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RJR: Recommended Bibliography 30 May 2026 at 01:55 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-05-27
CmpDate: 2026-05-27
Recent updates in human leukocyte antigen B27-associated uveitis.
Indian journal of ophthalmology, 74(6):817-820.
There has been progressive understanding in etiopathogenesis, clinical presentation, and effective treatment of anterior uveitis (AU) over the years. Sudden onset, symptomatic acute anterior uveitis (AAU) in a young adult, often male, classically arouses suspicion for human leukocyte antigen (HLA) B27-related uveitis. While the ocular presentation is frequently the earliest manifestation, its systemic counterparts within the spectrum, viz., spondyloarthropathies (SpA), including ankylosing spondylitis (AS), reactive arthritis (RA), psoriatic arthritis (PA), and inflammatory bowel disease-associated inflammation, pose greater diagnostic and therapeutic challenges for rheumatologists and internists. This places the ophthalmologist in a uniquely advantageous yet responsible position in initiating etiologic evaluation and facilitating early systemic recognition. Rapid advances in immunology and molecular medicine have significantly expanded the diagnostic and therapeutic landscape of HLA B27-related disease. Emerging insights implicating the gut microbiome, autoinflammatory mechanisms, and innate immune dysregulation have reshaped traditional concepts of pathogenesis. Concurrently, an improved understanding of cytokine networks and immune signaling pathways has led to the development of targeted biologic and synthetic disease-modifying therapies. Given the dynamic, multisystem nature of HLA B27-associated disease and its variable organ involvement, optimal management necessitates close multidisciplinary collaboration among ophthalmologists, rheumatologists, gastroenterologists, and internists. This article briefly explores the evolving concepts of the complex enigma of the HLA B27 molecule and the basis for recent trends in its understanding at the cellular, molecular, biochemical, and clinical levels.
Additional Links: PMID-42200732
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@article {pmid42200732,
year = {2026},
author = {Narain, S and Gupta, P and Pyare, R and Shroff, D and Rath, PD},
title = {Recent updates in human leukocyte antigen B27-associated uveitis.},
journal = {Indian journal of ophthalmology},
volume = {74},
number = {6},
pages = {817-820},
doi = {10.4103/IJO.IJO_64_26},
pmid = {42200732},
issn = {1998-3689},
mesh = {Humans ; *HLA-B27 Antigen/immunology ; *Uveitis, Anterior/immunology/diagnosis ; },
abstract = {There has been progressive understanding in etiopathogenesis, clinical presentation, and effective treatment of anterior uveitis (AU) over the years. Sudden onset, symptomatic acute anterior uveitis (AAU) in a young adult, often male, classically arouses suspicion for human leukocyte antigen (HLA) B27-related uveitis. While the ocular presentation is frequently the earliest manifestation, its systemic counterparts within the spectrum, viz., spondyloarthropathies (SpA), including ankylosing spondylitis (AS), reactive arthritis (RA), psoriatic arthritis (PA), and inflammatory bowel disease-associated inflammation, pose greater diagnostic and therapeutic challenges for rheumatologists and internists. This places the ophthalmologist in a uniquely advantageous yet responsible position in initiating etiologic evaluation and facilitating early systemic recognition. Rapid advances in immunology and molecular medicine have significantly expanded the diagnostic and therapeutic landscape of HLA B27-related disease. Emerging insights implicating the gut microbiome, autoinflammatory mechanisms, and innate immune dysregulation have reshaped traditional concepts of pathogenesis. Concurrently, an improved understanding of cytokine networks and immune signaling pathways has led to the development of targeted biologic and synthetic disease-modifying therapies. Given the dynamic, multisystem nature of HLA B27-associated disease and its variable organ involvement, optimal management necessitates close multidisciplinary collaboration among ophthalmologists, rheumatologists, gastroenterologists, and internists. This article briefly explores the evolving concepts of the complex enigma of the HLA B27 molecule and the basis for recent trends in its understanding at the cellular, molecular, biochemical, and clinical levels.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*HLA-B27 Antigen/immunology
*Uveitis, Anterior/immunology/diagnosis
RevDate: 2026-05-27
Impact of advanced therapy initiation on antibiotic dependence in chronic pouchitis.
Inflammatory bowel diseases pii:8696123 [Epub ahead of print].
BACKGROUND: A quarter of patients with ulcerative colitis who undergo total proctocolectomy with ileal pouch-anal anastomosis experience chronic pouchitis. While advanced therapies (ATs) are effective in some patients, their impact on antibiotic dependence is unclear.
METHODS: In a multicenter, retrospective study, we identified adults with chronic pouchitis during treatment with AT. Those with complete pre-AT antibiotic data formed the "incident AT user" cohort. Those with only post-AT data formed the "prevalent AT user" cohort. Antibiotic prescription was modeled as percentage of time, calculated as the number of weeks of antibiotic prescription during the weeks of observed time. The pooled prevalence of antibiotic use during AT was calculated in a systematic review and meta-analysis,.
RESULTS: Of the 67 incident AT users, 24 (36%) initiated treatment with tumor necrosis factor-α antagonist, 17 (25%) with anti-integrin, 23 (34%), with interleukin (IL) inhibitors (anti-IL), and 3 (5%) with Janus kinase inhibitors. The mean time on antibiotics was unchanged from 38% to 33% after AT initiation, and 61% of patients (n = 44) had a reduction in antibiotic use. Compared to the patients without reduction, the reduction group had a higher proportion of patients on anti-IL (46% vs 15%, adjusted odds ratio [OR] 11.1; 95% CI, 2.12-57.62). There were no differences in disease-related parameters. Seventy-nine percent (22/28) of prevalent AT users required antibiotics. On meta-analysis, pooled prevalence of antibiotic use was 0.46 (95% CI, 0.35-0.57).
CONCLUSIONS: Just over half of patients on AT for chronic pouchitis saw reduced antibiotic use; however, further studies are needed to identify impact of AT on antibiotic use and define which patients benefit from immune-mediated vs microbiome-directed therapy.
Additional Links: PMID-42200819
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PubMed:
Citation:
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@article {pmid42200819,
year = {2026},
author = {Pan, Y and Dunleavy, KA and Ananthakrishnan, AN},
title = {Impact of advanced therapy initiation on antibiotic dependence in chronic pouchitis.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag086},
pmid = {42200819},
issn = {1536-4844},
support = {R38AG070229/NH/NIH HHS/United States ; /NH/NIH HHS/United States ; },
abstract = {BACKGROUND: A quarter of patients with ulcerative colitis who undergo total proctocolectomy with ileal pouch-anal anastomosis experience chronic pouchitis. While advanced therapies (ATs) are effective in some patients, their impact on antibiotic dependence is unclear.
METHODS: In a multicenter, retrospective study, we identified adults with chronic pouchitis during treatment with AT. Those with complete pre-AT antibiotic data formed the "incident AT user" cohort. Those with only post-AT data formed the "prevalent AT user" cohort. Antibiotic prescription was modeled as percentage of time, calculated as the number of weeks of antibiotic prescription during the weeks of observed time. The pooled prevalence of antibiotic use during AT was calculated in a systematic review and meta-analysis,.
RESULTS: Of the 67 incident AT users, 24 (36%) initiated treatment with tumor necrosis factor-α antagonist, 17 (25%) with anti-integrin, 23 (34%), with interleukin (IL) inhibitors (anti-IL), and 3 (5%) with Janus kinase inhibitors. The mean time on antibiotics was unchanged from 38% to 33% after AT initiation, and 61% of patients (n = 44) had a reduction in antibiotic use. Compared to the patients without reduction, the reduction group had a higher proportion of patients on anti-IL (46% vs 15%, adjusted odds ratio [OR] 11.1; 95% CI, 2.12-57.62). There were no differences in disease-related parameters. Seventy-nine percent (22/28) of prevalent AT users required antibiotics. On meta-analysis, pooled prevalence of antibiotic use was 0.46 (95% CI, 0.35-0.57).
CONCLUSIONS: Just over half of patients on AT for chronic pouchitis saw reduced antibiotic use; however, further studies are needed to identify impact of AT on antibiotic use and define which patients benefit from immune-mediated vs microbiome-directed therapy.},
}
RevDate: 2026-05-29
CmpDate: 2026-05-27
A One Health Perspective on Cancer: A Narrative Review.
Medical sciences (Basel, Switzerland), 14(2):.
Cancer is a major public health challenge worldwide, with increasing incidence and a growing economic and societal burden. Despite therapeutic advances, prevention remains the most effective strategy to reduce its impact. The One Health approach, which recognizes the interconnection between human, animal, and environmental health, provides a valuable framework to address cancer risk factors in a more integrated and sustainable way. This narrative review addresses cancer through a One Health lens. Human health aspects include the global burden, major lifestyle and infectious risk factors, and key prevention strategies. Environmental determinants of cancer are summarized with emphasis on climate change, air pollution, occupational exposures, microplastics, ultraviolet radiation, and nutrition/food safety. Animal health contributions include insights from comparative oncology, which offer translational opportunities for prevention, diagnosis, and treatment, and from microbiome research revealing promising biomarkers for early detection and treatment response. Integrating cancer prevention into the One Health framework is essential for addressing the complex interplay between environmental, animal, and human health. A multidisciplinary approach can enhance public health policies, promote sustainable prevention measures, and improve early detection and treatment strategies, ultimately reducing healthcare costs and advancing global health outcomes.
Additional Links: PMID-42201013
PubMed:
Citation:
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@article {pmid42201013,
year = {2026},
author = {Duarte, SAC and Pinto-Leite, R and Queiroga, FL},
title = {A One Health Perspective on Cancer: A Narrative Review.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {2},
pages = {},
pmid = {42201013},
issn = {2076-3271},
support = {UID/00772/2025//Fundação para a Ciência e Tecnologia/ ; },
mesh = {Humans ; *Neoplasms/prevention & control/epidemiology/etiology ; Animals ; *One Health ; Risk Factors ; Public Health ; },
abstract = {Cancer is a major public health challenge worldwide, with increasing incidence and a growing economic and societal burden. Despite therapeutic advances, prevention remains the most effective strategy to reduce its impact. The One Health approach, which recognizes the interconnection between human, animal, and environmental health, provides a valuable framework to address cancer risk factors in a more integrated and sustainable way. This narrative review addresses cancer through a One Health lens. Human health aspects include the global burden, major lifestyle and infectious risk factors, and key prevention strategies. Environmental determinants of cancer are summarized with emphasis on climate change, air pollution, occupational exposures, microplastics, ultraviolet radiation, and nutrition/food safety. Animal health contributions include insights from comparative oncology, which offer translational opportunities for prevention, diagnosis, and treatment, and from microbiome research revealing promising biomarkers for early detection and treatment response. Integrating cancer prevention into the One Health framework is essential for addressing the complex interplay between environmental, animal, and human health. A multidisciplinary approach can enhance public health policies, promote sustainable prevention measures, and improve early detection and treatment strategies, ultimately reducing healthcare costs and advancing global health outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Neoplasms/prevention & control/epidemiology/etiology
Animals
*One Health
Risk Factors
Public Health
RevDate: 2026-05-27
Oral microbiota diversity and composition in patients with oral lichen planus: An observational molecular analysis study.
Dental and medical problems [Epub ahead of print].
BACKGROUND: Oral lichen planus (OLP) is a chronic inflammatory condition affecting the oral mucosa. The oral microbiome has been identified as a potential contributing factor to OLP.
OBJECTIVES: The aim of the study was to evaluate the prevalence and diversity of the oral microbiota in patients with OLP.
MATERIAL AND METHODS: This observational study included 78 patients with clinically and histopathologically confirmed OLP, recruited in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines. Buccal mucosa samples were collected using standardized protocols. DNA was extracted from 12 high-quality samples and subjected to 16S rRNA gene amplification and sequencing. Alpha and beta diversity indices were calculated using the Quantitative Insights Into Microbial Ecology (QIIME) platform. Statistical analyses were performed using the IBM SPSS Statistics for Windows software, v. 26.0 (IBM Corp., Armonk, USA) (p < 0.05).
RESULTS: Intratissue bacterial communities exhibited decreased alpha diversity and increased beta diversity compared with those present on the mucosal surface. Streptococcus, a genus within the Firmicutes phylum, was found to be the most abundant, with 5 Streptococcus strains identified in the OLP samples. Following Streptococci, Bacilli and Clostridia displayed considerable diversity. Other frequently detected species included Klebsiella pneumoniae, Escherichia coli, Pseudomonas aeruginosa, Eikenella corrodens, Actinobacillus, as well as members of the Proteobacteria phylum, which are commonly found in high quantities in the oral cavity. Prevotella and Capnocytophaga, belonging to the Bacteroidetes phylum, were also frequently observed. Alpha diversity analysis revealed significant differences in the colony numbers of the investigated species across studied samples.
CONCLUSIONS: The findings indicate an association between the composition of the oral microbiota and OLP. The microbial populations obtained from affected individuals exhibited distinct bacterial compositions. Modulation of the oral microbiome may represent a potential strategy for improving the management of OLP.
Additional Links: PMID-42201256
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PubMed:
Citation:
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@article {pmid42201256,
year = {2026},
author = {Saberian, E and Petrášová, A and Jenča, A and Jenčová, J and Shirali, K and Jenča, A and Więckiewicz, MA and Zare-Zardini, H and Ebrahimi Far, M},
title = {Oral microbiota diversity and composition in patients with oral lichen planus: An observational molecular analysis study.},
journal = {Dental and medical problems},
volume = {},
number = {},
pages = {},
doi = {10.17219/dmp/210087},
pmid = {42201256},
issn = {2300-9020},
abstract = {BACKGROUND: Oral lichen planus (OLP) is a chronic inflammatory condition affecting the oral mucosa. The oral microbiome has been identified as a potential contributing factor to OLP.
OBJECTIVES: The aim of the study was to evaluate the prevalence and diversity of the oral microbiota in patients with OLP.
MATERIAL AND METHODS: This observational study included 78 patients with clinically and histopathologically confirmed OLP, recruited in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines. Buccal mucosa samples were collected using standardized protocols. DNA was extracted from 12 high-quality samples and subjected to 16S rRNA gene amplification and sequencing. Alpha and beta diversity indices were calculated using the Quantitative Insights Into Microbial Ecology (QIIME) platform. Statistical analyses were performed using the IBM SPSS Statistics for Windows software, v. 26.0 (IBM Corp., Armonk, USA) (p < 0.05).
RESULTS: Intratissue bacterial communities exhibited decreased alpha diversity and increased beta diversity compared with those present on the mucosal surface. Streptococcus, a genus within the Firmicutes phylum, was found to be the most abundant, with 5 Streptococcus strains identified in the OLP samples. Following Streptococci, Bacilli and Clostridia displayed considerable diversity. Other frequently detected species included Klebsiella pneumoniae, Escherichia coli, Pseudomonas aeruginosa, Eikenella corrodens, Actinobacillus, as well as members of the Proteobacteria phylum, which are commonly found in high quantities in the oral cavity. Prevotella and Capnocytophaga, belonging to the Bacteroidetes phylum, were also frequently observed. Alpha diversity analysis revealed significant differences in the colony numbers of the investigated species across studied samples.
CONCLUSIONS: The findings indicate an association between the composition of the oral microbiota and OLP. The microbial populations obtained from affected individuals exhibited distinct bacterial compositions. Modulation of the oral microbiome may represent a potential strategy for improving the management of OLP.},
}
RevDate: 2026-05-27
Shorter Wound-healing Times Associated With Select Perioperative Medical Therapies in Hidradenitis Suppurativa Surgery, and a Limited Clinical Role of Intraoperative Cultures: A 194-Case Retrospective Review.
Annals of plastic surgery pii:00000637-990000000-01172 [Epub ahead of print].
BACKGROUND: Hidradenitis suppurativa (HS) is a chronic inflammatory disease of apocrine gland-bearing areas characterized by abscesses, tunneling, scarring, and recurrent flares. Surgical excision is central in refractory disease, but perioperative protocols are variable. We evaluated whether specific perioperative medical therapies are associated with shorter time to documented postoperative wound-healing progress after HS surgery, and whether intraoperative cultures meaningfully guide antibiotic management.
METHODS: We conducted a retrospective cohort study of 194 HS surgeries performed at a quaternary care center between January 1, 2013, and July 1, 2021. We abstracted perioperative medical therapies (including antibiotics and spironolactone), intraoperative culture results, postoperative antibiotics, and healing times from the medical record. Healing was defined as days from surgery to the first follow-up note documenting substantial wound-healing progress. Time to healing was analyzed with Kaplan-Meier survival curves and Cox proportional hazards models. We also examined whether intraoperative cultures were associated with postoperative antibiotic selection.
RESULTS: Perioperative trimethoprim-sulfamethoxazole was associated with shorter time to documented healing [hazard ratio (HR) 2.55, 95% CI: 1.46-4.46, P=0.00099]. Preoperative cephalexin was also associated with shorter time to heal (HR: 4.17, 95% CI: 1.40-12.44, P=0.01), whereas postoperative cephalexin was not (HR: 0.89, 95% CI: 0.44-1.79, P=0.74). Perioperative spironolactone was associated with faster healing (HR: 5.72, 95% CI: 2.08-15.74, P=0.00073). Intraoperative cultures were collected in 28% of surgeries, yielded gram-positive, gram-negative, and anaerobic organisms, showed only weak, nonsignificant associations with preoperative antibiotic exposure, and were not significantly associated with postoperative antibiotic choice.
CONCLUSIONS: Perioperative trimethoprim-sulfamethoxazole, cephalexin, and spironolactone were each associated with shorter time to documented wound-healing progress after HS surgery in this retrospective cohort. Routine intraoperative cultures demonstrated limited observed clinical utility in guiding immediate postsurgical antibiotics. These findings support efforts to streamline perioperative care while de-emphasizing routine intraoperative culture collection in HS surgery.
Additional Links: PMID-42201339
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PubMed:
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@article {pmid42201339,
year = {2026},
author = {Sekhon, S and Tompkins-Rhoades, C and Uzoekwe, M and Rajaii, R and Trinh, M and Sheff, S and Hansen, SL},
title = {Shorter Wound-healing Times Associated With Select Perioperative Medical Therapies in Hidradenitis Suppurativa Surgery, and a Limited Clinical Role of Intraoperative Cultures: A 194-Case Retrospective Review.},
journal = {Annals of plastic surgery},
volume = {},
number = {},
pages = {},
doi = {10.1097/SAP.0000000000004777},
pmid = {42201339},
issn = {1536-3708},
abstract = {BACKGROUND: Hidradenitis suppurativa (HS) is a chronic inflammatory disease of apocrine gland-bearing areas characterized by abscesses, tunneling, scarring, and recurrent flares. Surgical excision is central in refractory disease, but perioperative protocols are variable. We evaluated whether specific perioperative medical therapies are associated with shorter time to documented postoperative wound-healing progress after HS surgery, and whether intraoperative cultures meaningfully guide antibiotic management.
METHODS: We conducted a retrospective cohort study of 194 HS surgeries performed at a quaternary care center between January 1, 2013, and July 1, 2021. We abstracted perioperative medical therapies (including antibiotics and spironolactone), intraoperative culture results, postoperative antibiotics, and healing times from the medical record. Healing was defined as days from surgery to the first follow-up note documenting substantial wound-healing progress. Time to healing was analyzed with Kaplan-Meier survival curves and Cox proportional hazards models. We also examined whether intraoperative cultures were associated with postoperative antibiotic selection.
RESULTS: Perioperative trimethoprim-sulfamethoxazole was associated with shorter time to documented healing [hazard ratio (HR) 2.55, 95% CI: 1.46-4.46, P=0.00099]. Preoperative cephalexin was also associated with shorter time to heal (HR: 4.17, 95% CI: 1.40-12.44, P=0.01), whereas postoperative cephalexin was not (HR: 0.89, 95% CI: 0.44-1.79, P=0.74). Perioperative spironolactone was associated with faster healing (HR: 5.72, 95% CI: 2.08-15.74, P=0.00073). Intraoperative cultures were collected in 28% of surgeries, yielded gram-positive, gram-negative, and anaerobic organisms, showed only weak, nonsignificant associations with preoperative antibiotic exposure, and were not significantly associated with postoperative antibiotic choice.
CONCLUSIONS: Perioperative trimethoprim-sulfamethoxazole, cephalexin, and spironolactone were each associated with shorter time to documented wound-healing progress after HS surgery in this retrospective cohort. Routine intraoperative cultures demonstrated limited observed clinical utility in guiding immediate postsurgical antibiotics. These findings support efforts to streamline perioperative care while de-emphasizing routine intraoperative culture collection in HS surgery.},
}
RevDate: 2026-05-27
Rosy Discolouration in an Alpine Chapel: Beyond Salt Dependence.
Microbial ecology pii:10.1007/s00248-026-02795-2 [Epub ahead of print].
Stone heritage is central to cultural identity, yet alpine monuments remain understudied and vulnerable to deterioration. In mountain environments, moisture and temperature fluctuations promote salt crystallisation in porous geomaterials, frequently associated with rosy discolouration attributed to pink biofilms, a phenomenon still poorly explored at higher elevations. Here, we investigated rosy discolouration at about 1000 m altitude on the walls of St. Cyprian Chapel (South Tyrol) using metabarcoding and chemical analyses. We compared two cases of rosy discolouration: one on the north wall, where salt efflorescence is present, and one on the south wall, where it is absent. The aim was to characterise how salt efflorescence modulates rosy discolouration by comparing the two walls and linking substrate chemistry and mineralogy to biofilm pigments, structure, and microbial community composition. Despite similar mineralogy, the north wall exhibited distinct surface chemistry consistent with salt efflorescence. Biofilm biomass was comparable between walls, and no photosynthetic organisms were detected in either biofilm, yet microbial communities differed markedly. The south wall hosted carotenoid-producing biomarkers, including Rubrobacter and Pontibacter, although Raman did not detect carotenoid signals, indicating low pigment expression. In contrast, the north wall showed stronger discolouration and clear detection of bacterioruberin. Notably, the north-wall biomarker Chryseobacterium may also contribute to the rosy discolouration through flexirubin-type pigments. Overall, salt efflorescence is not required for pink biofilm establishment, but salt-rich microhabitats appear to enhance pigment production. This study provides new insights into the drivers of rosy discolouration and contributes to the still-limited research on alpine cultural heritage.
Additional Links: PMID-42201411
Publisher:
PubMed:
Citation:
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@article {pmid42201411,
year = {2026},
author = {Marzanni, A and Landolfi, M and Tiziani, R and Bombardelli, S and Celi, D and Pittertschatscher, M and Buttarelli, A and Bruni, S and Pecchioni, E and Perito, B and Cnudde, V and Cappitelli, F and Mimmo, T and Villa, F and Borruso, L},
title = {Rosy Discolouration in an Alpine Chapel: Beyond Salt Dependence.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02795-2},
pmid = {42201411},
issn = {1432-184X},
abstract = {Stone heritage is central to cultural identity, yet alpine monuments remain understudied and vulnerable to deterioration. In mountain environments, moisture and temperature fluctuations promote salt crystallisation in porous geomaterials, frequently associated with rosy discolouration attributed to pink biofilms, a phenomenon still poorly explored at higher elevations. Here, we investigated rosy discolouration at about 1000 m altitude on the walls of St. Cyprian Chapel (South Tyrol) using metabarcoding and chemical analyses. We compared two cases of rosy discolouration: one on the north wall, where salt efflorescence is present, and one on the south wall, where it is absent. The aim was to characterise how salt efflorescence modulates rosy discolouration by comparing the two walls and linking substrate chemistry and mineralogy to biofilm pigments, structure, and microbial community composition. Despite similar mineralogy, the north wall exhibited distinct surface chemistry consistent with salt efflorescence. Biofilm biomass was comparable between walls, and no photosynthetic organisms were detected in either biofilm, yet microbial communities differed markedly. The south wall hosted carotenoid-producing biomarkers, including Rubrobacter and Pontibacter, although Raman did not detect carotenoid signals, indicating low pigment expression. In contrast, the north wall showed stronger discolouration and clear detection of bacterioruberin. Notably, the north-wall biomarker Chryseobacterium may also contribute to the rosy discolouration through flexirubin-type pigments. Overall, salt efflorescence is not required for pink biofilm establishment, but salt-rich microhabitats appear to enhance pigment production. This study provides new insights into the drivers of rosy discolouration and contributes to the still-limited research on alpine cultural heritage.},
}
RevDate: 2026-05-27
CmpDate: 2026-05-27
Mapping the research landscape on diabetes mellitus and periodontal disease: a scientometric study.
