensic body fluid identification.},
}
RevDate: 2025-02-21
Skin microbiome differences in pancreatic adenocarcinoma, other cancers, and healthy controls: a pilot study.
Frontiers in oncology, 15:1495500.
INTRODUCTION: Many studies have reported the importance of the human microbiome in relationship to the overall health of its host. While recent studies have explored the microbiome's role in various types of cancer compared to healthy patients, this pilot study is the first to investigate differences in the skin microbiome composition among pancreatic adenocarcinoma patients, individuals with other cancers, and cancer-free controls.
METHODS: The study characterizes the skin microbiome's potential associations with cancer status by analyzing skin swabs from the forehead and cheek of 58 participants using Next Generation Sequencing (NGS), differential abundance analysis, and machine learning techniques.
RESULTS: The study results indicated that the cancer group displayed a significantly higher mean alpha diversity compared to the control group. Additionally, a machine learning classification model achieved a mean F1 Score of 0.943 in predicting cancer status, indicating measurable differentiation in the skin microbiome between the study groups. This differentiation is supported by differential abundance methods, including ANCOM-BC and MaAsLin2.
DISCUSSION: This pilot study suggests that skin microbiome profiling could serve as a non-invasive biomarker for cancer detection and monitoring, which warrants a larger, longitudinal study to validate these results.
Additional Links: PMID-39980568
Full Text:
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PubMed:
Citation:
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@article {pmid39980568,
year = {2025},
author = {Davis, T and Decker, KT and Hosseini, D and Jameson, G and Borazanci, E},
title = {Skin microbiome differences in pancreatic adenocarcinoma, other cancers, and healthy controls: a pilot study.},
journal = {Frontiers in oncology},
volume = {15},
number = {},
pages = {1495500},
doi = {10.3389/fonc.2025.1495500},
pmid = {39980568},
issn = {2234-943X},
abstract = {INTRODUCTION: Many studies have reported the importance of the human microbiome in relationship to the overall health of its host. While recent studies have explored the microbiome's role in various types of cancer compared to healthy patients, this pilot study is the first to investigate differences in the skin microbiome composition among pancreatic adenocarcinoma patients, individuals with other cancers, and cancer-free controls.
METHODS: The study characterizes the skin microbiome's potential associations with cancer status by analyzing skin swabs from the forehead and cheek of 58 participants using Next Generation Sequencing (NGS), differential abundance analysis, and machine learning techniques.
RESULTS: The study results indicated that the cancer group displayed a significantly higher mean alpha diversity compared to the control group. Additionally, a machine learning classification model achieved a mean F1 Score of 0.943 in predicting cancer status, indicating measurable differentiation in the skin microbiome between the study groups. This differentiation is supported by differential abundance methods, including ANCOM-BC and MaAsLin2.
DISCUSSION: This pilot study suggests that skin microbiome profiling could serve as a non-invasive biomarker for cancer detection and monitoring, which warrants a larger, longitudinal study to validate these results.},
}
RevDate: 2025-02-20
CmpDate: 2025-02-21
Investigating the Anna Karenina principle of the breast microbiome.
BMC microbiology, 25(1):81.
The relationship between the microbiome and disease has long been a central focus of research in human microbiome. Inspired by Leo Tolstoy's dictum, the Anna Karenina Principle (AKP) offers a framework for understanding the complex dynamics of microbial communities in response to perturbations, suggesting that dysbiotic individuals exhibit greater variability/heterogeneity in their microbiome compared to healthy counterparts. While some studies have proved the alignment of microbiome responses to disease with the AKP effect, it remains uncertain whether the human breast microbiome responds similarly to breast disease. This study used beta-diversity and similarity in Hill numbers, along with shared species analysis (SSA), to explore this issue. We observed that during mastitis, changes in both the taxa richness and composition in the breast milk microbiome align with the AKP effect, while alterations in abundant taxa exhibit an anti-AKP effect. The response of breast tissue microbiome to breast cancer differs from that of milk microbiome to mastitis. Breast cancer induce anti-AKP effects in taxa richness, and non-AKP effects in common taxa and taxa composition. Overall, our findings identified different responses to breast diseases across taxa abundance in the breast microbiome. Mastitis primarily involves increasing the heterogeneity of rare taxa in the breast milk microbiome, while breast cancer associates with decreased dispersion of rare taxa in the tissue microbiome.