The Saudi dental journal, 38(6):.
To map the scientific landscape linking diabetes mellitus and periodontal disease using bibliometric methods, identify major thematic clusters, and examine how research supports clinical and educational perspectives relevant to integrated diabetes-oral health research. The central research question was: What are the dominant knowledge structures and interdisciplinary connections in the literature on diabetes mellitus and oral health? A bibliometric analysis was conducted using the Web of Science Core Collection (1995-2024). The search strategy combined diabetes related and oral health-related terms. After applying the eligibility criteria, 1,058 publications were included. Keyword preprocessing involved synonym unification, abbreviation harmonization, and manual validation. VOSviewer v1.6.18 was used for keyword co occurrence mapping. Potential sources of bias related to database selection and keyword variability were acknowledged. Eight thematic clusters were identified, covering periodontal disease, prevention, epidemiology, systemic comorbidities, microbiome research, quality of life, clinical interventions, and biomarkers. Cluster structure remained stable across sensitivity thresholds. The literature on diabetes and oral health exhibits recurring thematic patterns and interconnected research domains. While bibliometric clustering reflects co occurrence structures rather than conceptual maturity, the findings provide an analytical overview of how research areas relate to one another. The findings indicate recurring thematic patterns and interconnected research domains. The identified clusters outline priority domains relevant to risk assessment, prevention, and interdisciplinary care. Although bibliometric findings do not directly inform clinical decision making, they highlight areas where integrated diabetes-oral health strategies may be strengthened.
Additional Links: PMID-42201500
PubMed:
Citation:
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@article {pmid42201500,
year = {2026},
author = {Repanovici, A and Vîlcu, ME and Pantea, I},
title = {Mapping the research landscape on diabetes mellitus and periodontal disease: a scientometric study.},
journal = {The Saudi dental journal},
volume = {38},
number = {6},
pages = {},
pmid = {42201500},
issn = {1013-9052},
abstract = {To map the scientific landscape linking diabetes mellitus and periodontal disease using bibliometric methods, identify major thematic clusters, and examine how research supports clinical and educational perspectives relevant to integrated diabetes-oral health research. The central research question was: What are the dominant knowledge structures and interdisciplinary connections in the literature on diabetes mellitus and oral health? A bibliometric analysis was conducted using the Web of Science Core Collection (1995-2024). The search strategy combined diabetes related and oral health-related terms. After applying the eligibility criteria, 1,058 publications were included. Keyword preprocessing involved synonym unification, abbreviation harmonization, and manual validation. VOSviewer v1.6.18 was used for keyword co occurrence mapping. Potential sources of bias related to database selection and keyword variability were acknowledged. Eight thematic clusters were identified, covering periodontal disease, prevention, epidemiology, systemic comorbidities, microbiome research, quality of life, clinical interventions, and biomarkers. Cluster structure remained stable across sensitivity thresholds. The literature on diabetes and oral health exhibits recurring thematic patterns and interconnected research domains. While bibliometric clustering reflects co occurrence structures rather than conceptual maturity, the findings provide an analytical overview of how research areas relate to one another. The findings indicate recurring thematic patterns and interconnected research domains. The identified clusters outline priority domains relevant to risk assessment, prevention, and interdisciplinary care. Although bibliometric findings do not directly inform clinical decision making, they highlight areas where integrated diabetes-oral health strategies may be strengthened.},
}
RevDate: 2026-05-27
Gut microbiota and cancer immunotherapy: from dysbiosis to personalized immune checkpoint blockade optimization.
Folia microbiologica [Epub ahead of print].
Cancer has become one of the most prominent causes of death worldwide due to its increasing mortality rate. Immune checkpoint blockade therapy is an effective regimen for tumor control. Still, it faces challenges, including primary resistance and interindividual variations, thereby directing the field towards a new era of immunotherapy adjuncts. Recent studies have shown that the microbiota of cancer patients influences the outcomes of ICB (immune checkpoint blockade) therapy through microbiome-immune system crosstalk. Homeostatic commensal microbial consortia aid in combating tumors by enhancing immunity, whereas dysbiotic microbes facilitate cancer development by mediating immunosuppression. Microbiota modulation via microbiome-targeted interventions, including fecal microbiota transplantation or washed microbiota transplantation from responders, biotic supplements, and dietary modifications, can convert primary resistance to durable responses and thus augment immunotherapy responsiveness in cancer treatment. This review discusses the dual nature of microbiota in mediating the development and treatment of cancer, its crucial role in shaping ICB therapy responsiveness, and the identification of microbial biomarkers into a refined Discovery-Validation-Clinical (DVC) pipeline linked to multi-omics profiling and personalized microbiome-modulation interventions for ICB therapy optimization. In addition, it presents the translational clinical decision framework that highlights patient stratification, intervention timing, and implementation barriers to support clinical translation. Ultimately, the gut microbiome emerges as a "force multiplier" of cancer ICB therapy, thereby enabling microbiome-guided precision oncology and strengthening a roadmap toward personalized cancer care.
Additional Links: PMID-42201625
PubMed:
Citation:
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@article {pmid42201625,
year = {2026},
author = {Akram, F and Zainab, S and Shabbir, I and Haq, IU},
title = {Gut microbiota and cancer immunotherapy: from dysbiosis to personalized immune checkpoint blockade optimization.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42201625},
issn = {1874-9356},
abstract = {Cancer has become one of the most prominent causes of death worldwide due to its increasing mortality rate. Immune checkpoint blockade therapy is an effective regimen for tumor control. Still, it faces challenges, including primary resistance and interindividual variations, thereby directing the field towards a new era of immunotherapy adjuncts. Recent studies have shown that the microbiota of cancer patients influences the outcomes of ICB (immune checkpoint blockade) therapy through microbiome-immune system crosstalk. Homeostatic commensal microbial consortia aid in combating tumors by enhancing immunity, whereas dysbiotic microbes facilitate cancer development by mediating immunosuppression. Microbiota modulation via microbiome-targeted interventions, including fecal microbiota transplantation or washed microbiota transplantation from responders, biotic supplements, and dietary modifications, can convert primary resistance to durable responses and thus augment immunotherapy responsiveness in cancer treatment. This review discusses the dual nature of microbiota in mediating the development and treatment of cancer, its crucial role in shaping ICB therapy responsiveness, and the identification of microbial biomarkers into a refined Discovery-Validation-Clinical (DVC) pipeline linked to multi-omics profiling and personalized microbiome-modulation interventions for ICB therapy optimization. In addition, it presents the translational clinical decision framework that highlights patient stratification, intervention timing, and implementation barriers to support clinical translation. Ultimately, the gut microbiome emerges as a "force multiplier" of cancer ICB therapy, thereby enabling microbiome-guided precision oncology and strengthening a roadmap toward personalized cancer care.},
}
RevDate: 2026-05-27
β-Elemene Rescues Radiation-Induced Enteritis by Orchestrating a Host-Microbiome Circuit That Fuels Epigenetic DNA Repair.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Radiation-induced enteritis (RIE) is a severe, dose-limiting toxicity of cancer radiotherapy lacking mechanism-based therapies. While the gut microbiome regulates radiation injury, harnessing it therapeutically remains challenging. Here, we show that the natural product β-elemene protects against RIE through a synergistic mechanism coordinating host and microbial responses. β-elemene directly rescues the radiation-disrupted interaction between the lactate transporter MCT1 and its chaperone CD147 in intestinal epithelial cells, priming them for enhanced lactate uptake. Concurrently, β-elemene selectively enriches for Lactobacillus gasseri, increasing intestinal lactate production. The convergence of host priming and elevated lactate availability triggers a metabo-epigenetic cascade. Specifically, lactate drives the lactylation of the chromatin-associated protein RBBP4, which in turn recruits EP300 to activate the transcription of essential DNA damage repair genes. We further identify EP300 as a lactyl-transferase, establishing a self-amplifying positive feedback loop that robustly enhances the repair signal. Our findings delineate a complete drug-microbe-metabolite-epigenome axis, establishing a 'prime-and-fuel' therapeutic strategy where a single agent orchestrates inter-kingdom communication to promote tissue regeneration.
Additional Links: PMID-42201651
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@article {pmid42201651,
year = {2026},
author = {He, J and Bao, J and Deng, S and Zang, W and Yan, H and Zhao, Z and Zhang, G and Liu, R and Chen, J and Hu, Y and Xue, W},
title = {β-Elemene Rescues Radiation-Induced Enteritis by Orchestrating a Host-Microbiome Circuit That Fuels Epigenetic DNA Repair.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e21445},
doi = {10.1002/advs.202521445},
pmid = {42201651},
issn = {2198-3844},
support = {82473448//National Natural Science Foundation of China/ ; 82102720//National Natural Science Foundation of China/ ; 82203096//National Natural Science Foundation of China/ ; BK20221272//Natural Science Foundation of the Jiangsu Province, China/ ; YJXYY202204-2-YSC16 YJXYY202204-ZD18//Jiangsu Provincial Research Hospital/ ; YJXYY202204-2-YSB23//Jiangsu Provincial Research Hospital/ ; },
abstract = {Radiation-induced enteritis (RIE) is a severe, dose-limiting toxicity of cancer radiotherapy lacking mechanism-based therapies. While the gut microbiome regulates radiation injury, harnessing it therapeutically remains challenging. Here, we show that the natural product β-elemene protects against RIE through a synergistic mechanism coordinating host and microbial responses. β-elemene directly rescues the radiation-disrupted interaction between the lactate transporter MCT1 and its chaperone CD147 in intestinal epithelial cells, priming them for enhanced lactate uptake. Concurrently, β-elemene selectively enriches for Lactobacillus gasseri, increasing intestinal lactate production. The convergence of host priming and elevated lactate availability triggers a metabo-epigenetic cascade. Specifically, lactate drives the lactylation of the chromatin-associated protein RBBP4, which in turn recruits EP300 to activate the transcription of essential DNA damage repair genes. We further identify EP300 as a lactyl-transferase, establishing a self-amplifying positive feedback loop that robustly enhances the repair signal. Our findings delineate a complete drug-microbe-metabolite-epigenome axis, establishing a 'prime-and-fuel' therapeutic strategy where a single agent orchestrates inter-kingdom communication to promote tissue regeneration.},
}
RevDate: 2026-05-27
CmpDate: 2026-05-27
Histological and metagenomic analysis of microbial communities in archaeological human bones.
PloS one, 21(5):e0340244.
Buried archaeological bones tend to be heavily degraded by microorganisms. This type of biodegradation was already identified in the 19th century and remains a subject of continuous investigation. However, the underlying processes are still not fully understood, and the organisms responsible for the decay have not been clearly identified. Technological advances in genetic sequencing now allow detailed study of the bone microbiome. And yet, identifying the species causing the observed bioerosion has proven challenging. Relatively few studies have combined the investigation of bone degradation by microscopy, so-called histotaphonomy, with metagenomic analyses. This study aims to bridge this gap. We utilize a large set of human bone samples from medieval cemeteries in south-western Norway. Detailed microscopic analyses have been carried out, showing diverse levels of preservation. The extent of bioerosion is correlated with the results from metagenomic analyses as well as environmental factors. Microbiome diversity is greater and more evenly distributed in well-preserved bones with limited bioerosion, particularly those recovered from burials beneath church floors, contrasting with outdoor cemeteries. Fungal taxa were detected in only a single sample in the metagenomic data despite histological evidence of fungal structures, and their role in bone bioerosion remains unclear. Our findings show that preservation state is strongly associated with microbiome composition. The most prevalent genus found was Streptomyces, supporting previous research suggesting that bacteria within this group could be involved in bone bioerosion.
Additional Links: PMID-42201863
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Citation:
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@article {pmid42201863,
year = {2026},
author = {Kaptan, D and Flemming Elvers, AC and Kjær Knudsen, A and Schroeder, H and Hollund, HI},
title = {Histological and metagenomic analysis of microbial communities in archaeological human bones.},
journal = {PloS one},
volume = {21},
number = {5},
pages = {e0340244},
pmid = {42201863},
issn = {1932-6203},
mesh = {Humans ; *Bone and Bones/microbiology/pathology ; *Metagenomics/methods ; *Archaeology ; *Microbiota/genetics ; Bacteria/genetics/classification ; Fungi/genetics/classification/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Norway ; Phylogeny ; },
abstract = {Buried archaeological bones tend to be heavily degraded by microorganisms. This type of biodegradation was already identified in the 19th century and remains a subject of continuous investigation. However, the underlying processes are still not fully understood, and the organisms responsible for the decay have not been clearly identified. Technological advances in genetic sequencing now allow detailed study of the bone microbiome. And yet, identifying the species causing the observed bioerosion has proven challenging. Relatively few studies have combined the investigation of bone degradation by microscopy, so-called histotaphonomy, with metagenomic analyses. This study aims to bridge this gap. We utilize a large set of human bone samples from medieval cemeteries in south-western Norway. Detailed microscopic analyses have been carried out, showing diverse levels of preservation. The extent of bioerosion is correlated with the results from metagenomic analyses as well as environmental factors. Microbiome diversity is greater and more evenly distributed in well-preserved bones with limited bioerosion, particularly those recovered from burials beneath church floors, contrasting with outdoor cemeteries. Fungal taxa were detected in only a single sample in the metagenomic data despite histological evidence of fungal structures, and their role in bone bioerosion remains unclear. Our findings show that preservation state is strongly associated with microbiome composition. The most prevalent genus found was Streptomyces, supporting previous research suggesting that bacteria within this group could be involved in bone bioerosion.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Bone and Bones/microbiology/pathology
*Metagenomics/methods
*Archaeology
*Microbiota/genetics
Bacteria/genetics/classification
Fungi/genetics/classification/isolation & purification
RNA, Ribosomal, 16S/genetics
Norway
Phylogeny
RevDate: 2026-05-27
CmpDate: 2026-05-27
Modeling the microbial contribution to human energy balance using the Digestion, Absorption, and Microbial Metabolism (DAMM) model.
PloS one, 21(5):e0347668.
Colonic microorganisms have been linked to human health and disease, specifically metabolic disease states such as obesity, but causal relationships remain to be established. Previous work demonstrated that interactions between the host's diet and intestinal microbiome were associated with human energy balance by affecting the human's energy absorption, quantified by metabolizable energy. We developed the Digestion, Absorption and Microbial Metabolism (DAMM) model, which explicitly accounts for the energy contributions of the colonic microbial community in five steps. 1) The DAMM model breaks down the diet composition into the gross energy of the individual macronutrients. 2) It calculates direct absorption in the upper gastrointestinal tract. 3) It uses microbial stoichiometry to estimate the consumption of the remaining unabsorbed nutrients by microbes in the large intestine. 4) It quantitatively predicts microbial production of short-chain fatty acids (SCFA) and methane in the colon. 5) The DAMM model estimates absorption from the colonic tract to the host, including SCFAs. When used to predict the results from a clinical study that compared two distinctly different diets, the DAMM model captured the directionality and magnitude of change in measured metabolizable chemical oxygen demand (which can be converted to metabolizable energy), estimated substrate availability within the colon, and predicted rate of production of microbially derived short-chain fatty acids. It improved on the accuracy of metabolizable chemical oxygen demand predictions compared to the Atwater factors, increasing the fit from R2 = 88% (Atwater) to R2 = 96% (DAMM). The model reduced systematic bias on one of the diets and decreased the mean difference between measurement and predictions from -22.3 gCOD d-1 to -2.5 gCOD d-1. The DAMM model now can be linked to existing human models that predict changes in body energy stores to extend our understanding of how microbial metabolic processes affect macronutrient absorption and metabolizable energy.
Additional Links: PMID-42201874
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Citation:
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@article {pmid42201874,
year = {2026},
author = {Davis, TL and Dirks, B and Carnero, EA and Corbin, KD and Smith, SR and Marcus, A and Krajmalnik-Brown, R and Rittmann, BE},
title = {Modeling the microbial contribution to human energy balance using the Digestion, Absorption, and Microbial Metabolism (DAMM) model.},
journal = {PloS one},
volume = {21},
number = {5},
pages = {e0347668},
pmid = {42201874},
issn = {1932-6203},
mesh = {Humans ; *Energy Metabolism/physiology ; *Models, Biological ; *Digestion/physiology ; *Gastrointestinal Microbiome/physiology ; Colon/microbiology/metabolism ; Fatty Acids, Volatile/metabolism ; Intestinal Absorption ; Diet ; },
abstract = {Colonic microorganisms have been linked to human health and disease, specifically metabolic disease states such as obesity, but causal relationships remain to be established. Previous work demonstrated that interactions between the host's diet and intestinal microbiome were associated with human energy balance by affecting the human's energy absorption, quantified by metabolizable energy. We developed the Digestion, Absorption and Microbial Metabolism (DAMM) model, which explicitly accounts for the energy contributions of the colonic microbial community in five steps. 1) The DAMM model breaks down the diet composition into the gross energy of the individual macronutrients. 2) It calculates direct absorption in the upper gastrointestinal tract. 3) It uses microbial stoichiometry to estimate the consumption of the remaining unabsorbed nutrients by microbes in the large intestine. 4) It quantitatively predicts microbial production of short-chain fatty acids (SCFA) and methane in the colon. 5) The DAMM model estimates absorption from the colonic tract to the host, including SCFAs. When used to predict the results from a clinical study that compared two distinctly different diets, the DAMM model captured the directionality and magnitude of change in measured metabolizable chemical oxygen demand (which can be converted to metabolizable energy), estimated substrate availability within the colon, and predicted rate of production of microbially derived short-chain fatty acids. It improved on the accuracy of metabolizable chemical oxygen demand predictions compared to the Atwater factors, increasing the fit from R2 = 88% (Atwater) to R2 = 96% (DAMM). The model reduced systematic bias on one of the diets and decreased the mean difference between measurement and predictions from -22.3 gCOD d-1 to -2.5 gCOD d-1. The DAMM model now can be linked to existing human models that predict changes in body energy stores to extend our understanding of how microbial metabolic processes affect macronutrient absorption and metabolizable energy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Energy Metabolism/physiology
*Models, Biological
*Digestion/physiology
*Gastrointestinal Microbiome/physiology
Colon/microbiology/metabolism
Fatty Acids, Volatile/metabolism
Intestinal Absorption
Diet
RevDate: 2026-05-27
Biological responses to heat stress in livestock: From thermoregulation to cellular and epigenetic adaptation.
Journal of thermal biology, 139:104473 pii:S0306-4565(26)00106-3 [Epub ahead of print].
Climate change driven increases in ambient temperature have positioned heat stress (HS) as a major biological constraint on livestock productivity and welfare. Excessive thermal load disrupts thermoregulatory balance, reduces feed intake and digestive efficiency, and perturbs immune and endocrine function, culminating in impaired energy metabolism and systemic dysfunction. Reproductive processes show pronounced thermal sensitivity, as HS alters hypothalamic-pituitary-gonadal axis signaling, compromises gametogenesis, reduces embryo viability, and suppresses fertility. Productive traits, including milk yield, growth rate, egg production, and carcass quality, decline as cumulative heat load exceeds adaptive capacity. Emerging evidence identifies the gut-brain axis as a critical mediator of HS pathology, where heat-induced vascular redistribution, epithelial hypoxia, and microbiome dysbiosis amplify inflammatory and metabolic stress. At the cellular level, HS triggers mitochondrial dysfunction, oxidative imbalance, activation of heat shock responses, immune dysregulation, and epigenetic remodeling with potential long-term consequences. Current mitigation strategies encompass nutritional and phytogenic modulation of stress pathways, genetic selection for thermo-tolerance, microclimate control, and precision livestock farming (PLF) technologies for real-time detection of thermal strain. However, partial understanding of molecular thresholds, epigenetic plasticity, and integrative system responses limits effective translation. Addressing these gaps through mechanistically driven and interdisciplinary research is essential for enhancing thermal resilience and sustaining livestock production under ongoing climate warming.
Additional Links: PMID-42202371
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PubMed:
Citation:
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@article {pmid42202371,
year = {2026},
author = {Afzal, A},
title = {Biological responses to heat stress in livestock: From thermoregulation to cellular and epigenetic adaptation.},
journal = {Journal of thermal biology},
volume = {139},
number = {},
pages = {104473},
doi = {10.1016/j.jtherbio.2026.104473},
pmid = {42202371},
issn = {0306-4565},
abstract = {Climate change driven increases in ambient temperature have positioned heat stress (HS) as a major biological constraint on livestock productivity and welfare. Excessive thermal load disrupts thermoregulatory balance, reduces feed intake and digestive efficiency, and perturbs immune and endocrine function, culminating in impaired energy metabolism and systemic dysfunction. Reproductive processes show pronounced thermal sensitivity, as HS alters hypothalamic-pituitary-gonadal axis signaling, compromises gametogenesis, reduces embryo viability, and suppresses fertility. Productive traits, including milk yield, growth rate, egg production, and carcass quality, decline as cumulative heat load exceeds adaptive capacity. Emerging evidence identifies the gut-brain axis as a critical mediator of HS pathology, where heat-induced vascular redistribution, epithelial hypoxia, and microbiome dysbiosis amplify inflammatory and metabolic stress. At the cellular level, HS triggers mitochondrial dysfunction, oxidative imbalance, activation of heat shock responses, immune dysregulation, and epigenetic remodeling with potential long-term consequences. Current mitigation strategies encompass nutritional and phytogenic modulation of stress pathways, genetic selection for thermo-tolerance, microclimate control, and precision livestock farming (PLF) technologies for real-time detection of thermal strain. However, partial understanding of molecular thresholds, epigenetic plasticity, and integrative system responses limits effective translation. Addressing these gaps through mechanistically driven and interdisciplinary research is essential for enhancing thermal resilience and sustaining livestock production under ongoing climate warming.},
}
RevDate: 2026-05-27
From contaminated waters to living ecosystems: Heavy-metal remediation as a driver of aquatic habitat and biodiversity restoration.
Marine pollution bulletin, 231:119919 pii:S0025-326X(26)00706-X [Epub ahead of print].
Contaminations of soils by hydrocarbons are significant threats to both ecosystems and human health as a result of their persistent nature and potential to cause adverse toxicological effects along with bioaccumulation. This review will discuss the state-of-the-art nanotechnologies used for remediation of soils contaminated with hydrocarbons and their role in processes of adsorption, catalytic oxidation, photocatalysis, electron transfer, redox cycling, and stimulation of microorganisms. While most studies on this topic only highlight the efficiency of biodegradation, this work is going to integrate all aspects of physicochemical transformations of the contaminants, ecology, and sustainability of nanomaterials into one comprehensive overview. Metal nanoparticles, metal oxide nanoparticles, carbon-based nanomaterials, nanoscale zero-valent iron, magnetic nanocomposites, nanoscale zeolites, and hybrid nanomaterials will be analyzed in relation to their impact on the process of hydrocarbon mineralization and degradation rate. The importance of new technologies that involve green synthesis of nanomaterials, their surface modification, and their coupling with microorganisms will be discussed about the improvement of catalytic properties, selectivity, and safety of nanomaterials. Potential ecotoxicological risks such as nanoparticle aggregation, disturbance of the microbiome, bioaccumulation, and changes to the structure of the soil will be also considered.
Additional Links: PMID-42202591
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PubMed:
Citation:
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@article {pmid42202591,
year = {2026},
author = {Baba, IA and Mustapha, LS and Obayomi, OV and Obayomi, KS and Zhang, J},
title = {From contaminated waters to living ecosystems: Heavy-metal remediation as a driver of aquatic habitat and biodiversity restoration.},
journal = {Marine pollution bulletin},
volume = {231},
number = {},
pages = {119919},
doi = {10.1016/j.marpolbul.2026.119919},
pmid = {42202591},
issn = {1879-3363},
abstract = {Contaminations of soils by hydrocarbons are significant threats to both ecosystems and human health as a result of their persistent nature and potential to cause adverse toxicological effects along with bioaccumulation. This review will discuss the state-of-the-art nanotechnologies used for remediation of soils contaminated with hydrocarbons and their role in processes of adsorption, catalytic oxidation, photocatalysis, electron transfer, redox cycling, and stimulation of microorganisms. While most studies on this topic only highlight the efficiency of biodegradation, this work is going to integrate all aspects of physicochemical transformations of the contaminants, ecology, and sustainability of nanomaterials into one comprehensive overview. Metal nanoparticles, metal oxide nanoparticles, carbon-based nanomaterials, nanoscale zero-valent iron, magnetic nanocomposites, nanoscale zeolites, and hybrid nanomaterials will be analyzed in relation to their impact on the process of hydrocarbon mineralization and degradation rate. The importance of new technologies that involve green synthesis of nanomaterials, their surface modification, and their coupling with microorganisms will be discussed about the improvement of catalytic properties, selectivity, and safety of nanomaterials. Potential ecotoxicological risks such as nanoparticle aggregation, disturbance of the microbiome, bioaccumulation, and changes to the structure of the soil will be also considered.},
}
RevDate: 2026-05-27
Long-lasting gut microbiome and fecal metabolome alterations after colorectal adenoma removal and their relationship to colorectal cancer.
Cell host & microbe pii:S1931-3128(26)00177-0 [Epub ahead of print].
Although the gut microbiome is implicated in colorectal cancer (CRC), microbiome and metabolome alterations along the adenoma-carcinoma sequence remain unclear. Here, we profile stool metagenomes obtained from 354 women 12.1 ± 4.8 years following adenoma resection and from their 1:1-matched controls, as well as stool metabolomes from 184 pairs. Metagenomic profiles are compared with those from 14 independent CRC case-control studies. Microbial composition differs between adenoma cases and controls and agrees with CRC-associated alterations (Pearson's rho = 0.26, p < 0.0001). Thirty-one microbes, including Faecalibacterium prausnitzii and Flavonifractor plautii, are altered in both conditions and correlate with lifestyle factors. Thirty metabolites and 7 sub-pathways, particularly sphingolipids, are associated with adenomas. Adenomas also exhibit disease-specific microbe-metabolite associations, including those between Bilophila wadsworthia and alanine-containing dipeptides. These findings reveal gut microbial and metabolomic alterations detectable years after adenoma resection, supporting the presence of an altered microbiome along the adenoma-CRC continuum.
Additional Links: PMID-42202778
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PubMed:
Citation:
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@article {pmid42202778,
year = {2026},
author = {Nogal, A and Wang, K and Thompson, KN and Kim, H and Bhosle, A and Piccinno, G and Maharjan, S and Upreti, C and Nguyen, LH and Segata, N and Rimm, EB and Garrett, WS and Chan, AT and Huttenhower, C and Song, M},
title = {Long-lasting gut microbiome and fecal metabolome alterations after colorectal adenoma removal and their relationship to colorectal cancer.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.05.001},
pmid = {42202778},
issn = {1934-6069},
abstract = {Although the gut microbiome is implicated in colorectal cancer (CRC), microbiome and metabolome alterations along the adenoma-carcinoma sequence remain unclear. Here, we profile stool metagenomes obtained from 354 women 12.1 ± 4.8 years following adenoma resection and from their 1:1-matched controls, as well as stool metabolomes from 184 pairs. Metagenomic profiles are compared with those from 14 independent CRC case-control studies. Microbial composition differs between adenoma cases and controls and agrees with CRC-associated alterations (Pearson's rho = 0.26, p < 0.0001). Thirty-one microbes, including Faecalibacterium prausnitzii and Flavonifractor plautii, are altered in both conditions and correlate with lifestyle factors. Thirty metabolites and 7 sub-pathways, particularly sphingolipids, are associated with adenomas. Adenomas also exhibit disease-specific microbe-metabolite associations, including those between Bilophila wadsworthia and alanine-containing dipeptides. These findings reveal gut microbial and metabolomic alterations detectable years after adenoma resection, supporting the presence of an altered microbiome along the adenoma-CRC continuum.},
}
RevDate: 2026-05-27
Gut microbiome composition and functional potential associate with incident type 2 diabetes in 4,685 adults from a Swedish prospective cohort.
Cell reports. Medicine pii:S2666-3791(26)00252-1 [Epub ahead of print].
Cross-sectional studies link gut microbiome alterations to type 2 diabetes (T2D), but prospective evidence remains limited. We aim to identify taxonomic and functional features associated with future T2D risk. We analyze shotgun metagenomic data from 4,685 participants (mean age, 73.9 years; 49.0% women) in the Swedish SIMPLER cohort, followed for a median 5.3 years, during which 383 developed T2D. Six species are associated with increased T2D risk: Desulfovibrio piger, Alistipes communis, Alistipes finegoldii, Akkermansia muciniphila, Ruminococcus gnavus, and GGB3614_SGB4886 (Lachnospiraceae), while three are protective: Erysipelotrichaceae bacterium, Coprococcus catus, and Clostridia unclassified SGB6317. We observe context-specific associations, including a dietary fiber-modified effect for A. muciniphila indicative of diet-dependent patterns. Three gut metabolic modules are associated with incident T2D: asparagine degradation (higher risk), mannose degradation, and the non-oxidative pentose phosphate pathway (lower risk). These prospective findings offer insights into T2D etiology and may support microbiome-informed strategies for risk prediction and prevention.
Additional Links: PMID-42202790
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PubMed:
Citation:
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@article {pmid42202790,
year = {2026},
author = {Toubon, G and Boulund, F and Escobedo, CM and Brunius, C and Engstrand, L and Larsson, SC and Nordin, E and Schuppe-Koistinen, I and Wolk, A and Wittenbecher, C and Landberg, R},
title = {Gut microbiome composition and functional potential associate with incident type 2 diabetes in 4,685 adults from a Swedish prospective cohort.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102835},
doi = {10.1016/j.xcrm.2026.102835},
pmid = {42202790},
issn = {2666-3791},
abstract = {Cross-sectional studies link gut microbiome alterations to type 2 diabetes (T2D), but prospective evidence remains limited. We aim to identify taxonomic and functional features associated with future T2D risk. We analyze shotgun metagenomic data from 4,685 participants (mean age, 73.9 years; 49.0% women) in the Swedish SIMPLER cohort, followed for a median 5.3 years, during which 383 developed T2D. Six species are associated with increased T2D risk: Desulfovibrio piger, Alistipes communis, Alistipes finegoldii, Akkermansia muciniphila, Ruminococcus gnavus, and GGB3614_SGB4886 (Lachnospiraceae), while three are protective: Erysipelotrichaceae bacterium, Coprococcus catus, and Clostridia unclassified SGB6317. We observe context-specific associations, including a dietary fiber-modified effect for A. muciniphila indicative of diet-dependent patterns. Three gut metabolic modules are associated with incident T2D: asparagine degradation (higher risk), mannose degradation, and the non-oxidative pentose phosphate pathway (lower risk). These prospective findings offer insights into T2D etiology and may support microbiome-informed strategies for risk prediction and prevention.},
}
RevDate: 2026-05-29
Air purification modulates PM-associated nasal microbiota and exhaled metabolome to enhance cardiopulmonary health in children: A randomized crossover trial.
Environmental pollution (Barking, Essex : 1987), 403:128441 pii:S0269-7491(26)00811-0 [Epub ahead of print].
Recent studies have identified the association between exposure to environmental particulate matter (PM) and upper respiratory tract microbiota or lower respiratory tract metabolites; however, direct evidence linking the respiratory microbiome to metabolomic responses remains limited. This study examines how short-term air purification influences PM-related health outcomes, nasal microbiota, and exhaled breath condensate (EBC) metabolites in children. In a randomized crossover trial involving 67 children living near a coking plant, the linear mixed-effects model analyses showed that PM exposure was associated with changes in vital capacity and heart rate. Moreover, PM exposure reduced the abundance of nasal Rothia, which was closely connected to changes in EBC metabolites, including hexylresorcinol and β-carotene. Network and mediation analyses revealed that the PM-Rothia-metabolite axis may exert a significant impact on cardiopulmonary function, among which β-carotene is likely to mediate the effect of PM on vital capacity. Our findings indicate that short-term air purification can reduce PM-associated cardiopulmonary risks in children by modulating Rothia-dependent metabolic pathways.
Additional Links: PMID-42203014
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PubMed:
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@article {pmid42203014,
year = {2026},
author = {Wang, S and Cheng, H and Shao, J and Wang, Y and Feng, C and Yan, S and Zhang, X},
title = {Air purification modulates PM-associated nasal microbiota and exhaled metabolome to enhance cardiopulmonary health in children: A randomized crossover trial.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {403},
number = {},
pages = {128441},
doi = {10.1016/j.envpol.2026.128441},
pmid = {42203014},
issn = {1873-6424},
abstract = {Recent studies have identified the association between exposure to environmental particulate matter (PM) and upper respiratory tract microbiota or lower respiratory tract metabolites; however, direct evidence linking the respiratory microbiome to metabolomic responses remains limited. This study examines how short-term air purification influences PM-related health outcomes, nasal microbiota, and exhaled breath condensate (EBC) metabolites in children. In a randomized crossover trial involving 67 children living near a coking plant, the linear mixed-effects model analyses showed that PM exposure was associated with changes in vital capacity and heart rate. Moreover, PM exposure reduced the abundance of nasal Rothia, which was closely connected to changes in EBC metabolites, including hexylresorcinol and β-carotene. Network and mediation analyses revealed that the PM-Rothia-metabolite axis may exert a significant impact on cardiopulmonary function, among which β-carotene is likely to mediate the effect of PM on vital capacity. Our findings indicate that short-term air purification can reduce PM-associated cardiopulmonary risks in children by modulating Rothia-dependent metabolic pathways.},
}
RevDate: 2026-05-28
Early-life exposure to phthalates and nanoplastics alters gut microbiota and intestinal morphophysiology in rat dams and male offspring.
Toxicology, 525:154510 pii:S0300-483X(26)00117-4 [Epub ahead of print].
Phthalates and nanoplastics, common contaminants in everyday products and a result of their degradation, respectively, are linked to environmental degradation and human exposure. Research suggests that these substances can affect the gut microbiota and morphology, especially during pregnancy and lactation. Changes in the maternal microbiota can have lasting immunological and inflammatory effects on the offspring. This study investigated the effects of gestational (design 1) and gestational and lactational (design 2) exposure to a mixture of phthalates (PM) and nanoplastics (NPs), isolated or in combination, on colon histology and gut microbiota composition of directly exposed mothers (1), and of the male pups of these mothers (2). Pregnant Sprague Dawley rats were randomly divided into 4 groups: CTR (control; vehicle), PM (20 μg/kg/day of phthalate mixture), NPs (1 mg/kg/day nanoplastics NPs-100nm), PM+NPs (20 μg/kg/day PM + 1 mg/kg/day NPs-100nm). Treatment was administered orally from gestational day 5 (GD5) to GD20 for maternal fecal collection (design 1), or from GD10 to postnatal day 22 (PND22) for fecal collection from male pups (design 2). At the end of the treatment period, pregnant rats (GD20) and post-weaning male rats (PND22), 5-6 rats from each group, were euthanized. Colon samples and feces were collected for morphological and microbiome composition analysis, respectively. PM exposure increased goblet cells and reduced class and order Erysipelothichia/Erysipelotrichales at GD20, and reduced class and order Clostridia/Clostridiales at PND22. In addition, PM+NPs exposure increased goblet cells and class and order Bacilli/Lactobacillales and Gammaproteobacteria/Enterobacteriales at GD20. These findings provide evidence that exposure to PM+NPs during gestation affects the maternal microbiota and goblet cells; while this exposure during gestation and lactation causes alterations in the gut microbiota of the offspring, without histological changes. This may also provide information about the mechanistic effects of co-exposure in humans.
Additional Links: PMID-42203025
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@article {pmid42203025,
year = {2026},
author = {Magosso, N and Fioretto, MN and Fávaro, I and de Souza, PV and Moreira, MF and Rocha, VA and Barbosa, FC and Rodrigues, J and Scarano, WR},
title = {Early-life exposure to phthalates and nanoplastics alters gut microbiota and intestinal morphophysiology in rat dams and male offspring.},
journal = {Toxicology},
volume = {525},
number = {},
pages = {154510},
doi = {10.1016/j.tox.2026.154510},
pmid = {42203025},
issn = {1879-3185},
abstract = {Phthalates and nanoplastics, common contaminants in everyday products and a result of their degradation, respectively, are linked to environmental degradation and human exposure. Research suggests that these substances can affect the gut microbiota and morphology, especially during pregnancy and lactation. Changes in the maternal microbiota can have lasting immunological and inflammatory effects on the offspring. This study investigated the effects of gestational (design 1) and gestational and lactational (design 2) exposure to a mixture of phthalates (PM) and nanoplastics (NPs), isolated or in combination, on colon histology and gut microbiota composition of directly exposed mothers (1), and of the male pups of these mothers (2). Pregnant Sprague Dawley rats were randomly divided into 4 groups: CTR (control; vehicle), PM (20 μg/kg/day of phthalate mixture), NPs (1 mg/kg/day nanoplastics NPs-100nm), PM+NPs (20 μg/kg/day PM + 1 mg/kg/day NPs-100nm). Treatment was administered orally from gestational day 5 (GD5) to GD20 for maternal fecal collection (design 1), or from GD10 to postnatal day 22 (PND22) for fecal collection from male pups (design 2). At the end of the treatment period, pregnant rats (GD20) and post-weaning male rats (PND22), 5-6 rats from each group, were euthanized. Colon samples and feces were collected for morphological and microbiome composition analysis, respectively. PM exposure increased goblet cells and reduced class and order Erysipelothichia/Erysipelotrichales at GD20, and reduced class and order Clostridia/Clostridiales at PND22. In addition, PM+NPs exposure increased goblet cells and class and order Bacilli/Lactobacillales and Gammaproteobacteria/Enterobacteriales at GD20. These findings provide evidence that exposure to PM+NPs during gestation affects the maternal microbiota and goblet cells; while this exposure during gestation and lactation causes alterations in the gut microbiota of the offspring, without histological changes. This may also provide information about the mechanistic effects of co-exposure in humans.},
}
RevDate: 2026-05-27
Valorizing renewable biomass into potential prebiotic oligosaccharides: Enzymatic, microbial, and synthetic biology strategies.
Bioresource technology pii:S0960-8524(26)01056-4 [Epub ahead of print].
Biomass valorization has become a central strategy in the transition toward a circular bioeconomy, enabling the conversion of underutilized terrestrial and marine resources into value-added functional ingredients. The production of prebiotic oligosaccharides (POs) has garnered increasing attention owing to their demonstrated health benefits, scalability, and compatibility with existing food systems. This review summarizes recent advances in enzymatic and microbial technologies for producing potential POs-including neoand agarooligosaccharides, cello-oligosaccharides, xylo-oligosaccharides, and pectin oligosaccharides-from renewable biomass, such as marine macroalgae, lignocellulosic residues, and pectin-rich crops. These oligosaccharides act as prebiotics that modulate the gut microbiota and promote the formation of bioactive metabolites, which include short-chain fatty acids, indole-3-lactic acid, and spermidine. With advances in metabolic engineering and synthetic biology, progress has also enabled the microbial biosynthesis of lacto-N-neotetraose and 2'-fucosyllactose, which are human milk oligosaccharides, from biomass-derived sugars using GRAS-designated microbial hosts. These biotechnologies offer sustainable and scalable alternatives to conventional extraction or chemical synthesis. We also discuss recent developments in enzyme engineering, bioprocess optimization, and microbial co-culture systems aimed at enhancing product yield and specificity. This review highlights the industrial applications and beneficial health effects of biomass-derived oligosaccharides, emphasizing their role as next-generation functional ingredients in personalized nutrition and microbiome-targeted therapies.
Additional Links: PMID-42203116
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PubMed:
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@article {pmid42203116,
year = {2026},
author = {Yun, YR and Kim, S and Lee, DY and Yu, S and Kim, KH and Yun, EJ},
title = {Valorizing renewable biomass into potential prebiotic oligosaccharides: Enzymatic, microbial, and synthetic biology strategies.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {134974},
doi = {10.1016/j.biortech.2026.134974},
pmid = {42203116},
issn = {1873-2976},
abstract = {Biomass valorization has become a central strategy in the transition toward a circular bioeconomy, enabling the conversion of underutilized terrestrial and marine resources into value-added functional ingredients. The production of prebiotic oligosaccharides (POs) has garnered increasing attention owing to their demonstrated health benefits, scalability, and compatibility with existing food systems. This review summarizes recent advances in enzymatic and microbial technologies for producing potential POs-including neoand agarooligosaccharides, cello-oligosaccharides, xylo-oligosaccharides, and pectin oligosaccharides-from renewable biomass, such as marine macroalgae, lignocellulosic residues, and pectin-rich crops. These oligosaccharides act as prebiotics that modulate the gut microbiota and promote the formation of bioactive metabolites, which include short-chain fatty acids, indole-3-lactic acid, and spermidine. With advances in metabolic engineering and synthetic biology, progress has also enabled the microbial biosynthesis of lacto-N-neotetraose and 2'-fucosyllactose, which are human milk oligosaccharides, from biomass-derived sugars using GRAS-designated microbial hosts. These biotechnologies offer sustainable and scalable alternatives to conventional extraction or chemical synthesis. We also discuss recent developments in enzyme engineering, bioprocess optimization, and microbial co-culture systems aimed at enhancing product yield and specificity. This review highlights the industrial applications and beneficial health effects of biomass-derived oligosaccharides, emphasizing their role as next-generation functional ingredients in personalized nutrition and microbiome-targeted therapies.},
}
RevDate: 2026-05-27
From multi-omics insights to single-strain proof: How traditional agricultural system enhances fish flavor via the microbiome-gut-muscle axis.
Bioresource technology pii:S0960-8524(26)01074-6 [Epub ahead of print].
Intensive aquaculture has significantly boosted aquatic product yields, but it often compromises sensory quality and remains constrained by reliance on unsustainable fishmeal. The Mulberry-dyke and Fish-pond system, used in China for millennia, suggests a circular approach, yet the underlying mechanism remains poorly understood. In this study, silkworm excrement (SE) from traditional sericulture (TSE) and modern insect factories (ISE) was evaluated as a functional aquafeed. Body weight, gut histology, and immunohistochemistry were employed to assess host health. Gut microbiome, electronic tongue analysis, and muscle metabolomics were conducted to assess fish flavor and identify flavor-related microorganisms. A single-strain feeding experiment further validated the microbiome-gut-muscle axis using electronic tongue analysis, gut transcriptomics, and determination of free amino acids and nucleotides. SE supplementation maintained fish yield while improving intestinal structure. Compared with commercial feed (CF), both SE treatments increased gut microbial diversity and community stability, and more than half of the significantly different ASVs were shared between the TSE and ISE groups, mainly involving immune regulation, nutrient metabolism, and flavor formation. SE, particularly TSE, enhanced antioxidant capacity and reduced lipid peroxidation, possibly through microbial regulation of lysophosphatidylcholines. As consistently indicated by electronic tongue and muscle metabolomics analyses, SE significantly improved fish flavor, with increased umami and reduced bitterness. Network analysis and single-strain feeding further suggested that Methylorubrum populi, Gemmobacter aquatilis, and Rhodobacter sphaeroides contributed to flavor improvement by regulating host amino acid and nucleotide metabolism along the microbiome-gut-muscle axis. These findings highlight SE as a promising sustainable bioresource for aquaculture.
Additional Links: PMID-42203119
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PubMed:
Citation:
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@article {pmid42203119,
year = {2026},
author = {Shen, X and Lei, X and Zhang, H and Guo, E and Chen, L and Sun, C and Muhammad, A and Shao, Y},
title = {From multi-omics insights to single-strain proof: How traditional agricultural system enhances fish flavor via the microbiome-gut-muscle axis.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {134992},
doi = {10.1016/j.biortech.2026.134992},
pmid = {42203119},
issn = {1873-2976},
abstract = {Intensive aquaculture has significantly boosted aquatic product yields, but it often compromises sensory quality and remains constrained by reliance on unsustainable fishmeal. The Mulberry-dyke and Fish-pond system, used in China for millennia, suggests a circular approach, yet the underlying mechanism remains poorly understood. In this study, silkworm excrement (SE) from traditional sericulture (TSE) and modern insect factories (ISE) was evaluated as a functional aquafeed. Body weight, gut histology, and immunohistochemistry were employed to assess host health. Gut microbiome, electronic tongue analysis, and muscle metabolomics were conducted to assess fish flavor and identify flavor-related microorganisms. A single-strain feeding experiment further validated the microbiome-gut-muscle axis using electronic tongue analysis, gut transcriptomics, and determination of free amino acids and nucleotides. SE supplementation maintained fish yield while improving intestinal structure. Compared with commercial feed (CF), both SE treatments increased gut microbial diversity and community stability, and more than half of the significantly different ASVs were shared between the TSE and ISE groups, mainly involving immune regulation, nutrient metabolism, and flavor formation. SE, particularly TSE, enhanced antioxidant capacity and reduced lipid peroxidation, possibly through microbial regulation of lysophosphatidylcholines. As consistently indicated by electronic tongue and muscle metabolomics analyses, SE significantly improved fish flavor, with increased umami and reduced bitterness. Network analysis and single-strain feeding further suggested that Methylorubrum populi, Gemmobacter aquatilis, and Rhodobacter sphaeroides contributed to flavor improvement by regulating host amino acid and nucleotide metabolism along the microbiome-gut-muscle axis. These findings highlight SE as a promising sustainable bioresource for aquaculture.},
}
RevDate: 2026-05-27
Beyond Suppression: The Plasticity, Dysfunction, and Therapeutic Reprogramming of Regulatory T Cells in Inflammatory Bowel Disease.
Journal of leukocyte biology pii:8696358 [Epub ahead of print].
Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory disorder of the gut, whose pathogenesis is closely related to immune dysregulation. Regulatory T cells (Tregs), as a key cell population maintaining intestinal immune tolerance, exhibit not only reduced frequency but, more critically, profound functional deficiencies, including the generation of pro-inflammatory ex-Tregs, and loss of lineage stability in the inflamed gut microenvironment of IBD. This review systematically delineates the sophisticated biological characteristics of Tregs, with a particular focus on the epigenetic and metabolic checkpoints that govern their stability. We critically summarize the aberrant changes of Tregs in IBD, emphasizing mechanisms such as inflammatory cytokine-induced Treg plasticity (e.g., Th1-like or Th17-like conversion) and microbiota-metabolite axis-mediated functional modulation. Furthermore, we provide an in-depth analysis of emerging therapeutic strategies aimed at restoring Treg suppressive capacity, including selective cytokine therapy (e.g., low-dose/engineered IL-2), adoptive transfer of engineered antigen-specific Tregs (including CAR-Tregs), microbiome/dietary interventions, and pharmacological modulation of Treg differentiation. We also discuss the disrupted crosstalk between Tregs and other innate and adaptive immune cells within the IBD milieu. Finally, this review highlights how cutting-edge technologies like single-cell multi-omics and spatial transcriptomics are delineating the heterogeneous landscape and uncovering novel, disease-specific Treg subpopulations, thereby paving the way for precise Treg-targeting therapies. Unlike previous reviews that broadly catalog Treg abnormalities, this review offers a refined conceptual framework centered on the critical distinction between lineage-defective ex-Tregs and exhausted effector Tregs (eTregs), and integrates recent multi-omics insights to redefine Treg functional failure in IBD.
Additional Links: PMID-42203202
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PubMed:
Citation:
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@article {pmid42203202,
year = {2026},
author = {Shao, Y and Yu, S and Zhang, M and Huang, Y and Dou, Z and Tian, B and Lu, J},
title = {Beyond Suppression: The Plasticity, Dysfunction, and Therapeutic Reprogramming of Regulatory T Cells in Inflammatory Bowel Disease.},
journal = {Journal of leukocyte biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jleuko/qiag067},
pmid = {42203202},
issn = {1938-3673},
abstract = {Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory disorder of the gut, whose pathogenesis is closely related to immune dysregulation. Regulatory T cells (Tregs), as a key cell population maintaining intestinal immune tolerance, exhibit not only reduced frequency but, more critically, profound functional deficiencies, including the generation of pro-inflammatory ex-Tregs, and loss of lineage stability in the inflamed gut microenvironment of IBD. This review systematically delineates the sophisticated biological characteristics of Tregs, with a particular focus on the epigenetic and metabolic checkpoints that govern their stability. We critically summarize the aberrant changes of Tregs in IBD, emphasizing mechanisms such as inflammatory cytokine-induced Treg plasticity (e.g., Th1-like or Th17-like conversion) and microbiota-metabolite axis-mediated functional modulation. Furthermore, we provide an in-depth analysis of emerging therapeutic strategies aimed at restoring Treg suppressive capacity, including selective cytokine therapy (e.g., low-dose/engineered IL-2), adoptive transfer of engineered antigen-specific Tregs (including CAR-Tregs), microbiome/dietary interventions, and pharmacological modulation of Treg differentiation. We also discuss the disrupted crosstalk between Tregs and other innate and adaptive immune cells within the IBD milieu. Finally, this review highlights how cutting-edge technologies like single-cell multi-omics and spatial transcriptomics are delineating the heterogeneous landscape and uncovering novel, disease-specific Treg subpopulations, thereby paving the way for precise Treg-targeting therapies. Unlike previous reviews that broadly catalog Treg abnormalities, this review offers a refined conceptual framework centered on the critical distinction between lineage-defective ex-Tregs and exhausted effector Tregs (eTregs), and integrates recent multi-omics insights to redefine Treg functional failure in IBD.},
}
RevDate: 2026-05-27
Profiling of the Guadalupe Fur Seal (Arctocephalus philippii townsendii) Fecal Bacteriome in Relation to Alopecic Syndrome.