Additional Links: PMID-39979818
PubMed:
Citation:
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@article {pmid39979818,
year = {2025},
author = {Li, W and Yang, J},
title = {Investigating the Anna Karenina principle of the breast microbiome.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {81},
pmid = {39979818},
issn = {1471-2180},
support = {202203021222244//Basic Research Program of Shanxi Province/ ; TYSGJ202201//Critical Talent Workstation Project/ ; 202105AC160030//Top Experts training Project for the Academy and Technology in Yunnan province/ ; XDYC-MY-2022-0005//Famous doctor project of Xingdian talent plan in Yunnan province/ ; 202201AY070001-232//The Scientific Research Fund of Yunnan province of China, Kunming Medical University Joint Research Project/ ; 2024EKKFKT-03//Neonatal Key Specialty of Yunnan province/ ; L-2024015//Yunnan health training project of high level talents/ ; },
mesh = {Humans ; *Microbiota ; Female ; *Mastitis/microbiology/veterinary ; *Milk, Human/microbiology/chemistry ; *Bacteria/classification/isolation & purification/genetics ; *Breast/microbiology ; Breast Neoplasms/microbiology ; RNA, Ribosomal, 16S/genetics ; Adult ; },
abstract = {The relationship between the microbiome and disease has long been a central focus of research in human microbiome. Inspired by Leo Tolstoy's dictum, the Anna Karenina Principle (AKP) offers a framework for understanding the complex dynamics of microbial communities in response to perturbations, suggesting that dysbiotic individuals exhibit greater variability/heterogeneity in their microbiome compared to healthy counterparts. While some studies have proved the alignment of microbiome responses to disease with the AKP effect, it remains uncertain whether the human breast microbiome responds similarly to breast disease. This study used beta-diversity and similarity in Hill numbers, along with shared species analysis (SSA), to explore this issue. We observed that during mastitis, changes in both the taxa richness and composition in the breast milk microbiome align with the AKP effect, while alterations in abundant taxa exhibit an anti-AKP effect. The response of breast tissue microbiome to breast cancer differs from that of milk microbiome to mastitis. Breast cancer induce anti-AKP effects in taxa richness, and non-AKP effects in common taxa and taxa composition. Overall, our findings identified different responses to breast diseases across taxa abundance in the breast microbiome. Mastitis primarily involves increasing the heterogeneity of rare taxa in the breast milk microbiome, while breast cancer associates with decreased dispersion of rare taxa in the tissue microbiome.},
}
MeSH Terms:
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Humans
*Microbiota
Female
*Mastitis/microbiology/veterinary
*Milk, Human/microbiology/chemistry
*Bacteria/classification/isolation & purification/genetics
*Breast/microbiology
Breast Neoplasms/microbiology
RNA, Ribosomal, 16S/genetics
Adult
RevDate: 2025-02-20
Targeting both the enzymatic and non-enzymatic functions of DHODH as a therapeutic vulnerability in c-Myc-driven cancer.
Cell reports, 44(3):115327 pii:S2211-1247(25)00098-1 [Epub ahead of print].
c-Myc (Myc)-driven cancers exhibit aggressive phenotypes and therapeutic resistance. Here, integrating CRISPR-Cas9 screening, we identify dihydroorotate dehydrogenase (DHODH) as a promising target in Myc-driven cancer. Mechanistically, DHODH interacts with Myc to stabilize it independently of its enzymatic activity, thereby antagonizing SKP2-mediated polyubiquitination and proteasomal degradation. EN4, a Myc transcriptional activity inhibitor, disrupts DHODH-Myc interaction, promoting Myc degradation via SKP2. Additionally, Myc transcriptionally activates DHODH, enhancing pyrimidine biosynthesis and ferroptosis defense, processes dependent on DHODH enzymatic activity. Clinically, DHODH positively correlates with Myc, activating pyrimidine metabolism and ferroptosis defense in Myc-driven cancers. Hyperactivation of the DHODH-Myc axis is linked to colorectal cancer progression and poor prognosis. Therapeutically, combining EN4 with a DHODH enzymatic inhibitor demonstrates potent antitumor efficacy in Myc-driven colorectal cancer. Overall, our findings elucidate the metabolic and non-metabolic roles of DHODH in Myc-driven cancer, underscoring its dual potential as a therapeutic target addressing both enzymatic and non-enzymatic functions.
Additional Links: PMID-39977268
Publisher:
PubMed:
Citation:
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@article {pmid39977268,
year = {2025},
author = {Zhang, Q and Cui, K and Kong, Y and Yu, J and Luo, Z and Yang, X and Gong, L and Xie, Y and Lin, J and Liu, C and Zhang, Z and Liu, Y and Liu, B and Liang, D and Zeng, W and He, Z and Lan, P},
title = {Targeting both the enzymatic and non-enzymatic functions of DHODH as a therapeutic vulnerability in c-Myc-driven cancer.},
journal = {Cell reports},
volume = {44},
number = {3},
pages = {115327},
doi = {10.1016/j.celrep.2025.115327},
pmid = {39977268},
issn = {2211-1247},
abstract = {c-Myc (Myc)-driven cancers exhibit aggressive phenotypes and therapeutic resistance. Here, integrating CRISPR-Cas9 screening, we identify dihydroorotate dehydrogenase (DHODH) as a promising target in Myc-driven cancer. Mechanistically, DHODH interacts with Myc to stabilize it independently of its enzymatic activity, thereby antagonizing SKP2-mediated polyubiquitination and proteasomal degradation. EN4, a Myc transcriptional activity inhibitor, disrupts DHODH-Myc interaction, promoting Myc degradation via SKP2. Additionally, Myc transcriptionally activates DHODH, enhancing pyrimidine biosynthesis and ferroptosis defense, processes dependent on DHODH enzymatic activity. Clinically, DHODH positively correlates with Myc, activating pyrimidine metabolism and ferroptosis defense in Myc-driven cancers. Hyperactivation of the DHODH-Myc axis is linked to colorectal cancer progression and poor prognosis. Therapeutically, combining EN4 with a DHODH enzymatic inhibitor demonstrates potent antitumor efficacy in Myc-driven colorectal cancer. Overall, our findings elucidate the metabolic and non-metabolic roles of DHODH in Myc-driven cancer, underscoring its dual potential as a therapeutic target addressing both enzymatic and non-enzymatic functions.},
}
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RJR Experience and Expertise
Researcher
Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.
Educator
Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.
Administrator
Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.
Technologist
Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.
Publisher
While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.
Speaker
Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.
Facilitator
Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.
Designer
Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.
RJR Picks from Around the Web (updated 11 MAY 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.