Journal of wildlife diseases pii:eJWD-D-25-00154 [Epub ahead of print].
Alopecic syndrome in Guadalupe fur seals, Arctocephalus philippii townsendii (GFSs), was first observed a decade ago, coinciding with an anomalous warm sea surface temperature event and shifts in foraging behaviors of otariid pinnipeds from Mexican North Pacific colonies. With no evidence of dermatophytes or ectoparasites commonly associated with alopecia, it has been proposed that nutritional or metabolic changes, secondary to altered foraging, may increase the risk of alopecia. We employed 16S rRNA gene deep sequencing to investigate changes in the fecal bacteriome of GFS with and without alopecia. We found no significant differences in species richness nor Simpson's diversity index, and alopecia accounted for less than 6% of the variation in bacteriome structure. However, five bacterial phyla (Bacteroidota, Firmicutes, Fusobacteriota, Proteobacteria, and Spirochaetota) were overrepresented, and two (Actinobacteriota and Campylobacterota) were underrepresented, in GFSs with alopecia. At the genus level, animals with alopecia had a higher abundance of various bacteria, including Parabacteroides, Bacteroides, Lachnospiraceae, Roseburia, and genera within Erysipelotrichaceae, which have been linked to alopecia in humans. The GFS fecal bacteriome revealed 322 distinct bacterial functional pathways, of which 163 varied significantly between cases and controls. The most prominent differences found in GFSs with alopecia were overrepresentation of critical precursors for bacterial cell wall components, aromatic amino acid biosynthesis and pantothenate and CoA biosynthesis, and underrepresentation of glucosyltransferases and bacterial surface antigens, nitrogen and sulfur metabolism, and bacterial secretion systems. Our study provides preliminary evidence that changes in enteric microbiota may contribute to the pathogenesis of alopecia in GFSs via three main mechanisms: dysregulation of immune modulation and sustained inflammation, altered metabolism, and reduced redox balance and detoxification in the gut. While future studies need to explore these possibilities, our findings offer insight into the role of the microbiome in emerging pathologies of wildlife.
Additional Links: PMID-42203230
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PubMed:
Citation:
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@article {pmid42203230,
year = {2026},
author = {Acevedo-Whitehouse, K and Domínguez-Sánchez, CA and Nieves-Martínez, DP},
title = {Profiling of the Guadalupe Fur Seal (Arctocephalus philippii townsendii) Fecal Bacteriome in Relation to Alopecic Syndrome.},
journal = {Journal of wildlife diseases},
volume = {},
number = {},
pages = {},
doi = {10.7589/JWD-D-25-00154},
pmid = {42203230},
issn = {1943-3700},
abstract = {Alopecic syndrome in Guadalupe fur seals, Arctocephalus philippii townsendii (GFSs), was first observed a decade ago, coinciding with an anomalous warm sea surface temperature event and shifts in foraging behaviors of otariid pinnipeds from Mexican North Pacific colonies. With no evidence of dermatophytes or ectoparasites commonly associated with alopecia, it has been proposed that nutritional or metabolic changes, secondary to altered foraging, may increase the risk of alopecia. We employed 16S rRNA gene deep sequencing to investigate changes in the fecal bacteriome of GFS with and without alopecia. We found no significant differences in species richness nor Simpson's diversity index, and alopecia accounted for less than 6% of the variation in bacteriome structure. However, five bacterial phyla (Bacteroidota, Firmicutes, Fusobacteriota, Proteobacteria, and Spirochaetota) were overrepresented, and two (Actinobacteriota and Campylobacterota) were underrepresented, in GFSs with alopecia. At the genus level, animals with alopecia had a higher abundance of various bacteria, including Parabacteroides, Bacteroides, Lachnospiraceae, Roseburia, and genera within Erysipelotrichaceae, which have been linked to alopecia in humans. The GFS fecal bacteriome revealed 322 distinct bacterial functional pathways, of which 163 varied significantly between cases and controls. The most prominent differences found in GFSs with alopecia were overrepresentation of critical precursors for bacterial cell wall components, aromatic amino acid biosynthesis and pantothenate and CoA biosynthesis, and underrepresentation of glucosyltransferases and bacterial surface antigens, nitrogen and sulfur metabolism, and bacterial secretion systems. Our study provides preliminary evidence that changes in enteric microbiota may contribute to the pathogenesis of alopecia in GFSs via three main mechanisms: dysregulation of immune modulation and sustained inflammation, altered metabolism, and reduced redox balance and detoxification in the gut. While future studies need to explore these possibilities, our findings offer insight into the role of the microbiome in emerging pathologies of wildlife.},
}
RevDate: 2026-05-27
CmpDate: 2026-05-27
Unveiling the Anti-tumor Actions and Therapeutic Potential of Calcitriol in Colorectal Cancer.
Anticancer research, 46(6):2985-3004.
Calcitriol (1,25-dihydroxyvitamin D3), the active form of vitamin D, signals through the vitamin D receptor (VDR) and has been linked to colorectal cancer (CRC) risk and progression. This review summarizes current evidence on calcitriol/VDR actions relevant to CRC prevention and therapy. A structured literature search of PubMed, Scopus, and Web of Science was conducted through December 2025 for studies on calcitriol, VDR, and CRC, including mechanistic, preclinical, epidemiological, and clinical trial reports. Evidence was synthesized narratively with an emphasis on pathways connecting epithelial biology, inflammation, and the tumor microenvironment. Across model systems and patient studies, calcitriol/VDR signaling is associated with reduced proliferation, enhanced differentiation and apoptosis, and repression of oncogenic programs including Wnt/beta catenin and MYC-driven transcription. Calcitriol can also shape the tumor immune milieu by limiting pro-inflammatory signaling (for example, NF-κB, COX 2, IL-6 and IL-8), supporting epithelial tight junctions, and modulating the microbiome and bile acid metabolism, which together may enhance immune surveillance and reduce tumor-permissive inflammation. Evidence from supplementation trials is mixed, suggesting heterogeneity in baseline vitamin D status, tumor stage and VDR pathway context. Calcitriol engages convergent epithelial and immune mechanisms that plausibly limit CRC initiation and progression, but optimal patient selection and dosing strategies remain unresolved. Future trials integrating molecular biomarkers and VDR-responsive gene signatures are needed to define when vitamin D-based interventions can provide meaningful benefit in CRC.
Additional Links: PMID-42203331
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PubMed:
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@article {pmid42203331,
year = {2026},
author = {Rafique, A and Koh, YS},
title = {Unveiling the Anti-tumor Actions and Therapeutic Potential of Calcitriol in Colorectal Cancer.},
journal = {Anticancer research},
volume = {46},
number = {6},
pages = {2985-3004},
doi = {10.21873/anticanres.18175},
pmid = {42203331},
issn = {1791-7530},
mesh = {Humans ; *Calcitriol/therapeutic use/pharmacology ; *Colorectal Neoplasms/drug therapy/metabolism/pathology ; Receptors, Calcitriol/metabolism ; Animals ; Signal Transduction/drug effects ; Tumor Microenvironment/drug effects ; *Antineoplastic Agents/therapeutic use/pharmacology ; },
abstract = {Calcitriol (1,25-dihydroxyvitamin D3), the active form of vitamin D, signals through the vitamin D receptor (VDR) and has been linked to colorectal cancer (CRC) risk and progression. This review summarizes current evidence on calcitriol/VDR actions relevant to CRC prevention and therapy. A structured literature search of PubMed, Scopus, and Web of Science was conducted through December 2025 for studies on calcitriol, VDR, and CRC, including mechanistic, preclinical, epidemiological, and clinical trial reports. Evidence was synthesized narratively with an emphasis on pathways connecting epithelial biology, inflammation, and the tumor microenvironment. Across model systems and patient studies, calcitriol/VDR signaling is associated with reduced proliferation, enhanced differentiation and apoptosis, and repression of oncogenic programs including Wnt/beta catenin and MYC-driven transcription. Calcitriol can also shape the tumor immune milieu by limiting pro-inflammatory signaling (for example, NF-κB, COX 2, IL-6 and IL-8), supporting epithelial tight junctions, and modulating the microbiome and bile acid metabolism, which together may enhance immune surveillance and reduce tumor-permissive inflammation. Evidence from supplementation trials is mixed, suggesting heterogeneity in baseline vitamin D status, tumor stage and VDR pathway context. Calcitriol engages convergent epithelial and immune mechanisms that plausibly limit CRC initiation and progression, but optimal patient selection and dosing strategies remain unresolved. Future trials integrating molecular biomarkers and VDR-responsive gene signatures are needed to define when vitamin D-based interventions can provide meaningful benefit in CRC.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Calcitriol/therapeutic use/pharmacology
*Colorectal Neoplasms/drug therapy/metabolism/pathology
Receptors, Calcitriol/metabolism
Animals
Signal Transduction/drug effects
Tumor Microenvironment/drug effects
*Antineoplastic Agents/therapeutic use/pharmacology
RevDate: 2026-05-27
CmpDate: 2026-05-27
Parasite-associated microbiomes: An unseen microenvironment.
Advances in parasitology, 131:31-70.
Parasites harbor diverse microbial ecosystems that include not only bacteria but also archaea, fungi, viruses and microbial eukaryotes. These parasite-associated microbiomes, long overlooked, are now recognized as important determinants of parasite development, fitness, virulence and interactions with hosts across medical, veterinary, agricultural and ecological systems. However, current understanding of parasite-associated microbiomes remains fragmented, with most studies focusing on a narrow set of human parasites, relying heavily on bacterial surveys and rarely capturing the full multi-kingdom diversity of microbial partners. Important challenges include expanding research to encompass neglected parasite groups and their non-bacterial associates, establishing causal links between microbiome members and parasite phenotypes, and overcoming the technical barriers posed by low-biomass, host-contaminated and/or experimentally intractable systems. Progress will also depend on developing robust reference genomes and analytical tools that can resolve multi-kingdom communities and integrate parasite and symbiont biology. This chapter synthesizes current knowledge across helminths, protozoa, ectoparasites and plant-infecting parasites. We consider how microbiome manipulation may contribute to parasite control while recognizing the evolutionary and ecological complexities involved in altering host-parasite-microbiome interactions. Embracing an explicitly multi-kingdom, holobiont-focused perspective promises to illuminate fundamental aspects of parasitism. Such knowledge may contribute to new avenues for mitigating the impact of parasitic diseases on human and animal health, food security and ecosystems.
Additional Links: PMID-42203372
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PubMed:
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@article {pmid42203372,
year = {2026},
author = {McCann, P and Megaw, J and Gobert, GN},
title = {Parasite-associated microbiomes: An unseen microenvironment.},
journal = {Advances in parasitology},
volume = {131},
number = {},
pages = {31-70},
doi = {10.1016/bs.apar.2026.03.001},
pmid = {42203372},
issn = {2163-6079},
mesh = {Animals ; Humans ; *Microbiota ; *Host-Parasite Interactions ; *Parasites/microbiology/physiology ; Symbiosis ; },
abstract = {Parasites harbor diverse microbial ecosystems that include not only bacteria but also archaea, fungi, viruses and microbial eukaryotes. These parasite-associated microbiomes, long overlooked, are now recognized as important determinants of parasite development, fitness, virulence and interactions with hosts across medical, veterinary, agricultural and ecological systems. However, current understanding of parasite-associated microbiomes remains fragmented, with most studies focusing on a narrow set of human parasites, relying heavily on bacterial surveys and rarely capturing the full multi-kingdom diversity of microbial partners. Important challenges include expanding research to encompass neglected parasite groups and their non-bacterial associates, establishing causal links between microbiome members and parasite phenotypes, and overcoming the technical barriers posed by low-biomass, host-contaminated and/or experimentally intractable systems. Progress will also depend on developing robust reference genomes and analytical tools that can resolve multi-kingdom communities and integrate parasite and symbiont biology. This chapter synthesizes current knowledge across helminths, protozoa, ectoparasites and plant-infecting parasites. We consider how microbiome manipulation may contribute to parasite control while recognizing the evolutionary and ecological complexities involved in altering host-parasite-microbiome interactions. Embracing an explicitly multi-kingdom, holobiont-focused perspective promises to illuminate fundamental aspects of parasitism. Such knowledge may contribute to new avenues for mitigating the impact of parasitic diseases on human and animal health, food security and ecosystems.},
}
MeSH Terms:
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Animals
Humans
*Microbiota
*Host-Parasite Interactions
*Parasites/microbiology/physiology
Symbiosis
RevDate: 2026-05-27
CmpDate: 2026-05-27
The Role of the Respiratory Microbiome in Pneumonia.
Clinics in chest medicine, 47(2):199-213.
The lung microbiome field has matured into a promising area of translational research. Emerging evidence from the past decade, including studies of COVID pneumonia, indicates a role for respiratory microbiota in pneumonia pathogenesis. Here, the authors discuss areas of investigation that will be essential to refine an ecology-based conceptual framework of pneumonia pathogenesis, which will ultimately guide the development of microbiome-targeted diagnostics and therapeutics for pneumonia management.
Additional Links: PMID-42203413
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PubMed:
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@article {pmid42203413,
year = {2026},
author = {Baker, JM and Dickson, RP},
title = {The Role of the Respiratory Microbiome in Pneumonia.},
journal = {Clinics in chest medicine},
volume = {47},
number = {2},
pages = {199-213},
doi = {10.1016/j.ccm.2025.12.004},
pmid = {42203413},
issn = {1557-8216},
mesh = {Humans ; *Microbiota ; COVID-19 ; *Lung/microbiology ; SARS-CoV-2 ; *Pneumonia, Viral/microbiology ; Pandemics ; *Pneumonia/microbiology ; Betacoronavirus ; },
abstract = {The lung microbiome field has matured into a promising area of translational research. Emerging evidence from the past decade, including studies of COVID pneumonia, indicates a role for respiratory microbiota in pneumonia pathogenesis. Here, the authors discuss areas of investigation that will be essential to refine an ecology-based conceptual framework of pneumonia pathogenesis, which will ultimately guide the development of microbiome-targeted diagnostics and therapeutics for pneumonia management.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Microbiota
COVID-19
*Lung/microbiology
SARS-CoV-2
*Pneumonia, Viral/microbiology
Pandemics
*Pneumonia/microbiology
Betacoronavirus
RevDate: 2026-05-27
CmpDate: 2026-05-27
The Evolving Etiology of Hospital-Acquired and Ventilator-Associated Pneumonia.
Clinics in chest medicine, 47(2):321-329.
Nosocomial pneumonia (NP), including hospital-acquired and ventilator-associated pneumonia, remains a major threat to hospitalized patients. NP arises from aspiration of pathogens in the setting of alterations in the pulmonary microbiome and weakened host defenses. Pseudomonas aeruginosa and Staphylococcus aureus predominate, though there has been a rise in carbapenem-resistant gram negatives, complicating treatment and increasing mortality. Viral and fungal pathogens further contribute to the NP burden. Diagnostic challenges persist due to nonspecific clinical features, though multiplex polymerase chain reaction testing is improving pathogen identification. This article highlights emerging trends in NP epidemiology, antibiotic resistance, and novel diagnostics.
Additional Links: PMID-42203422
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PubMed:
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@article {pmid42203422,
year = {2026},
author = {Van Besien, RF and Vazquez Guillamet, MC},
title = {The Evolving Etiology of Hospital-Acquired and Ventilator-Associated Pneumonia.},
journal = {Clinics in chest medicine},
volume = {47},
number = {2},
pages = {321-329},
doi = {10.1016/j.ccm.2025.12.013},
pmid = {42203422},
issn = {1557-8216},
mesh = {Humans ; *Pneumonia, Ventilator-Associated/microbiology/epidemiology/etiology/diagnosis/drug therapy ; *Healthcare-Associated Pneumonia/microbiology/epidemiology/diagnosis/etiology/drug therapy ; *Cross Infection/microbiology/epidemiology ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Nosocomial pneumonia (NP), including hospital-acquired and ventilator-associated pneumonia, remains a major threat to hospitalized patients. NP arises from aspiration of pathogens in the setting of alterations in the pulmonary microbiome and weakened host defenses. Pseudomonas aeruginosa and Staphylococcus aureus predominate, though there has been a rise in carbapenem-resistant gram negatives, complicating treatment and increasing mortality. Viral and fungal pathogens further contribute to the NP burden. Diagnostic challenges persist due to nonspecific clinical features, though multiplex polymerase chain reaction testing is improving pathogen identification. This article highlights emerging trends in NP epidemiology, antibiotic resistance, and novel diagnostics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Pneumonia, Ventilator-Associated/microbiology/epidemiology/etiology/diagnosis/drug therapy
*Healthcare-Associated Pneumonia/microbiology/epidemiology/diagnosis/etiology/drug therapy
*Cross Infection/microbiology/epidemiology
Anti-Bacterial Agents/therapeutic use
RevDate: 2026-05-27
CmpDate: 2026-05-27
Non-antibiotic Treatments for Pneumonia: Host-Directed Therapies, Next-Steps and Future Directions.
Clinics in chest medicine, 47(2):383-397.
Pneumonia is one of the deadliest and most common infections worldwide. Traditional management has focused on pathogen-directed therapy with antimicrobial drugs. However, continued increase of antimicrobial resistance represents a growing health care crisis and heightens the urgency of shifting the treatment focus outside of the traditional paradigm. Adjunctive and host-directed therapies (HDT) target the response to infection by either enhancing the host immune response or mitigating immunopathology. They encompass a broad range of treatments, repurposed medications, and interventions that alter how the host responds to infections. This review summarizes adjunctive and HDTs for bacterial, tuberculous, fungal, and viral pneumonia.
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@article {pmid42203427,
year = {2026},
author = {Pantaleón García, J and Chung, CJ and Flowers, RC and Evans, SE and Wu, BG},
title = {Non-antibiotic Treatments for Pneumonia: Host-Directed Therapies, Next-Steps and Future Directions.},
journal = {Clinics in chest medicine},
volume = {47},
number = {2},
pages = {383-397},
doi = {10.1016/j.ccm.2025.12.018},
pmid = {42203427},
issn = {1557-8216},
mesh = {Humans ; *Host-Directed Therapy ; *Pneumonia/therapy/microbiology/drug therapy ; },
abstract = {Pneumonia is one of the deadliest and most common infections worldwide. Traditional management has focused on pathogen-directed therapy with antimicrobial drugs. However, continued increase of antimicrobial resistance represents a growing health care crisis and heightens the urgency of shifting the treatment focus outside of the traditional paradigm. Adjunctive and host-directed therapies (HDT) target the response to infection by either enhancing the host immune response or mitigating immunopathology. They encompass a broad range of treatments, repurposed medications, and interventions that alter how the host responds to infections. This review summarizes adjunctive and HDTs for bacterial, tuberculous, fungal, and viral pneumonia.},
}
MeSH Terms:
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Humans
*Host-Directed Therapy
*Pneumonia/therapy/microbiology/drug therapy
RevDate: 2026-05-27
Stage-Associated Subgingival Dysbiosis Across the Periodontal Disease Spectrum in a Thai Cohort.
Journal of clinical periodontology [Epub ahead of print].
AIMS: This cross-sectional study aimed to investigate the subgingival microbiota and predict functional profiles across the 2018 EFP/AAP periodontal disease spectrum in a Thai clinical cohort.
MATERIALS AND METHODS: Subgingival plaque from 100 participants (gingivitis, n = 30; Stage II-IV periodontitis, n = 70) was analysed by 16S rRNA gene sequencing with taxonomic assignment using the Human Oral Microbiome Database.
RESULTS: Peptostreptococcaceae-related taxa, Dialister pneumosintes, Shuttleworthia satelles, Prevotella sp. HMT-304, and Bacteroidetes [G-3] bacterium HMT-280 were recurrently identified across differential abundance and penalised regression analyses. Penalised regression models showed limited stage-discriminative performance (multinomial AUC 0.68-0.78), with gingivitis achieving the highest classification accuracy (63%) and Stage IV the lowest, consistent with overlapping microbial profiles across stages. Nonetheless, some stage-enriched taxa included Campylobacter species in Stage III and Porphyromonas gingivalis with Odoribacter bacterium HMT-516 in Stage IV. Stage-enriched taxa correlated with anaerobic fermentation pathways, while co-occurrence networks became less dense but broader across stages.
CONCLUSION: Stage-associated microbiome shifts were detectable using a gingivitis reference group, with a disease-associated core and accompanying anaerobic functional enrichment. The findings suggest that subgingival dysbiosis across periodontitis stages does not follow a simple linear trajectory and that clinical stage is not determined by microbiome composition alone.
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@article {pmid42203454,
year = {2026},
author = {Sawangpanyangkura, T and Suparan, K and Wechwithayakhlung, C and Kunasol, C and Chattipakorn, N and Chattipakorn, SC},
title = {Stage-Associated Subgingival Dysbiosis Across the Periodontal Disease Spectrum in a Thai Cohort.},
journal = {Journal of clinical periodontology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jcpe.70147},
pmid = {42203454},
issn = {1600-051X},
support = {N42A660301//National Research Council of Thailand/ ; N42A670125//National Research Council of Thailand/ ; N42A690147//National Research Council of Thailand/ ; //Chiang Mai University Excellent Center award/ ; JRCMU2566R_023//CMU Junior Research Fellowship Program/ ; },
abstract = {AIMS: This cross-sectional study aimed to investigate the subgingival microbiota and predict functional profiles across the 2018 EFP/AAP periodontal disease spectrum in a Thai clinical cohort.
MATERIALS AND METHODS: Subgingival plaque from 100 participants (gingivitis, n = 30; Stage II-IV periodontitis, n = 70) was analysed by 16S rRNA gene sequencing with taxonomic assignment using the Human Oral Microbiome Database.
RESULTS: Peptostreptococcaceae-related taxa, Dialister pneumosintes, Shuttleworthia satelles, Prevotella sp. HMT-304, and Bacteroidetes [G-3] bacterium HMT-280 were recurrently identified across differential abundance and penalised regression analyses. Penalised regression models showed limited stage-discriminative performance (multinomial AUC 0.68-0.78), with gingivitis achieving the highest classification accuracy (63%) and Stage IV the lowest, consistent with overlapping microbial profiles across stages. Nonetheless, some stage-enriched taxa included Campylobacter species in Stage III and Porphyromonas gingivalis with Odoribacter bacterium HMT-516 in Stage IV. Stage-enriched taxa correlated with anaerobic fermentation pathways, while co-occurrence networks became less dense but broader across stages.
CONCLUSION: Stage-associated microbiome shifts were detectable using a gingivitis reference group, with a disease-associated core and accompanying anaerobic functional enrichment. The findings suggest that subgingival dysbiosis across periodontitis stages does not follow a simple linear trajectory and that clinical stage is not determined by microbiome composition alone.},
}
RevDate: 2026-05-27
Gut microbial metabolites for potentiating cancer therapy.
Trends in cancer pii:S2405-8033(26)00080-4 [Epub ahead of print].
The gut microbiome exerts distant and local effects on tumours, healthy epithelial cells, and the immune system through the production of bioactive metabolites. This influences cancer therapy responses across treatment modalities and cancer types. In this review, we discuss promising approaches to boost beneficial microbiota-derived metabolites to enhance existing cancer therapies, including prebiotics, probiotics, postbiotics, and live biotherapeutic products. Each approach faces challenges in achieving physiological concentrations and tissue distribution, as well as different regulatory regimes and commercial landscapes. With promising early clinical trials and significant scientific and commercial activity in these areas, there is hope that targeted, metabolite-focused interventions will soon benefit cancer patients.
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@article {pmid42203551,
year = {2026},
author = {Kamrad, S and Gagliani, N and Lawley, TD and Patil, KR and Tintelnot, J},
title = {Gut microbial metabolites for potentiating cancer therapy.},
journal = {Trends in cancer},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.trecan.2026.04.005},
pmid = {42203551},
issn = {2405-8025},
abstract = {The gut microbiome exerts distant and local effects on tumours, healthy epithelial cells, and the immune system through the production of bioactive metabolites. This influences cancer therapy responses across treatment modalities and cancer types. In this review, we discuss promising approaches to boost beneficial microbiota-derived metabolites to enhance existing cancer therapies, including prebiotics, probiotics, postbiotics, and live biotherapeutic products. Each approach faces challenges in achieving physiological concentrations and tissue distribution, as well as different regulatory regimes and commercial landscapes. With promising early clinical trials and significant scientific and commercial activity in these areas, there is hope that targeted, metabolite-focused interventions will soon benefit cancer patients.},
}
RevDate: 2026-05-27
Dual human milk oligosaccharide-fibre utilisation is a selection cue for the weaning gut microbiome.
Nature communications pii:10.1038/s41467-026-73297-5 [Epub ahead of print].
Gut microbiome (GM) maturation in early life follows organised taxonomic successions, yet how the weaning diet impacts these trajectories remains underexplored. Here, we collected faecal samples at pre-, early and late weaning from seven mother-infant dyads forming the Milkome cohort, designed to evaluate the contribution of human milk oligosaccharides (HMOs) to GM maturation during weaning (NCT07026526). Surprisingly, all preweaning infant faecal consortia grew on multiple dietary fibres, consistent with the prevalence of fibre-degradation genes in their metagenomes. Utilisation of both HMOs and dietary fibres was discovered as a metabolic hallmark of the weaning GM, as supported by metagenomics and the growth of faecal consortia on HMOs, following their enrichment on fibres. The growth of a defined consortium on weaning-mimic substrates, further showed that distinct Clostridia simultaneously deploy HMO and fibre utilisation pathways, which confers competitive growth against HMO- or fibre-utilising bifidobacteria. Metagenomics, culturomics and HMO-utilisation profiles of 137 maternal isolates were concordant with retention of the HMO-utilisation capacity by the adult GM. Our findings highlight dual HMO-fibre utilisation as an unrecognised selection cue of core adult GM species during weaning, which outlines a plausible mechanism of GM maturation in early life and extends the importance of HMOs to the weaning transition.
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@article {pmid42203770,
year = {2026},
author = {So, Y and Pichler, MJ and Kappel, SS and Jin, C and Eriksen, C and Chatzigiannidou, I and Andersen, MHB and Tsiamis, V and Lukassen, MV and Skytthe, LE and Teneberg, S and Kristiansen, K and Brix, S and Aunsholt, L and Abou Hachem, M},
title = {Dual human milk oligosaccharide-fibre utilisation is a selection cue for the weaning gut microbiome.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-73297-5},
pmid = {42203770},
issn = {2041-1723},
support = {1026-00386B//Natur og Univers, Det Frie Forskningsråd (Natural Sciences, Danish Council for Independent Research)/ ; },
abstract = {Gut microbiome (GM) maturation in early life follows organised taxonomic successions, yet how the weaning diet impacts these trajectories remains underexplored. Here, we collected faecal samples at pre-, early and late weaning from seven mother-infant dyads forming the Milkome cohort, designed to evaluate the contribution of human milk oligosaccharides (HMOs) to GM maturation during weaning (NCT07026526). Surprisingly, all preweaning infant faecal consortia grew on multiple dietary fibres, consistent with the prevalence of fibre-degradation genes in their metagenomes. Utilisation of both HMOs and dietary fibres was discovered as a metabolic hallmark of the weaning GM, as supported by metagenomics and the growth of faecal consortia on HMOs, following their enrichment on fibres. The growth of a defined consortium on weaning-mimic substrates, further showed that distinct Clostridia simultaneously deploy HMO and fibre utilisation pathways, which confers competitive growth against HMO- or fibre-utilising bifidobacteria. Metagenomics, culturomics and HMO-utilisation profiles of 137 maternal isolates were concordant with retention of the HMO-utilisation capacity by the adult GM. Our findings highlight dual HMO-fibre utilisation as an unrecognised selection cue of core adult GM species during weaning, which outlines a plausible mechanism of GM maturation in early life and extends the importance of HMOs to the weaning transition.},
}
RevDate: 2026-05-27
Heritable gut microbiota decreases fat accumulation in pregnant sows and optimizes gestational outcomes.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-00998-6 [Epub ahead of print].
This study investigates the interplay between host genetics and gut microbiota in regulating fat deposition and reproductive outcomes in sows. Integrating multiomics data from 348 Yorkshire sows-including whole-genome sequencing, 16S rRNA sequencing, and metabolomic profiling-we identified 37 microbial taxa significantly associated with thick backfat (TBP) through microbiome-wide association studies (MWAS). Microbial genome-wide association analysis (mGWAS) revealed heritable genera, including Ezakiella and Corynebacterium, and implicated host genes such as MED17 and VSTM5 in microbial modulation. Concurrently, genome-wide association studies (GWAS) identified MC4R and MEDAG as candidate genes directly influencing TBP. Metabolomic analysis highlighted acetate, a short-chain fatty acid, as a key mediator in host adipogenesis. Functional validation in experimental models demonstrated that exogenous acetate supplementation alters lipid metabolism and enhances reproductive performance. These findings elucidate a mechanistic axis wherein host genetics shape gut microbial composition, which in turn modulates fat metabolism via acetate production, ultimately affecting pregnancy outcomes. This integrated approach provides insights into host-microbe co-regulation of metabolic traits and highlights potential targets for improving reproductive efficiency in livestock.
Additional Links: PMID-42203795
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Citation:
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@article {pmid42203795,
year = {2026},
author = {Wang, M and Zhang, L and Li, S and Cha, E and Guo, A and Sun, B and Li, X and Wu, S and Yu, T},
title = {Heritable gut microbiota decreases fat accumulation in pregnant sows and optimizes gestational outcomes.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00998-6},
pmid = {42203795},
issn = {2055-5008},
support = {HAAS2023RCOD01//the Research and Development of Key Technology for Precise and Efficient Breeding of Local Pigs in Hainan Province/ ; YSPTZX202304//Academician Workstation/ ; 2021YFD1301205//the Breeding and Promotion of New Varieties of Qinling Black Pigs/ ; 2022GD-TSLD-46//the Shaanxi Livestock and Poultry Breeding Double-chain Fusion Key Project/ ; 2023-YBNY-106//the Key Research and Development Plan of Shaanxi Province/ ; },
abstract = {This study investigates the interplay between host genetics and gut microbiota in regulating fat deposition and reproductive outcomes in sows. Integrating multiomics data from 348 Yorkshire sows-including whole-genome sequencing, 16S rRNA sequencing, and metabolomic profiling-we identified 37 microbial taxa significantly associated with thick backfat (TBP) through microbiome-wide association studies (MWAS). Microbial genome-wide association analysis (mGWAS) revealed heritable genera, including Ezakiella and Corynebacterium, and implicated host genes such as MED17 and VSTM5 in microbial modulation. Concurrently, genome-wide association studies (GWAS) identified MC4R and MEDAG as candidate genes directly influencing TBP. Metabolomic analysis highlighted acetate, a short-chain fatty acid, as a key mediator in host adipogenesis. Functional validation in experimental models demonstrated that exogenous acetate supplementation alters lipid metabolism and enhances reproductive performance. These findings elucidate a mechanistic axis wherein host genetics shape gut microbial composition, which in turn modulates fat metabolism via acetate production, ultimately affecting pregnancy outcomes. This integrated approach provides insights into host-microbe co-regulation of metabolic traits and highlights potential targets for improving reproductive efficiency in livestock.},
}
RevDate: 2026-05-27
CmpDate: 2026-05-27
Shotgun metagenomic mapping of saliva reveals insights into diversity and function of the oral microbiome in pregnancy.
Scientific reports, 16(1):.
The oral microbiome is a complex and dynamic microecosystem that fluctuates continually throughout the lifespan of a woman. Nevertheless, the function of the oral microbiome in reproductive health is not yet fully understood. Monitoring oral health and providing necessary dental care before and during pregnancy could help maintain a balanced oral microecology and support healthier microbial transfer to newborns. Here, we aimed to compare the salivary microbiome of pregnant and non-pregnant women using shotgun metagenomics to describe their taxonomic and functional composition and assess whether the resulting data is better explained by the reproductive stage. We conducted a comparative cross-sectional study involving pregnant women (n = 71; gestational age 37-42 weeks) and non-pregnant women (n = 143 with regular menstrual cycles; 3 saliva samples per participant across different menstrual phases). Shallow shotgun metagenomic sequencing was used to characterize both taxonomic and functional profiles of the oral microbiome. Socransky's color complex analysis was performed to assess group differences in key microbial complexes. Quantitative PCR was used to validate the abundance of selected oral bacteria. Participant data, including demographic, behavioral, clinical, and oral health variables (such as dentist visits), were collected and incorporated as covariates to adjust for potential confounding effects. Additionally, a sensitivity analysis was performed by excluding participants with identified behavioral or clinical risk factors. Ten phyla including Actinomycetota, Bacteroidota, Chloroflexota Bacillota, Fusobacteriota, Pseudomonadota, Spirochaetota, Synergistota Candidatus Saccharimonadota and Mycoplasmatota, 102 genera, and 410 species were identified. Pregnant women had lower saliva microbiome diversity, driven by reduced richness but unchanged evenness. The microbial composition varied between the groups, even after adjusting for confounding factors. Differential abundance analysis, adjusted for potential confounders, identified 25 species that significantly differed between groups (q < 0.05), with 13 taxa more than three-fold higher in pregnant women. Notably, red complex species were more abundant in pregnant women (p < 0.05). Functional pathway analysis identified 40 modules that differed by pregnancy status. These results further suggest a connection between pregnancy and changes to the oral microbiome in women. As many of these changes are in a pro-inflammatory direction, further research is warranted to assess its potential impact on pregnant women and their newborns.
Additional Links: PMID-42203854
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@article {pmid42203854,
year = {2026},
author = {Bostanci, N and Antony, AT and Silbereisen, A and Esmaili, T and Krog, MC and Sterpu, I and Bashir, Z and Engstrand, L and Wiberg-Itzel, E and Nielsen, HS and Hugerth, LW and Schuppe-Koistinen, I},
title = {Shotgun metagenomic mapping of saliva reveals insights into diversity and function of the oral microbiome in pregnancy.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42203854},
issn = {2045-2322},
mesh = {Humans ; Female ; Pregnancy ; *Saliva/microbiology ; *Microbiota/genetics ; *Metagenomics/methods ; Adult ; *Mouth/microbiology ; Shotgun Sequencing ; Cross-Sectional Studies ; Metagenome ; Bacteria/genetics/classification ; },
abstract = {The oral microbiome is a complex and dynamic microecosystem that fluctuates continually throughout the lifespan of a woman. Nevertheless, the function of the oral microbiome in reproductive health is not yet fully understood. Monitoring oral health and providing necessary dental care before and during pregnancy could help maintain a balanced oral microecology and support healthier microbial transfer to newborns. Here, we aimed to compare the salivary microbiome of pregnant and non-pregnant women using shotgun metagenomics to describe their taxonomic and functional composition and assess whether the resulting data is better explained by the reproductive stage. We conducted a comparative cross-sectional study involving pregnant women (n = 71; gestational age 37-42 weeks) and non-pregnant women (n = 143 with regular menstrual cycles; 3 saliva samples per participant across different menstrual phases). Shallow shotgun metagenomic sequencing was used to characterize both taxonomic and functional profiles of the oral microbiome. Socransky's color complex analysis was performed to assess group differences in key microbial complexes. Quantitative PCR was used to validate the abundance of selected oral bacteria. Participant data, including demographic, behavioral, clinical, and oral health variables (such as dentist visits), were collected and incorporated as covariates to adjust for potential confounding effects. Additionally, a sensitivity analysis was performed by excluding participants with identified behavioral or clinical risk factors. Ten phyla including Actinomycetota, Bacteroidota, Chloroflexota Bacillota, Fusobacteriota, Pseudomonadota, Spirochaetota, Synergistota Candidatus Saccharimonadota and Mycoplasmatota, 102 genera, and 410 species were identified. Pregnant women had lower saliva microbiome diversity, driven by reduced richness but unchanged evenness. The microbial composition varied between the groups, even after adjusting for confounding factors. Differential abundance analysis, adjusted for potential confounders, identified 25 species that significantly differed between groups (q < 0.05), with 13 taxa more than three-fold higher in pregnant women. Notably, red complex species were more abundant in pregnant women (p < 0.05). Functional pathway analysis identified 40 modules that differed by pregnancy status. These results further suggest a connection between pregnancy and changes to the oral microbiome in women. As many of these changes are in a pro-inflammatory direction, further research is warranted to assess its potential impact on pregnant women and their newborns.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
Pregnancy
*Saliva/microbiology
*Microbiota/genetics
*Metagenomics/methods
Adult
*Mouth/microbiology
Shotgun Sequencing
Cross-Sectional Studies
Metagenome
Bacteria/genetics/classification
RevDate: 2026-05-27
Gut microbiota alteration contributes to bone marrow mesenchymal stem cells connexin43 response to high-fat diet induced obesity in mice.
International journal of obesity (2005) [Epub ahead of print].
BACKGROUND/ OBJECTIVE: Bone marrow mesenchymal stem cells (BMSCs) contribute to controlling adipose tissue homeostasis and may be a potential target for obesity therapy. Since lack of connexin43(Cx43) in mesenchymal stem cells (MSCs) is known to combat high-fat diet (HFD)-induced adiposity. Also, HFD is a well-known risk factor for gut microbiota dysbiosis. Here we attempt to address the interaction between HFD, gut microbiota, and Cx43 deficiency in BMSCs during the development of obesity.
METHODS: BMSC-specific Cx43 knockout (Prrx1-Cre;Cx43[flox/flox](cKO)) and control littermate (Cx43[flox/flox](flox))mice were fed a regular chow diet or a HFD for 8 weeks. Cecal microbiome composition was assessed by 16S ribosomal RNA (rRNA) sequencing, and further analyzing correlation between gut microbiota and obesogenic parameters. Moreover, transplantation fecal microbiota was used to probe the salutary effect of BMSC Cx43.
RESULTS: HFD fed cKO mice notably altered cecal microbiome composition as proved by a distinctively clustered separation from flox mice. Concomitantly, Allobaculum induced by HFD was strongly correlated positively with body weight, glucose intolerance, and adipose mass. The recipients with gut microbiota from cKO mice displayed anti-obesity phenotype as the donors.
CONCLUSIONS: Gut microbiota alteration may be one main reason for the salutary effect of BMSC Cx43 knockout on body adiposity.
Additional Links: PMID-42203970
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@article {pmid42203970,
year = {2026},
author = {Ning, K and Chen, Y and Yang, X and Dou, X and Liu, S and Wang, DE and Niu, Y and Xu, H},
title = {Gut microbiota alteration contributes to bone marrow mesenchymal stem cells connexin43 response to high-fat diet induced obesity in mice.},
journal = {International journal of obesity (2005)},
volume = {},
number = {},
pages = {},
pmid = {42203970},
issn = {1476-5497},
abstract = {BACKGROUND/ OBJECTIVE: Bone marrow mesenchymal stem cells (BMSCs) contribute to controlling adipose tissue homeostasis and may be a potential target for obesity therapy. Since lack of connexin43(Cx43) in mesenchymal stem cells (MSCs) is known to combat high-fat diet (HFD)-induced adiposity. Also, HFD is a well-known risk factor for gut microbiota dysbiosis. Here we attempt to address the interaction between HFD, gut microbiota, and Cx43 deficiency in BMSCs during the development of obesity.
METHODS: BMSC-specific Cx43 knockout (Prrx1-Cre;Cx43[flox/flox](cKO)) and control littermate (Cx43[flox/flox](flox))mice were fed a regular chow diet or a HFD for 8 weeks. Cecal microbiome composition was assessed by 16S ribosomal RNA (rRNA) sequencing, and further analyzing correlation between gut microbiota and obesogenic parameters. Moreover, transplantation fecal microbiota was used to probe the salutary effect of BMSC Cx43.
RESULTS: HFD fed cKO mice notably altered cecal microbiome composition as proved by a distinctively clustered separation from flox mice. Concomitantly, Allobaculum induced by HFD was strongly correlated positively with body weight, glucose intolerance, and adipose mass. The recipients with gut microbiota from cKO mice displayed anti-obesity phenotype as the donors.
CONCLUSIONS: Gut microbiota alteration may be one main reason for the salutary effect of BMSC Cx43 knockout on body adiposity.},
}
RevDate: 2026-05-27
CmpDate: 2026-05-27
Intervening at the microbial crossroads: targeting inflammation across the oral-gut-reproductive microbiome crosstalk in atherosclerosis.
Antonie van Leeuwenhoek, 119(7):.
Despite the increasing burden of mortality due to cardiovascular disease, the traditional risk factors fail to explain the complexity of the pathology of cardiovascular disease, especially in the context of chronic inflammation. Emerging scientific evidence indicates that dysbiosis of the oral, gut, and reproductive microbiome is associated with systemic vascular dysfunction. This review comprehensively discusses the available scientific data on the interactions between the mucosal colonizing microbiota and their modulation of whole-body inflammation and cardiovascular disease pathogenesis. It underlines the roles of microbial metabolites, including trimethylamine N-oxide and lipopolysaccharides, in immune activation, epithelial barrier cell injury, and their effects in endothelial activation, vascular remodeling and dysfunction, oxidative stress, and inflammation. This review describes the mechanistic interplay that drives atherosclerosis and vascular dysfunction, mediated by immune activation and cytokine-driven inflammatory cascades. Sex hormones influence the composition of the microbiota and the host immune responses, thereby influencing vascular disease manifestations and responses to therapy. These mechanisms present the potential of intervening at the microbial crossroads through microbiome-targeted approaches as an effective treatment strategy for cardiovascular disease.
Additional Links: PMID-42203993
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@article {pmid42203993,
year = {2026},
author = {Saka, WA and Oyedokun, PA and Alade, TA and Oyeleke, BT and Oyelaran, AO and Oyedokun, MD and Irozuoke, CA and Olayemi, OM and Oladepo, S and Ndako, JA},
title = {Intervening at the microbial crossroads: targeting inflammation across the oral-gut-reproductive microbiome crosstalk in atherosclerosis.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {7},
pages = {},
pmid = {42203993},
issn = {1572-9699},
mesh = {Humans ; *Atherosclerosis/microbiology ; *Gastrointestinal Microbiome ; *Inflammation/microbiology ; Animals ; Dysbiosis/microbiology ; *Mouth/microbiology ; },
abstract = {Despite the increasing burden of mortality due to cardiovascular disease, the traditional risk factors fail to explain the complexity of the pathology of cardiovascular disease, especially in the context of chronic inflammation. Emerging scientific evidence indicates that dysbiosis of the oral, gut, and reproductive microbiome is associated with systemic vascular dysfunction. This review comprehensively discusses the available scientific data on the interactions between the mucosal colonizing microbiota and their modulation of whole-body inflammation and cardiovascular disease pathogenesis. It underlines the roles of microbial metabolites, including trimethylamine N-oxide and lipopolysaccharides, in immune activation, epithelial barrier cell injury, and their effects in endothelial activation, vascular remodeling and dysfunction, oxidative stress, and inflammation. This review describes the mechanistic interplay that drives atherosclerosis and vascular dysfunction, mediated by immune activation and cytokine-driven inflammatory cascades. Sex hormones influence the composition of the microbiota and the host immune responses, thereby influencing vascular disease manifestations and responses to therapy. These mechanisms present the potential of intervening at the microbial crossroads through microbiome-targeted approaches as an effective treatment strategy for cardiovascular disease.},
}
MeSH Terms:
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Humans
*Atherosclerosis/microbiology
*Gastrointestinal Microbiome
*Inflammation/microbiology
Animals
Dysbiosis/microbiology
*Mouth/microbiology
RevDate: 2026-05-27
Advocating for return-of-results to participants in microbiome research.
Nature microbiology [Epub ahead of print].
Additional Links: PMID-42204344
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Citation:
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@article {pmid42204344,
year = {2026},
author = {Olubayo, L and Hazelhurst, S},
title = {Advocating for return-of-results to participants in microbiome research.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42204344},
issn = {2058-5276},
support = {TW 012077//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; },
}
RevDate: 2026-05-28
MetaTree: an interactive web platform for aligned hierarchical data visualization and multi-group comparison.
BMC bioinformatics pii:10.1186/s12859-026-06475-3 [Epub ahead of print].
BACKGROUND: Hierarchical quantitative profiles are widely used in microbiome studies and other domains. However, comparing multiple samples and experimental groups while preserving hierarchical structure remains challenging. Many existing workflows require extensive manual figure assembly or do not support aligned comparisons across conditions on a shared hierarchy.
RESULTS: We developed MetaTree, an open-source platform that runs in a web browser for interactive visualization and comparative analysis of hierarchical quantitative data. MetaTree anchors samples, groups, and contrasts between groups to a shared reference hierarchy, preserving one-to-one node correspondence so that the same clade is compared in the same position across views. In addition to visualization, MetaTree integrates statistical testing for comparisons between two groups with false discovery rate (FDR) control, enabling users to identify clades with consistent differences between conditions and interpret them in hierarchical context. MetaTree also provides user configurable controls for visual encoding, filtering thresholds, label density, and layout, allowing figures to be adapted to different datasets and reporting needs. The interface remains usable for large hierarchies through interactive navigation, adaptive label handling, and branch collapsing.
CONCLUSIONS: MetaTree is an installation-free web platform (https://byemaxx.github.io/MetaTree) for topology-consistent visualization and comparison of hierarchical profiles, supporting coordinated multi-panel exploration and automated comparison matrices to enable rapid generation of publication-ready figures for microbiome and other hierarchical datasets.
Additional Links: PMID-42204477
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PubMed:
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@article {pmid42204477,
year = {2026},
author = {Wu, Q and Zhang, A and Ning, Z and Figeys, D},
title = {MetaTree: an interactive web platform for aligned hierarchical data visualization and multi-group comparison.},
journal = {BMC bioinformatics},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12859-026-06475-3},
pmid = {42204477},
issn = {1471-2105},
support = {RGPIN-03905-2018//Natural Sciences and Engineering Research Council of Canada/ ; },
abstract = {BACKGROUND: Hierarchical quantitative profiles are widely used in microbiome studies and other domains. However, comparing multiple samples and experimental groups while preserving hierarchical structure remains challenging. Many existing workflows require extensive manual figure assembly or do not support aligned comparisons across conditions on a shared hierarchy.
RESULTS: We developed MetaTree, an open-source platform that runs in a web browser for interactive visualization and comparative analysis of hierarchical quantitative data. MetaTree anchors samples, groups, and contrasts between groups to a shared reference hierarchy, preserving one-to-one node correspondence so that the same clade is compared in the same position across views. In addition to visualization, MetaTree integrates statistical testing for comparisons between two groups with false discovery rate (FDR) control, enabling users to identify clades with consistent differences between conditions and interpret them in hierarchical context. MetaTree also provides user configurable controls for visual encoding, filtering thresholds, label density, and layout, allowing figures to be adapted to different datasets and reporting needs. The interface remains usable for large hierarchies through interactive navigation, adaptive label handling, and branch collapsing.
CONCLUSIONS: MetaTree is an installation-free web platform (https://byemaxx.github.io/MetaTree) for topology-consistent visualization and comparison of hierarchical profiles, supporting coordinated multi-panel exploration and automated comparison matrices to enable rapid generation of publication-ready figures for microbiome and other hierarchical datasets.},
}
RevDate: 2026-05-28
The mycobiome, virome and archaeome in gastrointestinal cancers: molecular pathogenesis and therapeutic intervention.
Molecular cancer pii:10.1186/s12943-026-02698-3 [Epub ahead of print].
Gastrointestinal (GI) cancers remain a significant global health challenge. For decades, research has concentrated on the bacterial microbiome's role in tumour development, largely neglecting the important roles of the non-bacterial kingdoms, including mycobiome (fungi), the virome (viruses), and archaeome (archaea). These elements represent an underexplored and crucial "dark matter" of the microbiome. This review aims to systematically summarize current evidence on the compositional alterations of viruses, fungi, and archaea across the major types of GI cancer, including colorectal, hepatocellular, gastric, pancreatic and esophageal/oral cancers. We critically examine how viruses, fungi, and archaea directly affect host cellular processes and indirectly influence cancer risk through complex cross-kingdom interactions with the bacterial microbiota and the host immune system. Additionally, we explore the significant translational potential of this knowledge, emphasizing opportunities to use these non-bacterial communities in developing new diagnostic biomarkers and therapeutic strategies. Finally, we highlight the importance of future multi-kingdom integrative analyses to fully understand the microbial ecosystem involved in GI oncogenesis and to translate these insights into clinical practice.
Additional Links: PMID-42204538
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PubMed:
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@article {pmid42204538,
year = {2026},
author = {Cheng, CH and Wong, CC},
title = {The mycobiome, virome and archaeome in gastrointestinal cancers: molecular pathogenesis and therapeutic intervention.},
journal = {Molecular cancer},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12943-026-02698-3},
pmid = {42204538},
issn = {1476-4598},
support = {2023ZD0501400; 2023ZD0500200//Noncommunicable Chronic Diseases-National Science and Technology Major Project/ ; 14101725; 14107924; 14101322//Research Grants Council-General Research Fund/ ; C4008-23WF, C4042-24GF//RGC-Collaborative Research Fund/ ; },
abstract = {Gastrointestinal (GI) cancers remain a significant global health challenge. For decades, research has concentrated on the bacterial microbiome's role in tumour development, largely neglecting the important roles of the non-bacterial kingdoms, including mycobiome (fungi), the virome (viruses), and archaeome (archaea). These elements represent an underexplored and crucial "dark matter" of the microbiome. This review aims to systematically summarize current evidence on the compositional alterations of viruses, fungi, and archaea across the major types of GI cancer, including colorectal, hepatocellular, gastric, pancreatic and esophageal/oral cancers. We critically examine how viruses, fungi, and archaea directly affect host cellular processes and indirectly influence cancer risk through complex cross-kingdom interactions with the bacterial microbiota and the host immune system. Additionally, we explore the significant translational potential of this knowledge, emphasizing opportunities to use these non-bacterial communities in developing new diagnostic biomarkers and therapeutic strategies. Finally, we highlight the importance of future multi-kingdom integrative analyses to fully understand the microbial ecosystem involved in GI oncogenesis and to translate these insights into clinical practice.},
}
RevDate: 2026-05-28
Role of gut microbiota in cancer modulation: molecular mechanisms and emerging therapeutic strategies.
Infectious agents and cancer pii:10.1186/s13027-026-00767-2 [Epub ahead of print].
The gut microbiota exerts profound effects on host physiology, immunity, and disease susceptibility, with growing evidence implicating its role in cancer initiation, progression, and therapy response. Dysbiosis and microbial-derived metabolites contribute to oncogenesis by modulating epithelial signalling, immune regulation, and systemic inflammation. This review synthesises current knowledge on the crosstalk between the gut microbiome and cancer, spanning molecular mechanisms, site-specific malignancies, and treatment outcomes. We discuss how microbial pathways, including NF-κB, STAT3, Wnt/β-catenin, and inflammasome activation, shape tumour biology, and how microbiota profiles correlate with cancer risk and progression in colorectal, gastric, liver, breast, gynaecological, and pulmonary cancers. Furthermore, we highlight the microbiome's impact on responses to chemotherapy, radiotherapy, and immunotherapy. Finally, we evaluate therapeutic strategies targeting the microbiota, from conventional dietary and probiotic interventions to cutting-edge approaches such as faecal microbiota transplantation, engineered bacterial strains, and microbiome-based biomarkers. Understanding these complex interactions offers novel opportunities to integrate microbiome science into precision oncology.
Additional Links: PMID-42204557
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PubMed:
Citation:
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@article {pmid42204557,
year = {2026},
author = {Preetam, S and Bora, J and Porna Dutta, S and Talukdar, N and Rustagi, S and Thapliyal, S and Malik, S and Choudhary, N and Kumar, D and Kondaveeti, SB},
title = {Role of gut microbiota in cancer modulation: molecular mechanisms and emerging therapeutic strategies.},
journal = {Infectious agents and cancer},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13027-026-00767-2},
pmid = {42204557},
issn = {1750-9378},
abstract = {The gut microbiota exerts profound effects on host physiology, immunity, and disease susceptibility, with growing evidence implicating its role in cancer initiation, progression, and therapy response. Dysbiosis and microbial-derived metabolites contribute to oncogenesis by modulating epithelial signalling, immune regulation, and systemic inflammation. This review synthesises current knowledge on the crosstalk between the gut microbiome and cancer, spanning molecular mechanisms, site-specific malignancies, and treatment outcomes. We discuss how microbial pathways, including NF-κB, STAT3, Wnt/β-catenin, and inflammasome activation, shape tumour biology, and how microbiota profiles correlate with cancer risk and progression in colorectal, gastric, liver, breast, gynaecological, and pulmonary cancers. Furthermore, we highlight the microbiome's impact on responses to chemotherapy, radiotherapy, and immunotherapy. Finally, we evaluate therapeutic strategies targeting the microbiota, from conventional dietary and probiotic interventions to cutting-edge approaches such as faecal microbiota transplantation, engineered bacterial strains, and microbiome-based biomarkers. Understanding these complex interactions offers novel opportunities to integrate microbiome science into precision oncology.},
}
RevDate: 2026-05-28
The formation and function of tertiary lymphoid structures.
Biomarker research pii:10.1186/s40364-026-00939-7 [Epub ahead of print].
Tertiary lymphoid structures (TLSs) are immune cell aggregates that emerge in nonlymphoid tissues during various disease states, including chronic inflammation, autoimmunity, and cancer. TLSs are structurally and functionally analogous to secondary lymphoid organs, and exhibit a maturation continuum (progressing from initial aggregation to mature structures with germinal centers). TLS formation is synergistically regulated by local chemokine networks (e.g. CXCL13, CCL19, and CCL21), lymphotoxin signaling axes, stromal cells, metabolic reprogramming, and the microbiome. This review comprehensively elucidates the biological foundations of TLSs, including their cellular composition, spatial architecture, and developmental dynamics of maturation. We explore the crucial roles of TLSs as favorable prognostic factors and predictors of the immunotherapy response in various solid tumors, including melanoma, breast cancer, lung cancer, hepatocellular carcinoma, and colorectal cancer. Additionally, we analyze their "pathogenic" role in causing tissue damage and disease progression in autoimmune disorders such as rheumatoid arthritis and Sjögren's syndrome, as well as chronic inflammatory diseases such as COPD, IgA nephropathy, and atherosclerosis. In addition, we thoroughly examine TLS research methodologies, covering a wide range of approaches from conventional hematoxylin and eosin (H&E) and immunohistochemical staining to advanced multiplex fluorescence staining, imaging mass spectrometry, and spatial transcriptomic techniques. We summarize multiple gene expression signatures (e.g. the 12-chemokine signature and TLS score) for TLS identification and quantification. Finally, we highlight multiple strategies for artificially inducing TLS formation, including cytokine delivery, immunotherapy, engineered scaffolds, microbiome modulation, and organoid technologies, designed to enhance antitumor immunity or reverse immunopathology. This review provides a comprehensive framework for understanding the complex functions of TLSs in human disease and explores their clinical translation potential as biomarkers and therapeutic targets.
Additional Links: PMID-42204605
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PubMed:
Citation:
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@article {pmid42204605,
year = {2026},
author = {Zhang, C and Lv, P and Hou, Y and Yao, Z and Jiang, S and Chen, K and Liu, Z and Liu, L},
title = {The formation and function of tertiary lymphoid structures.},
journal = {Biomarker research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40364-026-00939-7},
pmid = {42204605},
issn = {2050-7771},
abstract = {Tertiary lymphoid structures (TLSs) are immune cell aggregates that emerge in nonlymphoid tissues during various disease states, including chronic inflammation, autoimmunity, and cancer. TLSs are structurally and functionally analogous to secondary lymphoid organs, and exhibit a maturation continuum (progressing from initial aggregation to mature structures with germinal centers). TLS formation is synergistically regulated by local chemokine networks (e.g. CXCL13, CCL19, and CCL21), lymphotoxin signaling axes, stromal cells, metabolic reprogramming, and the microbiome. This review comprehensively elucidates the biological foundations of TLSs, including their cellular composition, spatial architecture, and developmental dynamics of maturation. We explore the crucial roles of TLSs as favorable prognostic factors and predictors of the immunotherapy response in various solid tumors, including melanoma, breast cancer, lung cancer, hepatocellular carcinoma, and colorectal cancer. Additionally, we analyze their "pathogenic" role in causing tissue damage and disease progression in autoimmune disorders such as rheumatoid arthritis and Sjögren's syndrome, as well as chronic inflammatory diseases such as COPD, IgA nephropathy, and atherosclerosis. In addition, we thoroughly examine TLS research methodologies, covering a wide range of approaches from conventional hematoxylin and eosin (H&E) and immunohistochemical staining to advanced multiplex fluorescence staining, imaging mass spectrometry, and spatial transcriptomic techniques. We summarize multiple gene expression signatures (e.g. the 12-chemokine signature and TLS score) for TLS identification and quantification. Finally, we highlight multiple strategies for artificially inducing TLS formation, including cytokine delivery, immunotherapy, engineered scaffolds, microbiome modulation, and organoid technologies, designed to enhance antitumor immunity or reverse immunopathology. This review provides a comprehensive framework for understanding the complex functions of TLSs in human disease and explores their clinical translation potential as biomarkers and therapeutic targets.},
}
RevDate: 2026-05-28
Insights into the microbiota profile of Pediculus humanus capitis using metagenomic next-generation sequencing and molecular detection of unexpected pathogen DNA in Hunan Province, China.
Parasites & vectors pii:10.1186/s13071-026-07471-5 [Epub ahead of print].
BACKGROUND: The head louse, Pediculus humanus capitis, remains a significant public health concern affecting millions of people worldwide and has been implicated as a potential vector for multiple human pathogens. Characterization of the microbiota of head lice could improve our understanding of their public health significance and potential role in pathogen transmission. Here, we characterize the microbiota of head lice and investigate microbiota differences among different clades of head lice.
METHODS: Head lice were collected from Hunan Province, China, and classified into clade A and clade B (CACB) using polymerase chain reaction (PCR)-based genotyping. The microbiota of pooled CACB of head lice samples (n = 46) was investigated by metagenomic shotgun sequencing and comparatively analysed at the phylum, genus, and species levels. In addition, the prevalence of potential pathogen DNA in head lice samples (n = 204) was assessed using real-time PCR with stringent negative controls.
RESULTS: We obtained non-redundant CACB microbial gene catalog comprising 79,232 genes, of which 4.70% (3,722 genes) were taxonomically assigned. The relative abundance of bacteria (2.52%) was higher than that of eukaryotes (2.04%), viruses (0.11%), and archaea (0.02%). Comparative analysis identified 655 and 750 unique genes in CACB, respectively. The dominant phyla in the CACB of head lice were Proteobacteria. At the genus level, DNA sequences corresponding to Anaplasma (25.98%; 53/204), Mycobacterium (24.02%; 49/204), Chlamydia (23.53%; 48/204), Ehrlichia (10.29%; 21/204), and Vibrio (0.49%; 1/204) were detected, suggesting the presence of bacterial DNA from these taxa.
CONCLUSIONS: Our results provide a preliminary characterization of the annotated fraction of the CACB microbiome in head lice. The high proportion of unannotated genes (>95%) underscores the limited representation of louse-associated microbial genomes in public databases and suggests substantial, yet unexplored, microbial diversity. The detection of pathogen DNA does not confirm organism viability or vector competence,however it may suggest prior exposure, mechanical carriage, or residual DNA from blood meals. These exploratory findings contribute new insights into the microbiota associated with human lice.
Additional Links: PMID-42204631
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PubMed:
Citation:
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@article {pmid42204631,
year = {2026},
author = {Fu, YT and Deng, YP and Duan, DY and Peng, YY and Liu, YL and Zhang, Y and Xu, ZK and Elsheikha, HM and Liu, GH},
title = {Insights into the microbiota profile of Pediculus humanus capitis using metagenomic next-generation sequencing and molecular detection of unexpected pathogen DNA in Hunan Province, China.},
journal = {Parasites & vectors},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13071-026-07471-5},
pmid = {42204631},
issn = {1756-3305},
support = {2024JJ6548//the Hunan Natural Science Foundation Youth Fund Project/ ; 32473057//the National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: The head louse, Pediculus humanus capitis, remains a significant public health concern affecting millions of people worldwide and has been implicated as a potential vector for multiple human pathogens. Characterization of the microbiota of head lice could improve our understanding of their public health significance and potential role in pathogen transmission. Here, we characterize the microbiota of head lice and investigate microbiota differences among different clades of head lice.
METHODS: Head lice were collected from Hunan Province, China, and classified into clade A and clade B (CACB) using polymerase chain reaction (PCR)-based genotyping. The microbiota of pooled CACB of head lice samples (n = 46) was investigated by metagenomic shotgun sequencing and comparatively analysed at the phylum, genus, and species levels. In addition, the prevalence of potential pathogen DNA in head lice samples (n = 204) was assessed using real-time PCR with stringent negative controls.
RESULTS: We obtained non-redundant CACB microbial gene catalog comprising 79,232 genes, of which 4.70% (3,722 genes) were taxonomically assigned. The relative abundance of bacteria (2.52%) was higher than that of eukaryotes (2.04%), viruses (0.11%), and archaea (0.02%). Comparative analysis identified 655 and 750 unique genes in CACB, respectively. The dominant phyla in the CACB of head lice were Proteobacteria. At the genus level, DNA sequences corresponding to Anaplasma (25.98%; 53/204), Mycobacterium (24.02%; 49/204), Chlamydia (23.53%; 48/204), Ehrlichia (10.29%; 21/204), and Vibrio (0.49%; 1/204) were detected, suggesting the presence of bacterial DNA from these taxa.
CONCLUSIONS: Our results provide a preliminary characterization of the annotated fraction of the CACB microbiome in head lice. The high proportion of unannotated genes (>95%) underscores the limited representation of louse-associated microbial genomes in public databases and suggests substantial, yet unexplored, microbial diversity. The detection of pathogen DNA does not confirm organism viability or vector competence,however it may suggest prior exposure, mechanical carriage, or residual DNA from blood meals. These exploratory findings contribute new insights into the microbiota associated with human lice.},
}
RevDate: 2026-05-28
Decoding the microbiome-immune crosstalk in cancer: from mechanisms to therapeutic translation.
Biomarker research pii:10.1186/s40364-026-00930-2 [Epub ahead of print].
The gut microbiome plays a critical role in shaping host immunity and profoundly affects the efficacy of cancer immunotherapy. Accumulating evidence suggests that interventions designed to alter the microbial community, including fecal microbiota transplantation, probiotics, and engineered bacteria, can reprogram the tumor-immune microenvironment and enhance clinical efficacy. This Review provides a comprehensive overview of the molecular and cellular mechanisms through which the gut microbiota influences antitumor immunity, and it highlights recent clinical studies evaluating these interventions. We further examine inherent challenges, including inter-individual variability in microbial composition, difficulties in achieving stable and durable colonization, technical barriers in delivery, and potential safety concerns associated with immune activation or off-target effects. Finally, we discuss future directions for translating microbiome-targeted therapies into oncology, emphasizing the need for mechanistic insight, standardized protocols, rigorous evaluation, and integration with precision immunotherapy strategies to optimize therapeutic outcomes.
Additional Links: PMID-42204645
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PubMed:
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@article {pmid42204645,
year = {2026},
author = {Zhao, N and Wu, L and Peng, S and Yang, H and Song, Y and Zhang, Y and Ding, L},
title = {Decoding the microbiome-immune crosstalk in cancer: from mechanisms to therapeutic translation.},
journal = {Biomarker research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40364-026-00930-2},
pmid = {42204645},
issn = {2050-7771},
support = {82303235//National Natural Science Foundation of China/ ; 2025SF-YBXM-358//Key Research and Development Projects of Shaanxi Province/ ; 2025JC-YBQN-1236//Natural Science Basic Research Program of Shaanxi Province/ ; NUHSRO/2023/005/Startup/3//NUS STARTUP grant/ ; MOH-OFIRG24jan-0001, MOH-OFIRG23jul-0007 and MOH-OFIRG21nov-0007//NUS-NJU Research Collaboration Fund 2025, OF-IRG grant from National Medical Research Council/ ; NRF, CRP28-2022RS-0001//CRP grant from National Research Foundation/ ; },
abstract = {The gut microbiome plays a critical role in shaping host immunity and profoundly affects the efficacy of cancer immunotherapy. Accumulating evidence suggests that interventions designed to alter the microbial community, including fecal microbiota transplantation, probiotics, and engineered bacteria, can reprogram the tumor-immune microenvironment and enhance clinical efficacy. This Review provides a comprehensive overview of the molecular and cellular mechanisms through which the gut microbiota influences antitumor immunity, and it highlights recent clinical studies evaluating these interventions. We further examine inherent challenges, including inter-individual variability in microbial composition, difficulties in achieving stable and durable colonization, technical barriers in delivery, and potential safety concerns associated with immune activation or off-target effects. Finally, we discuss future directions for translating microbiome-targeted therapies into oncology, emphasizing the need for mechanistic insight, standardized protocols, rigorous evaluation, and integration with precision immunotherapy strategies to optimize therapeutic outcomes.},
}
RevDate: 2026-05-28
Plant immune dysregulation disrupts microbe-induced growth promotion and microbiome compatibility.
Plant communications pii:S2590-3462(26)00235-X [Epub ahead of print].
Plants associate with diverse microbial communities that influence growth and health. Although the plant immune regulatory network balances defense activation and microbial accommodation during pathogen attack, how it coordinates beneficial plant-microbe interactions across complex microbial contexts remains unclear. Here, we performed a systematic screen of 39 immune-pathway mutants using individual plant growth-promoting bacteria (PGPBs), binary combinations, synthetic and natural communities. We identified the bik1-1 mutant as exhibiting a broad defect in growth promotion across multiple beneficial microbial systems. Extensive genetic analyses using independent BIK1 CRISPR and T-DNA insertion alleles, as well as overexpression lines, demonstrated that the growth promotion defect observed in the bik1-1 line is not caused by loss of BIK1 function but instead correlates with a chromosomal fragment duplication. Although ISR and beneficial bacteria-mediated pathogen protection remain intact in bik1-1, immune activation is elevated during beneficial interactions. Microbiome profiling revealed reduced diversity and altered community structure, and microbiome transfer experiments indicate that host immune status influences the selection of microbial taxa associated with growth promotion. These findings indicate that immune signaling balance is a key determinant of plant-microbiome compatibility across diverse microbial contexts.
Additional Links: PMID-42204817
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PubMed:
Citation:
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@article {pmid42204817,
year = {2026},
author = {Han, B and Rawat, A and Parween, S and Alzayed, W and Zhang, H and Alkhateeb, RS and Schmidt, T and Wu, Y and Rodriguez, CP and Saad, MM and Hirt, H},
title = {Plant immune dysregulation disrupts microbe-induced growth promotion and microbiome compatibility.},
journal = {Plant communications},
volume = {},
number = {},
pages = {101927},
doi = {10.1016/j.xplc.2026.101927},
pmid = {42204817},
issn = {2590-3462},
abstract = {Plants associate with diverse microbial communities that influence growth and health. Although the plant immune regulatory network balances defense activation and microbial accommodation during pathogen attack, how it coordinates beneficial plant-microbe interactions across complex microbial contexts remains unclear. Here, we performed a systematic screen of 39 immune-pathway mutants using individual plant growth-promoting bacteria (PGPBs), binary combinations, synthetic and natural communities. We identified the bik1-1 mutant as exhibiting a broad defect in growth promotion across multiple beneficial microbial systems. Extensive genetic analyses using independent BIK1 CRISPR and T-DNA insertion alleles, as well as overexpression lines, demonstrated that the growth promotion defect observed in the bik1-1 line is not caused by loss of BIK1 function but instead correlates with a chromosomal fragment duplication. Although ISR and beneficial bacteria-mediated pathogen protection remain intact in bik1-1, immune activation is elevated during beneficial interactions. Microbiome profiling revealed reduced diversity and altered community structure, and microbiome transfer experiments indicate that host immune status influences the selection of microbial taxa associated with growth promotion. These findings indicate that immune signaling balance is a key determinant of plant-microbiome compatibility across diverse microbial contexts.},
}
RevDate: 2026-05-28
Microbiota-derived indole derivatives as anticancer agents: mechanistic insights and major perspectives.
Future microbiology [Epub ahead of print].
Cancer remains a major global health challenge, and emerging research highlights the role of the gut microbiota in cancer development. This complex microbial community supports digestion, immunity, and even mental well-being, adapting to lifestyle factors like diet and exercise. One key function is the breakdown of tryptophan (Trp) into indole. Studies have linked these compounds to cancer, inflammatory conditions, and brain disorders. This review compiles evidence showing that indole derivatives produced by gut bacteria could serve as potential anticancer agents by targeting specific biochemical pathways. Mechanistically, these metabolites inhibit IDO1, lower kynurenine levels, decrease regulatory T cells, and increase CD8+ T cell responses. They also activate tumor-suppressive signaling pathways such as the aryl hydrocarbon receptor (AhR), pregnane X receptor (PXR), and nuclear factor erythroid 2-related factor 2 (NRF2), while regulating reactive oxygen species (ROS). In addition, some indole derivatives trigger interleukin-12 (IL-12)-mediated T cell activation, leading to metabolic stress in cancer cells by downregulating UHRF1 and activating AMP-activated protein kinase (AMPK), thereby depleting ATP and causing cell death. Relevant literature was identified from PubMed, Google Scholar, and Scopus up to January 2026. Collectively, understanding this link could support development of personalized diets and microbiota-based cancer therapies.
Additional Links: PMID-42204951
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PubMed:
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@article {pmid42204951,
year = {2026},
author = {Tomar, K and Khodlan, P and Malik, T and Rana, P and Tariq, M and Mishra, R and Mohan, A and Fatima, S and Gautam, H and Kumar, S and Abdin, MZ and Kumar, A},
title = {Microbiota-derived indole derivatives as anticancer agents: mechanistic insights and major perspectives.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-10},
doi = {10.1080/17460913.2026.2677452},
pmid = {42204951},
issn = {1746-0921},
abstract = {Cancer remains a major global health challenge, and emerging research highlights the role of the gut microbiota in cancer development. This complex microbial community supports digestion, immunity, and even mental well-being, adapting to lifestyle factors like diet and exercise. One key function is the breakdown of tryptophan (Trp) into indole. Studies have linked these compounds to cancer, inflammatory conditions, and brain disorders. This review compiles evidence showing that indole derivatives produced by gut bacteria could serve as potential anticancer agents by targeting specific biochemical pathways. Mechanistically, these metabolites inhibit IDO1, lower kynurenine levels, decrease regulatory T cells, and increase CD8+ T cell responses. They also activate tumor-suppressive signaling pathways such as the aryl hydrocarbon receptor (AhR), pregnane X receptor (PXR), and nuclear factor erythroid 2-related factor 2 (NRF2), while regulating reactive oxygen species (ROS). In addition, some indole derivatives trigger interleukin-12 (IL-12)-mediated T cell activation, leading to metabolic stress in cancer cells by downregulating UHRF1 and activating AMP-activated protein kinase (AMPK), thereby depleting ATP and causing cell death. Relevant literature was identified from PubMed, Google Scholar, and Scopus up to January 2026. Collectively, understanding this link could support development of personalized diets and microbiota-based cancer therapies.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Microbial Diversity in Airport Terminal Environments and Potential Aerosol Transmission Risks.
Biomedical and environmental sciences : BES, 39(5):512-528.
OBJECTIVE: To characterize the distribution of bacterial and fungal pathogens in airport terminal environments, compare airborne aerosol sampling methods, identify high-abundance pathogenic species based on the WHO priority pathogens list, and provide a scientific basis for optimizing microbiological monitoring and control measures.
METHODS: Sampling was conducted in the transit transfer area (A1), domestic arrivals area (A2), and domestic departures area (A3). Airborne aerosols were collected using cyclonic and filtration samplers, and surface samples were collected using sterile swabs. DNA analysis was performed using 2bRAD sequencing for microbiome profiling (2bRAD-M). Microbial community diversity and compositional differences were assessed using α-diversity indices (Chao1, Shannon, and Simpson) and β-diversity metrics.
RESULTS: Bacteria dominated the indoor air microbiota of the airport terminal (98.4%), with Pseudomonadota (39.4%-62.9%) and Actinomycetota (18.9%-32.9%) as the predominant phyla. Microbial diversity was significantly higher in surface samples than in airborne aerosols. High-frequency contact surfaces (e.g., handrails) were enriched with human commensal bacteria, including Cutibacterium acnes (9.71%-19.4%). Multiple WHO-prioritized pathogens were detected, including Acinetobacter baumannii (0.3%-1.4%) and Pseudomonas aeruginosa (0.01%-1.24%). The transit transfer area (A1), characterized by poorer ventilation, showed higher microbial richness. Filtration samplers captured more microorganisms per unit volume than cyclonic samplers, with significant differences in detection profiles.
CONCLUSION: Sampling methods, sample types, and environmental conditions influence microbial distribution patterns across terminals. Detection of WHO Critical and High priority pathogens indicates potential risks of aerosol and contact transmission. Enhanced ventilation and disinfection of high-frequency contact surfaces can mitigate public health risks.
GRAPHICAL ABSTRACT: available in www.besjournal.com.
Additional Links: PMID-42205017
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PubMed:
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@article {pmid42205017,
year = {2026},
author = {Zhang, ZN and Wang, Q and Dong, XY and Li, X and Lu, B and Xu, DQ},
title = {Microbial Diversity in Airport Terminal Environments and Potential Aerosol Transmission Risks.},
journal = {Biomedical and environmental sciences : BES},
volume = {39},
number = {5},
pages = {512-528},
doi = {10.3967/bes2026.018},
pmid = {42205017},
issn = {2214-0190},
mesh = {Aerosols/analysis ; *Air Microbiology ; *Bacteria/isolation & purification/classification ; *Airports ; Environmental Monitoring ; Humans ; *Fungi/isolation & purification/classification ; *Microbiota ; *Air Pollution, Indoor/analysis ; },
abstract = {OBJECTIVE: To characterize the distribution of bacterial and fungal pathogens in airport terminal environments, compare airborne aerosol sampling methods, identify high-abundance pathogenic species based on the WHO priority pathogens list, and provide a scientific basis for optimizing microbiological monitoring and control measures.
METHODS: Sampling was conducted in the transit transfer area (A1), domestic arrivals area (A2), and domestic departures area (A3). Airborne aerosols were collected using cyclonic and filtration samplers, and surface samples were collected using sterile swabs. DNA analysis was performed using 2bRAD sequencing for microbiome profiling (2bRAD-M). Microbial community diversity and compositional differences were assessed using α-diversity indices (Chao1, Shannon, and Simpson) and β-diversity metrics.
RESULTS: Bacteria dominated the indoor air microbiota of the airport terminal (98.4%), with Pseudomonadota (39.4%-62.9%) and Actinomycetota (18.9%-32.9%) as the predominant phyla. Microbial diversity was significantly higher in surface samples than in airborne aerosols. High-frequency contact surfaces (e.g., handrails) were enriched with human commensal bacteria, including Cutibacterium acnes (9.71%-19.4%). Multiple WHO-prioritized pathogens were detected, including Acinetobacter baumannii (0.3%-1.4%) and Pseudomonas aeruginosa (0.01%-1.24%). The transit transfer area (A1), characterized by poorer ventilation, showed higher microbial richness. Filtration samplers captured more microorganisms per unit volume than cyclonic samplers, with significant differences in detection profiles.
CONCLUSION: Sampling methods, sample types, and environmental conditions influence microbial distribution patterns across terminals. Detection of WHO Critical and High priority pathogens indicates potential risks of aerosol and contact transmission. Enhanced ventilation and disinfection of high-frequency contact surfaces can mitigate public health risks.
GRAPHICAL ABSTRACT: available in www.besjournal.com.},
}
MeSH Terms:
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Aerosols/analysis
*Air Microbiology
*Bacteria/isolation & purification/classification
*Airports
Environmental Monitoring
Humans
*Fungi/isolation & purification/classification
*Microbiota
*Air Pollution, Indoor/analysis
RevDate: 2026-05-28
Editorial: Maternal nutrition, gut microbiota, and endocrine programming in early life.
Frontiers in endocrinology, 17:1859900.
Additional Links: PMID-42205261
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@article {pmid42205261,
year = {2026},
author = {Gradisteanu Pircalabioru, G and Ionescu, MI and Bernstein, R},
title = {Editorial: Maternal nutrition, gut microbiota, and endocrine programming in early life.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1859900},
doi = {10.3389/fendo.2026.1859900},
pmid = {42205261},
issn = {1664-2392},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Problems in the use of chemical and functional nomenclatures for steroids in human physiology, biology and pharmacology.
RSC advances, 16(30):27678-27691.
Steroid compounds are important messengers in the human body that can be described using multiple nomenclature systems, each reflecting a different perspective on structure or function. Chemical nomenclature, based on IUPAC conventions, classifies steroids according to their ring structure and functional groups, whereas functional nomenclature reflects a compound's source, biological action, regulatory pathways, metabolism, or clinical application. These parallel systems are often applied inconsistently across disciplines, leading to ambiguity in interpretation and communication. This review outlines the foundations of chemical and functional naming, highlights circumstances in which nomenclature becomes inconsistent, and illustrates how physiology, molecular biology, receptor diversification, genetics, oncology, and the microbiome complicate terminology. Because clinicians, biochemists, pharmacologists, and researchers often apply different naming logics, coherent definitions and consistent usage are necessary for clear scientific discourse. This review proposes considerations to support more precise application of steroid nomenclature in academic publications.
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@article {pmid42205289,
year = {2026},
author = {Honour, JW},
title = {Problems in the use of chemical and functional nomenclatures for steroids in human physiology, biology and pharmacology.},
journal = {RSC advances},
volume = {16},
number = {30},
pages = {27678-27691},
pmid = {42205289},
issn = {2046-2069},
abstract = {Steroid compounds are important messengers in the human body that can be described using multiple nomenclature systems, each reflecting a different perspective on structure or function. Chemical nomenclature, based on IUPAC conventions, classifies steroids according to their ring structure and functional groups, whereas functional nomenclature reflects a compound's source, biological action, regulatory pathways, metabolism, or clinical application. These parallel systems are often applied inconsistently across disciplines, leading to ambiguity in interpretation and communication. This review outlines the foundations of chemical and functional naming, highlights circumstances in which nomenclature becomes inconsistent, and illustrates how physiology, molecular biology, receptor diversification, genetics, oncology, and the microbiome complicate terminology. Because clinicians, biochemists, pharmacologists, and researchers often apply different naming logics, coherent definitions and consistent usage are necessary for clear scientific discourse. This review proposes considerations to support more precise application of steroid nomenclature in academic publications.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Ecology-microbiome engineering in Sauce-flavor Baijiu via Single-Cell Raman Spectroscopy.
Biodesign research, 8(2):100089.
Sauce-flavor Baijiu owes its layered aroma to a diverse microbial consortium fermenting under extreme, open, solid-state conditions. High-throughput sequencing has revealed marked spatiotemporal heterogeneity in community composition, yet a fundamental composition-function disconnect persists: bulk omics average signals across heterogeneous micro-niches and cultivation recovers only a minor fraction of total diversity, leaving "who is doing what" unresolved. Closing this disconnect is a prerequisite for rational design of fermentation microbiomes and demands cell-resolved functional tools within an iterative engineering framework. This review proposes that Single-Cell Raman Spectroscopy (SCRS) and its derivatives, including D2O-Raman activity mapping, scRACS-Seq phenotype-to-genome linkage, scRACS-Culture recovery of rare functional strains, and Intra-Ramanome Correlation Analysis (IRCA) predictive metabolic phenotyping, collectively provide a label-free, culture-independent toolkit suited to this role in solid-state matrices. We delineate how these single-cell insights feed each stage of a Design-Build-Test-Learn (DBTL) cycle, from phenotype-informed strain selection through consortium assembly and functional validation to data-driven iterative optimization. This convergence of cell-resolved functional dissection, synthetic ecology, and process analytical technologies establishes the foundation for advancing Sauce-flavor Baijiu from experience-dependent craftsmanship toward intelligent brewing.
Additional Links: PMID-42205323
PubMed:
Citation:
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@article {pmid42205323,
year = {2026},
author = {Sun, X and Yi, X and Zhang, J},
title = {Ecology-microbiome engineering in Sauce-flavor Baijiu via Single-Cell Raman Spectroscopy.},
journal = {Biodesign research},
volume = {8},
number = {2},
pages = {100089},
pmid = {42205323},
issn = {2693-1257},
abstract = {Sauce-flavor Baijiu owes its layered aroma to a diverse microbial consortium fermenting under extreme, open, solid-state conditions. High-throughput sequencing has revealed marked spatiotemporal heterogeneity in community composition, yet a fundamental composition-function disconnect persists: bulk omics average signals across heterogeneous micro-niches and cultivation recovers only a minor fraction of total diversity, leaving "who is doing what" unresolved. Closing this disconnect is a prerequisite for rational design of fermentation microbiomes and demands cell-resolved functional tools within an iterative engineering framework. This review proposes that Single-Cell Raman Spectroscopy (SCRS) and its derivatives, including D2O-Raman activity mapping, scRACS-Seq phenotype-to-genome linkage, scRACS-Culture recovery of rare functional strains, and Intra-Ramanome Correlation Analysis (IRCA) predictive metabolic phenotyping, collectively provide a label-free, culture-independent toolkit suited to this role in solid-state matrices. We delineate how these single-cell insights feed each stage of a Design-Build-Test-Learn (DBTL) cycle, from phenotype-informed strain selection through consortium assembly and functional validation to data-driven iterative optimization. This convergence of cell-resolved functional dissection, synthetic ecology, and process analytical technologies establishes the foundation for advancing Sauce-flavor Baijiu from experience-dependent craftsmanship toward intelligent brewing.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Selling Clean Vaginas: An Examination of Feminine Hygiene Products' Health and Cultural Messaging and Its Implications for Black Women's Sexual Health.
International journal of sexual health : official journal of the World Association for Sexual Health, 38(2):390-403.
BACKGROUND: Feminine hygiene products (FHPs), including washes, deodorants, suppositories, and wipes, are widely marketed in the United States as essential to vaginal cleanliness, pH balance, and odor control. However, these products may contribute to adverse outcomes such as microbiome disruption, irritation, and infection. Black women disproportionately use FHPs and experience higher rates of reproductive health issues, yet the content and marketing of these products remain underexamined. This study investigates the health claims, ingredients, and marketing strategies of FHPs, with a focus on products explicitly marketed to Black women in the US.
METHODS: A conventional content analysis was conducted on 83 FHPs identified through US-based retail and e-commerce platforms between July 2022 and November 2024. Products were categorized by name, brand, claims, ingredients, point-of-sale (retail vs. e-commerce), and Black-owned. Products were also labeled "Black consumer focused" if they were produced by self-identified Black-owned brands and (1) marketed using culturally specific terms, language, or practices (e.g., "yoni", vaginal steaming), and/or (2) marketed claims related to health concerns disproportionately affecting Black women (e.g., fibroids, endometriosis).
RESULTS: Of the products analyzed, 63.8% claimed to balance vaginal pH, 33.7% targeted odor elimination, and 15.6% claimed to treat BV or yeast infections. Products often contained acidic ingredients (56.6%) and fragrances (28%), despite limited safety data. Products marketed to Black women disproportionately used spiritual or empowerment language such as "yoni," promoted herbal or botanical formulations (90%), and made unsubstantiated claims to treat reproductive conditions such as fibroids, infertility, and menstrual irregularities.
CONCLUSION: Marketing of FHPs reinforces myths about vaginal cleanliness and targets Black women with racially coded and scientifically unsupported claims. These practices may contribute to reproductive health disparities and warrant increased regulatory oversight, provider education, and culturally grounded health communication.
Additional Links: PMID-42205326
PubMed:
Citation:
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@article {pmid42205326,
year = {2026},
author = {Jenkins Hall, W and Garvey, I},
title = {Selling Clean Vaginas: An Examination of Feminine Hygiene Products' Health and Cultural Messaging and Its Implications for Black Women's Sexual Health.},
journal = {International journal of sexual health : official journal of the World Association for Sexual Health},
volume = {38},
number = {2},
pages = {390-403},
pmid = {42205326},
issn = {1931-762X},
abstract = {BACKGROUND: Feminine hygiene products (FHPs), including washes, deodorants, suppositories, and wipes, are widely marketed in the United States as essential to vaginal cleanliness, pH balance, and odor control. However, these products may contribute to adverse outcomes such as microbiome disruption, irritation, and infection. Black women disproportionately use FHPs and experience higher rates of reproductive health issues, yet the content and marketing of these products remain underexamined. This study investigates the health claims, ingredients, and marketing strategies of FHPs, with a focus on products explicitly marketed to Black women in the US.
METHODS: A conventional content analysis was conducted on 83 FHPs identified through US-based retail and e-commerce platforms between July 2022 and November 2024. Products were categorized by name, brand, claims, ingredients, point-of-sale (retail vs. e-commerce), and Black-owned. Products were also labeled "Black consumer focused" if they were produced by self-identified Black-owned brands and (1) marketed using culturally specific terms, language, or practices (e.g., "yoni", vaginal steaming), and/or (2) marketed claims related to health concerns disproportionately affecting Black women (e.g., fibroids, endometriosis).
RESULTS: Of the products analyzed, 63.8% claimed to balance vaginal pH, 33.7% targeted odor elimination, and 15.6% claimed to treat BV or yeast infections. Products often contained acidic ingredients (56.6%) and fragrances (28%), despite limited safety data. Products marketed to Black women disproportionately used spiritual or empowerment language such as "yoni," promoted herbal or botanical formulations (90%), and made unsubstantiated claims to treat reproductive conditions such as fibroids, infertility, and menstrual irregularities.
CONCLUSION: Marketing of FHPs reinforces myths about vaginal cleanliness and targets Black women with racially coded and scientifically unsupported claims. These practices may contribute to reproductive health disparities and warrant increased regulatory oversight, provider education, and culturally grounded health communication.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
The role of extracellular vesicles in intercellular communication within the oral cavity.
Journal of oral microbiology, 18(1):2673760.
BACKGROUND: Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, are nanoscale membrane-bound structures that mediate intercellular communication through the transfer of proteins, lipids, and nucleic acids. In the oral cavity, EVs are present in saliva and gingival crevicular fluid, where they contribute to immune regulation, epithelial barrier integrity, and host-microbiome interactions.
OBJECTIVE: This review aimed to critically summarize current knowledge regarding EV biogenesis, molecular composition, cellular and microbial sources, and their roles in oral homeostasis and disease pathogenesis.
RESULTS: Current evidence demonstrates that EVs derived from host cells and oral microorganisms actively regulate inflammatory responses, biofilm dynamics, tissue regeneration, and microbial colonization. Dysregulation of EV-mediated communication has been implicated in the development and progression of periodontal disease, oral candidiasis, and oral squamous cell carcinoma (OSCC). In addition, salivary EVs have emerged as promising non-invasive biomarkers and potential therapeutic tools in oral medicine. However, important methodological limitations remain, particularly regarding EV isolation, characterization, and standardization.
CONCLUSIONS: EVs represent central mediators of communication within the oral microenvironment and play dual roles in maintaining oral homeostasis and promoting disease progression. Further standardized and clinically relevant studies are required to better define EV biology and facilitate the translation of EV-based diagnostic and therapeutic strategies into clinical oral medicine.
Additional Links: PMID-42205570
PubMed:
Citation:
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@article {pmid42205570,
year = {2026},
author = {Semlali, A and Al-Zharani, M and Al-Ansari, J},
title = {The role of extracellular vesicles in intercellular communication within the oral cavity.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2673760},
pmid = {42205570},
issn = {2000-2297},
abstract = {BACKGROUND: Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, are nanoscale membrane-bound structures that mediate intercellular communication through the transfer of proteins, lipids, and nucleic acids. In the oral cavity, EVs are present in saliva and gingival crevicular fluid, where they contribute to immune regulation, epithelial barrier integrity, and host-microbiome interactions.
OBJECTIVE: This review aimed to critically summarize current knowledge regarding EV biogenesis, molecular composition, cellular and microbial sources, and their roles in oral homeostasis and disease pathogenesis.
RESULTS: Current evidence demonstrates that EVs derived from host cells and oral microorganisms actively regulate inflammatory responses, biofilm dynamics, tissue regeneration, and microbial colonization. Dysregulation of EV-mediated communication has been implicated in the development and progression of periodontal disease, oral candidiasis, and oral squamous cell carcinoma (OSCC). In addition, salivary EVs have emerged as promising non-invasive biomarkers and potential therapeutic tools in oral medicine. However, important methodological limitations remain, particularly regarding EV isolation, characterization, and standardization.
CONCLUSIONS: EVs represent central mediators of communication within the oral microenvironment and play dual roles in maintaining oral homeostasis and promoting disease progression. Further standardized and clinically relevant studies are required to better define EV biology and facilitate the translation of EV-based diagnostic and therapeutic strategies into clinical oral medicine.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Association between the oral microbiome and clinical indicators of resectable non-small cell lung cancer (NSCLC).
Journal of oral microbiology, 18(1):2675065.
BACKGROUND: Oral microbial implications for lung cancer outcomes and association with clinical markers are largely unknown.
OBJECTIVE: This work aimed to characterize the oral microbiome in relation to clinical indicators and identify oral microbial biomarkers associated with lung cancer outcomes in patients with non-small cell lung cancer (NSCLC).
DESIGN: This is an observational prospective study of saliva samples from patients undergoing curative surgery for NSCLC. Taxonomic and composition profiles were generated using full-length 16S rRNA gene sequencing (n=64). Differences in bacterial diversity and composition with cancer stage, histological subtype, overall survival (OS), and event-free survival (EFS) were examined.
RESULTS: Most alpha diversity measures were lower with stage III cancer compared to stage I. All other clinical features were not statistically associated with alpha diversity (P>0.05). The relative abundance of Haemophilus and Solobacterium was detected as significantly differentially abundant in participants with stage III NSCLC by at least 2 differentially abundant tools and an FDR-corrected p-value<0.1.
CONCLUSION: This study shows a significant association between cancer stage with oral bacterial diversity and the relative abundance of specific genera in relation to OS in participants with resectable NSCLC. This study is limited by sample size and needs to be confirmed in larger studies.
Additional Links: PMID-42205571
PubMed:
Citation:
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@article {pmid42205571,
year = {2026},
author = {DeClercq, V and Murphy, RE and Zinck, N and Langille, MGI and Wallace, A},
title = {Association between the oral microbiome and clinical indicators of resectable non-small cell lung cancer (NSCLC).},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2675065},
pmid = {42205571},
issn = {2000-2297},
abstract = {BACKGROUND: Oral microbial implications for lung cancer outcomes and association with clinical markers are largely unknown.
OBJECTIVE: This work aimed to characterize the oral microbiome in relation to clinical indicators and identify oral microbial biomarkers associated with lung cancer outcomes in patients with non-small cell lung cancer (NSCLC).
DESIGN: This is an observational prospective study of saliva samples from patients undergoing curative surgery for NSCLC. Taxonomic and composition profiles were generated using full-length 16S rRNA gene sequencing (n=64). Differences in bacterial diversity and composition with cancer stage, histological subtype, overall survival (OS), and event-free survival (EFS) were examined.
RESULTS: Most alpha diversity measures were lower with stage III cancer compared to stage I. All other clinical features were not statistically associated with alpha diversity (P>0.05). The relative abundance of Haemophilus and Solobacterium was detected as significantly differentially abundant in participants with stage III NSCLC by at least 2 differentially abundant tools and an FDR-corrected p-value<0.1.
CONCLUSION: This study shows a significant association between cancer stage with oral bacterial diversity and the relative abundance of specific genera in relation to OS in participants with resectable NSCLC. This study is limited by sample size and needs to be confirmed in larger studies.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Interaction ecology and functional stability: a mechanistic framework for managing plant microbiomes in drylands.
Frontiers in microbiology, 17:1816170.
Drylands are critical ecosystems that support grazing and agriculture, but they are increasingly constrained by environmental stresses such as altered precipitation, warming, salinity/alkalinity, soil pH variability and desertification, which limit plant performance and ecosystem stability. In these conditions, sustaining development through severe, pulse-driven stress is more important for plant "success" than optimizing growth. In addition, soil pH acts as a chemical regulator that modulates microbial activity and resource availability under arid conditions. Through an ecological perspective, this study summarizes how plant-associated microbiomes, particularly bacteria and fungus found in the root and rhizosphere, improve plant performance under arid conditions. Under this filters, microbial communities with functional redundancy, robust interaction networks, and microhabitat-forming characteristics are preferred over single-strain inoculants, which frequently fail under desiccation, UV exposure, temperature extremes, and competition. Key microbial traits, including biofilm formation and extracellular polymeric substances (EPS), contribute to plant resilience under dry conditions. The study further highlights landscape microbial infrastructures-biocrusts and fertility islands-as upstream drivers of microbial source pools and patch-scale resource maps. Finally, it outlines translational priorities for development of stress-adapted consortia and management plans aligned with dryland assembly rules and climate-driven variability.
Additional Links: PMID-42205580
PubMed:
Citation:
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@article {pmid42205580,
year = {2026},
author = {Sami, A and Mao, W and Wang, Q and Rui, G and Xu, Q and Wang, J and Wu, K and Li, J and Jiang, L},
title = {Interaction ecology and functional stability: a mechanistic framework for managing plant microbiomes in drylands.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1816170},
pmid = {42205580},
issn = {1664-302X},
abstract = {Drylands are critical ecosystems that support grazing and agriculture, but they are increasingly constrained by environmental stresses such as altered precipitation, warming, salinity/alkalinity, soil pH variability and desertification, which limit plant performance and ecosystem stability. In these conditions, sustaining development through severe, pulse-driven stress is more important for plant "success" than optimizing growth. In addition, soil pH acts as a chemical regulator that modulates microbial activity and resource availability under arid conditions. Through an ecological perspective, this study summarizes how plant-associated microbiomes, particularly bacteria and fungus found in the root and rhizosphere, improve plant performance under arid conditions. Under this filters, microbial communities with functional redundancy, robust interaction networks, and microhabitat-forming characteristics are preferred over single-strain inoculants, which frequently fail under desiccation, UV exposure, temperature extremes, and competition. Key microbial traits, including biofilm formation and extracellular polymeric substances (EPS), contribute to plant resilience under dry conditions. The study further highlights landscape microbial infrastructures-biocrusts and fertility islands-as upstream drivers of microbial source pools and patch-scale resource maps. Finally, it outlines translational priorities for development of stress-adapted consortia and management plans aligned with dryland assembly rules and climate-driven variability.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Editorial: Microbial-fungal symbioses: ecological implications, environmental impact, and biotechnological applications in natural and agricultural systems.
Frontiers in microbiology, 17:1861156.
Additional Links: PMID-42205583
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Citation:
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@article {pmid42205583,
year = {2026},
author = {Herrera, H and Sinha, A and Sarkar, S and Cambronero-Heinrichs, JC},
title = {Editorial: Microbial-fungal symbioses: ecological implications, environmental impact, and biotechnological applications in natural and agricultural systems.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1861156},
pmid = {42205583},
issn = {1664-302X},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
The gut mycobiome is shaped by interactions with the bacterial community in twins.
iScience, 29(6):115786.
The human gut microbiome comprises bacteria, viruses, and fungi, yet the fungal component (mycobiome) remains poorly characterized. Here, we investigated gut fungal composition and fungal-bacterial interactions in healthy monozygotic and dizygotic twins. Fungal communities showed substantially higher inter-individual variability than bacterial communities. Zygosity, age, and shared environment had no major influence on fungal abundance, similarity, or dominant genera. Candida was the most abundant genus (mean 5.2% in 161 individuals), followed by Geotrichum (3.7% in 132), whereas Saccharomyces was detected less frequently (0.8% in 92). Most bacterial genera were negatively correlated with Candida and Geotrichum, with stronger negative associations observed at higher bacterial abundances (up to rho = -0.6 for Alistipes). Network analysis revealed complex negative correlations among Bacteroides, Prevotella, and Candida. Overall, our findings reveal a highly variable gut mycobiome independent of host zygosity, pointing to a competitive bacterial-fungal interplay as a key regulator of fungal homeostasis in humans.
Additional Links: PMID-42205706
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Citation:
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@article {pmid42205706,
year = {2026},
author = {Lehr, K and Vilchez-Vargas, R and Skieceviciene, J and Hipler, NM and Gedgaudienė, G and Gustaityte, I and Kucinskas, L and Urba, M and Thon, C and Schanze, D and Zenker, M and Kupcinskas, J and Link, A},
title = {The gut mycobiome is shaped by interactions with the bacterial community in twins.},
journal = {iScience},
volume = {29},
number = {6},
pages = {115786},
pmid = {42205706},
issn = {2589-0042},
abstract = {The human gut microbiome comprises bacteria, viruses, and fungi, yet the fungal component (mycobiome) remains poorly characterized. Here, we investigated gut fungal composition and fungal-bacterial interactions in healthy monozygotic and dizygotic twins. Fungal communities showed substantially higher inter-individual variability than bacterial communities. Zygosity, age, and shared environment had no major influence on fungal abundance, similarity, or dominant genera. Candida was the most abundant genus (mean 5.2% in 161 individuals), followed by Geotrichum (3.7% in 132), whereas Saccharomyces was detected less frequently (0.8% in 92). Most bacterial genera were negatively correlated with Candida and Geotrichum, with stronger negative associations observed at higher bacterial abundances (up to rho = -0.6 for Alistipes). Network analysis revealed complex negative correlations among Bacteroides, Prevotella, and Candida. Overall, our findings reveal a highly variable gut mycobiome independent of host zygosity, pointing to a competitive bacterial-fungal interplay as a key regulator of fungal homeostasis in humans.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Cross-sectional analysis of feline gut microbiota reveals differences across age-defined groups under varying environments.
Frontiers in veterinary science, 13:1775401.
The gut microbiome plays a critical role in host health; however, its variation across age groups in domestic cats (Felis catus) remains unclear. This study characterized differences in the feline gut microbiota using 16S rRNA gene sequencing in 83 cats across five age-defined groups under varying environments: Pre-weaning (1.5 months, n = 16), Early kitten (3 months, n = 16), Late kitten (6-10 months, n = 15), Young adult (2 years, n = 20), and Mature adult (7-10 years, n = 16). Significant differences in microbial diversity and composition were observed across groups. Alpha-diversity was lowest in Pre-weaning kittens, peaking in Young adults, and declining in Mature adults. Beta-diversity revealed distinct clustering among groups (PERMANOVA, R [2] = 0.33, p = 0.001). Sensitivity analysis excluding the heterogeneous Mature adult group showed consistent patterns and increased the explanatory power of age (R [2] = 0.48). At the taxonomic level, Pre-weaning microbiota were enriched in Proteobacteria, particularly Escherichia-Shigella. Following weaning, the relative abundance of Negativibacillus increased, whereas Lactobacillus decreased. Bifidobacterium was more abundant in kitten stages, while Faecalibacterium exhibited higher abundance in Young adults. These patterns were generally consistent in sensitivity analyses. In contrast, the Mature adult group exhibited reduced Prevotella and increased Escherichia-Shigella relative to Young adults. Overall, this cross-sectional study identified compositional differences in the feline gut microbiota across age-defined groups under varying environments. These findings should be interpreted as group-level associations rather than independent age effects. Further controlled and longitudinal studies are needed to disentangle these effects.
Additional Links: PMID-42205797
PubMed:
Citation:
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@article {pmid42205797,
year = {2026},
author = {Wang, Y and Chen, Z and Hua, C and Mao, J and Geng, W and Feng, X and Ye, S and Song, S and Wang, H and Wang, X and Lin, L},
title = {Cross-sectional analysis of feline gut microbiota reveals differences across age-defined groups under varying environments.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1775401},
pmid = {42205797},
issn = {2297-1769},
abstract = {The gut microbiome plays a critical role in host health; however, its variation across age groups in domestic cats (Felis catus) remains unclear. This study characterized differences in the feline gut microbiota using 16S rRNA gene sequencing in 83 cats across five age-defined groups under varying environments: Pre-weaning (1.5 months, n = 16), Early kitten (3 months, n = 16), Late kitten (6-10 months, n = 15), Young adult (2 years, n = 20), and Mature adult (7-10 years, n = 16). Significant differences in microbial diversity and composition were observed across groups. Alpha-diversity was lowest in Pre-weaning kittens, peaking in Young adults, and declining in Mature adults. Beta-diversity revealed distinct clustering among groups (PERMANOVA, R [2] = 0.33, p = 0.001). Sensitivity analysis excluding the heterogeneous Mature adult group showed consistent patterns and increased the explanatory power of age (R [2] = 0.48). At the taxonomic level, Pre-weaning microbiota were enriched in Proteobacteria, particularly Escherichia-Shigella. Following weaning, the relative abundance of Negativibacillus increased, whereas Lactobacillus decreased. Bifidobacterium was more abundant in kitten stages, while Faecalibacterium exhibited higher abundance in Young adults. These patterns were generally consistent in sensitivity analyses. In contrast, the Mature adult group exhibited reduced Prevotella and increased Escherichia-Shigella relative to Young adults. Overall, this cross-sectional study identified compositional differences in the feline gut microbiota across age-defined groups under varying environments. These findings should be interpreted as group-level associations rather than independent age effects. Further controlled and longitudinal studies are needed to disentangle these effects.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Associations between prevalent unhealthy lifestyles and the gut microbiota: a comprehensive multi-database bibliometric analysis of pathogenic mechanisms and clinical trajectories.
Frontiers in medicine, 13:1834916.
BACKGROUND: Unhealthy lifestyles are associated with gut microbiota dysbiosis through complex inflammatory and immune-related pathways. Despite extensive primary research, comprehensive big-data syntheses mapping this field remain limited. This study systematically analyzes the research landscape, related pathophysiological processes, and emerging trends in the field of lifestyle-microbiome interactions using a multi-database bibliometric framework.
METHODS: A dual-database retrieval strategy utilized the Web of Science Core Collection (WoSCC) and PubMed. The analysis targeted five predominant unhealthy lifestyles: smoking, alcohol consumption, sleep disorders, sedentary behavior, and high-sugar diets. A primary dataset of 5,380 records published between January 1, 2001, and March 13, 2026, was extracted from WoSCC. A parallel clinical analysis incorporated 172 targeted studies from PubMed. Bibliometric analyses, encompassing publication trends, network topologies, citation bursts, keyword evolution, and clinical trajectories, were performed and visualized using Microsoft Excel 2024, VOSviewer, CiteSpace, SCImago, and R.
RESULTS: Publication output exhibited exponential growth from 2001 to 2026. China and the United States emerged as the dominant academic contributors. Thematic analyses identified inflammation, oxidative stress, obesity, metabolic dysfunction, and microbiome-associated metabolomics as core pathophysiological nodes. The literature frequently describes these elements as mediating the association between behavioral exposures and microbial dysbiosis. Clinical research trajectories demonstrated an evolution toward high-rigor methodological designs, systemic blood biomarker integration, and demographic stratification. The bibliometric data highlight targeted lifestyle intervention as a heavily researched non-pharmacological strategy for gut microbiota preservation.
CONCLUSION: This multi-database bibliometric study delineates the structural landscape of research on the association between unhealthy lifestyles and the gut microbiota. Inflammation, oxidative stress, and metabolic dysfunction emerge as central themes within the existing literature. These findings provide a systematic framework for understanding microenvironmental interactions and offer valuable insights to inform future research and the development of precise, lifestyle-oriented strategies for gastrointestinal health.
Additional Links: PMID-42205829
PubMed:
Citation:
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@article {pmid42205829,
year = {2026},
author = {Zhou, XJ and Chen, JL and Hu, CF and Li, ZK and Zheng, HB and Ding, TN and Chen, Y and Zhu, Y and Li, JN and Fu, Q and Fu, Y},
title = {Associations between prevalent unhealthy lifestyles and the gut microbiota: a comprehensive multi-database bibliometric analysis of pathogenic mechanisms and clinical trajectories.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1834916},
pmid = {42205829},
issn = {2296-858X},
abstract = {BACKGROUND: Unhealthy lifestyles are associated with gut microbiota dysbiosis through complex inflammatory and immune-related pathways. Despite extensive primary research, comprehensive big-data syntheses mapping this field remain limited. This study systematically analyzes the research landscape, related pathophysiological processes, and emerging trends in the field of lifestyle-microbiome interactions using a multi-database bibliometric framework.
METHODS: A dual-database retrieval strategy utilized the Web of Science Core Collection (WoSCC) and PubMed. The analysis targeted five predominant unhealthy lifestyles: smoking, alcohol consumption, sleep disorders, sedentary behavior, and high-sugar diets. A primary dataset of 5,380 records published between January 1, 2001, and March 13, 2026, was extracted from WoSCC. A parallel clinical analysis incorporated 172 targeted studies from PubMed. Bibliometric analyses, encompassing publication trends, network topologies, citation bursts, keyword evolution, and clinical trajectories, were performed and visualized using Microsoft Excel 2024, VOSviewer, CiteSpace, SCImago, and R.
RESULTS: Publication output exhibited exponential growth from 2001 to 2026. China and the United States emerged as the dominant academic contributors. Thematic analyses identified inflammation, oxidative stress, obesity, metabolic dysfunction, and microbiome-associated metabolomics as core pathophysiological nodes. The literature frequently describes these elements as mediating the association between behavioral exposures and microbial dysbiosis. Clinical research trajectories demonstrated an evolution toward high-rigor methodological designs, systemic blood biomarker integration, and demographic stratification. The bibliometric data highlight targeted lifestyle intervention as a heavily researched non-pharmacological strategy for gut microbiota preservation.
CONCLUSION: This multi-database bibliometric study delineates the structural landscape of research on the association between unhealthy lifestyles and the gut microbiota. Inflammation, oxidative stress, and metabolic dysfunction emerge as central themes within the existing literature. These findings provide a systematic framework for understanding microenvironmental interactions and offer valuable insights to inform future research and the development of precise, lifestyle-oriented strategies for gastrointestinal health.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Oral microbiota alterations in radiographic axial spondyloarthritis.
Frontiers in medicine, 13:1815404.
OBJECTIVE: To investigate alterations in the oral microbiome of patients with radiographic axial spondyloarthritis (r-axSpA), to identify microbial taxa associated with disease status and structural progression, and to explore potential links between oral microbiota composition and systemic immunological profiles.
METHODS: An observational cross-sectional study was conducted including 57 radiographic axial spondyloarthritis patients and 41 healthy controls. Oral samples were analyzed using 16S rRNA gene sequencing; amplicon sequence variants (ASVs) were generated using LotuS2/DADA2 and taxonomically annotated with SILVA, Greengenes, and HITdb. Alpha and beta diversity were assessed using ACE, Pielou indexes, and UniFrac distances with PERMANOVA and ANOSIM. Differential abundance was determined via LEfSe (LDA > 2, p < 0.05). Associations between microbial taxa, disease activity, structural damage, and immunological markers were evaluated using linear modeling and Spearman correlation analysis.
RESULTS: R-axSpA patients showed alterations in oral microbiome composition compared with controls, although alpha diversity remained largely comparable. Actinobacteria, Spirochaetes, and Synergistetes tended to be enriched in r-axSpA patients, mainly driven by an increased abundance of Actinomyces and Selenomonas. Several key periodontal pathogens, including Porphyromonas gingivalis and Actinomyces species, were more abundant in the r-axSpA group. Within the r-axSpA group, the abundance of Porphyromonas and Saccharimonadaceae showed associations with the severity of sacroiliitis and ankylosis. These taxa also exhibited positive correlations with systemic pro-inflammatory cytokines (such as IL-17), which may suggest a possible link between oral dysbiosis and enhanced Th17-driven inflammation in r-axSpA.
CONCLUSION: Patients may exhibit a distinct proinflammatory oral microbiome profile, with increased representation of Actinomyces and Porphyromonas species. Certain microbial taxa, including members of Porphyromonadaceae and Patescibacteria, have been reported to correlate with cytokines implicated in the immunopathogenesis of radiographic axial spondyloarthritis. These observations suggest that oral dysbiosis could play a role in the maintenance or modulation of systemic inflammation in r-axSpA, and that the oral microbiome might serve as a potential source of biomarkers or a target for future therapeutic strategies.
Additional Links: PMID-42205836
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@article {pmid42205836,
year = {2026},
author = {Abuova, A and Meiramova, A and Zueva, Y and Kunz, J and Chulenbayeva, L and Issilbayeva, A and Jarmukhanov, Z and Vinogradova, E and Ainabekova, B and Kozhakhmetov, S and Kushugulova, A},
title = {Oral microbiota alterations in radiographic axial spondyloarthritis.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1815404},
pmid = {42205836},
issn = {2296-858X},
abstract = {OBJECTIVE: To investigate alterations in the oral microbiome of patients with radiographic axial spondyloarthritis (r-axSpA), to identify microbial taxa associated with disease status and structural progression, and to explore potential links between oral microbiota composition and systemic immunological profiles.
METHODS: An observational cross-sectional study was conducted including 57 radiographic axial spondyloarthritis patients and 41 healthy controls. Oral samples were analyzed using 16S rRNA gene sequencing; amplicon sequence variants (ASVs) were generated using LotuS2/DADA2 and taxonomically annotated with SILVA, Greengenes, and HITdb. Alpha and beta diversity were assessed using ACE, Pielou indexes, and UniFrac distances with PERMANOVA and ANOSIM. Differential abundance was determined via LEfSe (LDA > 2, p < 0.05). Associations between microbial taxa, disease activity, structural damage, and immunological markers were evaluated using linear modeling and Spearman correlation analysis.
RESULTS: R-axSpA patients showed alterations in oral microbiome composition compared with controls, although alpha diversity remained largely comparable. Actinobacteria, Spirochaetes, and Synergistetes tended to be enriched in r-axSpA patients, mainly driven by an increased abundance of Actinomyces and Selenomonas. Several key periodontal pathogens, including Porphyromonas gingivalis and Actinomyces species, were more abundant in the r-axSpA group. Within the r-axSpA group, the abundance of Porphyromonas and Saccharimonadaceae showed associations with the severity of sacroiliitis and ankylosis. These taxa also exhibited positive correlations with systemic pro-inflammatory cytokines (such as IL-17), which may suggest a possible link between oral dysbiosis and enhanced Th17-driven inflammation in r-axSpA.
CONCLUSION: Patients may exhibit a distinct proinflammatory oral microbiome profile, with increased representation of Actinomyces and Porphyromonas species. Certain microbial taxa, including members of Porphyromonadaceae and Patescibacteria, have been reported to correlate with cytokines implicated in the immunopathogenesis of radiographic axial spondyloarthritis. These observations suggest that oral dysbiosis could play a role in the maintenance or modulation of systemic inflammation in r-axSpA, and that the oral microbiome might serve as a potential source of biomarkers or a target for future therapeutic strategies.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Metagenomic profiling of endophytic microbiomes associated with fruit pulp and seed kernels of different mango varieties reveals conservation of bacterial communities in seed kernels.
3 Biotech, 16(6):222.
UNLABELLED: Bacterial and fungal communities associated with mango pulp and seed kernels from eight Indian mango varieties were profiled using 16 S rRNA and ITS amplicon sequencing. Bacterial diversity was consistently higher in seed kernels (647 ± 238 OTUs) than in pulp tissues (196 ± 112 OTUs). Seed kernel-associated bacterial communities were dominated by Firmicutes (35.8-44.0%) and Bacteroidota (16.8-35.8%) and showed high compositional consistency across varieties, with core genera including Prevotella, Ruminiclostridium, and Lachnoclostridium. In contrast, pulp-associated bacterial communities were enriched in Proteobacteria (6.5-88.5%) and Actinobacteria (4.4-34.6%) and exhibited pronounced inter-varietal variability, particularly in the relative abundance of Bacteroidota (0.8-53.8%). Fungal communities displayed lower richness (14-72 OTUs) and higher variability, with Candida kruisii (15-67%) and Hanseniaspora uvarum (up to 86%) as dominant taxa. Non-metric multidimensional scaling and hierarchical clustering revealed clear tissue-driven segregation of bacterial communities, whereas fungal assemblages showed weaker tissue-associated structuring. Seed kernels harbored approximately 3.3-fold more unique bacterial OTUs than pulp tissues, with the Amrapali seedkernel exhibiting the highest richness (789 OTUs). Across varieties, 82% of kernel-associated bacterial OTUs were shared, compared with 31% in pulp, indicating a conserved kernel microbiome and a more variable, cultivar-specific pulp microbiome. These results highlight strong tissue-level compartmentalization of mango-associated bacterial communities across cultivars.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04848-2.
Additional Links: PMID-42205899
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@article {pmid42205899,
year = {2026},
author = {Patil, BL and Shanmugaraj, C and Madhusudan, M},
title = {Metagenomic profiling of endophytic microbiomes associated with fruit pulp and seed kernels of different mango varieties reveals conservation of bacterial communities in seed kernels.},
journal = {3 Biotech},
volume = {16},
number = {6},
pages = {222},
pmid = {42205899},
issn = {2190-572X},
abstract = {UNLABELLED: Bacterial and fungal communities associated with mango pulp and seed kernels from eight Indian mango varieties were profiled using 16 S rRNA and ITS amplicon sequencing. Bacterial diversity was consistently higher in seed kernels (647 ± 238 OTUs) than in pulp tissues (196 ± 112 OTUs). Seed kernel-associated bacterial communities were dominated by Firmicutes (35.8-44.0%) and Bacteroidota (16.8-35.8%) and showed high compositional consistency across varieties, with core genera including Prevotella, Ruminiclostridium, and Lachnoclostridium. In contrast, pulp-associated bacterial communities were enriched in Proteobacteria (6.5-88.5%) and Actinobacteria (4.4-34.6%) and exhibited pronounced inter-varietal variability, particularly in the relative abundance of Bacteroidota (0.8-53.8%). Fungal communities displayed lower richness (14-72 OTUs) and higher variability, with Candida kruisii (15-67%) and Hanseniaspora uvarum (up to 86%) as dominant taxa. Non-metric multidimensional scaling and hierarchical clustering revealed clear tissue-driven segregation of bacterial communities, whereas fungal assemblages showed weaker tissue-associated structuring. Seed kernels harbored approximately 3.3-fold more unique bacterial OTUs than pulp tissues, with the Amrapali seedkernel exhibiting the highest richness (789 OTUs). Across varieties, 82% of kernel-associated bacterial OTUs were shared, compared with 31% in pulp, indicating a conserved kernel microbiome and a more variable, cultivar-specific pulp microbiome. These results highlight strong tissue-level compartmentalization of mango-associated bacterial communities across cultivars.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04848-2.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Fecal functional metagenomics reveals increased gut Bacillota/Pseudomonadota (Firmicutes/Proteobacteria) ratio and altered bacterial CAZyme profile in human colorectal cancer.
3 Biotech, 16(6):230.
UNLABELLED: Gut microbial dysbiosis has been implicated in the onset and/or progression of colorectal cancer (CC). We recently identified the emergence of low-abundance bacterial taxa affiliated with the phylum Bacillota in the gut microbiome of CC patients, as revealed by 16S rRNA gene amplicon sequencing. Here, we subjected the fecal samples from CC (n = 4) and healthy control (HC, n = 4) participants to functional metagenomics using the Illumina Novaseq 6000 platform. Metagenome-assembled genomes (MAGs) showed compositional differences among bacterial phylotypes in CC and HC. Species observed, richness (Chao1), and diversity (Shannon's) were high in CC, whereas species abundance peaked in HC. The Bacillota to Pseudomonadota ratio was high (> 3-fold) in CC (2.45) as compared to HC (0.70). MAGs revealed a decline in the distribution frequency of COGs involved in carbohydrate transport and metabolism (G), inorganic ion transport and metabolism (P), and unknown function (S) in CC. However, CC and HC samples exhibited marginal variations in terms of G/P (1.29 and 1.18, respectively) and G/S (0.35 and 0.40, respectively) ratios. Analysis further revealed a significant increment in glycosyltransferases GT1, GT2 and GT4, particularly in CC. In contrast, the glycoside hydrolases GH5 and GH9 declined in CC. GT/GH ratios were found to increase > 2-fold in CC (3.94) compared with HC (1.37). The present pilot-scale dataset-specific work reflects perseverance of Bacillota, significant decline in Pseudomonadota, a stable G/P and G/S ratios and enrichment of glycosyltransfererases in CC. Further transcriptomic-based studies in larger cohorts are warranted to gain insights into the implications of dysbiosis and its pathophysiological relevance.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04882-0.
Additional Links: PMID-42205903
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@article {pmid42205903,
year = {2026},
author = {Hameed, A and Ghate, SD and Shastry, RP},
title = {Fecal functional metagenomics reveals increased gut Bacillota/Pseudomonadota (Firmicutes/Proteobacteria) ratio and altered bacterial CAZyme profile in human colorectal cancer.},
journal = {3 Biotech},
volume = {16},
number = {6},
pages = {230},
pmid = {42205903},
issn = {2190-572X},
abstract = {UNLABELLED: Gut microbial dysbiosis has been implicated in the onset and/or progression of colorectal cancer (CC). We recently identified the emergence of low-abundance bacterial taxa affiliated with the phylum Bacillota in the gut microbiome of CC patients, as revealed by 16S rRNA gene amplicon sequencing. Here, we subjected the fecal samples from CC (n = 4) and healthy control (HC, n = 4) participants to functional metagenomics using the Illumina Novaseq 6000 platform. Metagenome-assembled genomes (MAGs) showed compositional differences among bacterial phylotypes in CC and HC. Species observed, richness (Chao1), and diversity (Shannon's) were high in CC, whereas species abundance peaked in HC. The Bacillota to Pseudomonadota ratio was high (> 3-fold) in CC (2.45) as compared to HC (0.70). MAGs revealed a decline in the distribution frequency of COGs involved in carbohydrate transport and metabolism (G), inorganic ion transport and metabolism (P), and unknown function (S) in CC. However, CC and HC samples exhibited marginal variations in terms of G/P (1.29 and 1.18, respectively) and G/S (0.35 and 0.40, respectively) ratios. Analysis further revealed a significant increment in glycosyltransferases GT1, GT2 and GT4, particularly in CC. In contrast, the glycoside hydrolases GH5 and GH9 declined in CC. GT/GH ratios were found to increase > 2-fold in CC (3.94) compared with HC (1.37). The present pilot-scale dataset-specific work reflects perseverance of Bacillota, significant decline in Pseudomonadota, a stable G/P and G/S ratios and enrichment of glycosyltransfererases in CC. Further transcriptomic-based studies in larger cohorts are warranted to gain insights into the implications of dysbiosis and its pathophysiological relevance.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-026-04882-0.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
A randomised controlled trial of EP395, a novel anti-inflammatory macrolide, in stable COPD patients.
ERJ open research, 12(3):.
BACKGROUND: Macrolide antibiotics have immunomodulatory activity and when taken chronically reduce exacerbations of COPD. However, chronic use can cause bacterial resistance. EP395 (glasmacinal), a novel macrolide, is being developed as a treatment to reduce exacerbations of COPD without inducing antimicrobial resistance.
METHODS: In this double-blind, placebo-controlled, phase 2a trial (NCT05572333), patients (≥45 years old, diagnosed with COPD for ≥2 years and stable on at least one maintenance inhaled therapy) were randomised (2:1) to EP395 or placebo daily for 12 weeks. The primary objective was safety, with key secondary objectives assessing pharmacodynamic effects of EP395.
RESULTS: A total of 61 patients were randomised (42 EP395, 19 placebo). A 12-week course of EP395 was well tolerated: no serious adverse events were considered related to EP395, and adverse events occurred in similar proportions in both groups (64.3% EP395, 63.2% placebo). Four patients were withdrawn due to adverse events (three EP395, one placebo). Sputum neutrophil elastase and myeloperoxidase, mediators of neutrophil activation, were reduced with EP395 (treatment difference (log scale): neutrophil elastase -0.415 ng·mL[-1], 95% CI -0.787 to -0.043 ng·mL[-1], p=0.030; myeloperoxidase -0.282 ng·mL[-1], 95% CI -0.640 to 0.076 ng·mL[-1], p=0.119). Relative changes in neutrophil elastase and myeloperoxidase from baseline with EP395 were 66% and 75%, respectively, of those observed with placebo. Exploratory 16S rRNA sequencing of sputum showed EP395 had no detectable effect on the lung microbiome, including the proportion of pathogenic Proteobacteria species.
CONCLUSION: In patients with stable COPD, EP395 for 12 weeks was well tolerated, demonstrated selective anti-inflammatory activity and had no detectable effect on the lung microbiome.
Additional Links: PMID-42206016
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Citation:
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@article {pmid42206016,
year = {2026},
author = {Watz, H and Korn, S and Kornmann, O and Singh, D and Wilkinson, T and Hanrott, K and Staples, KJ and Ackland, J and Norris, V},
title = {A randomised controlled trial of EP395, a novel anti-inflammatory macrolide, in stable COPD patients.},
journal = {ERJ open research},
volume = {12},
number = {3},
pages = {},
pmid = {42206016},
issn = {2312-0541},
abstract = {BACKGROUND: Macrolide antibiotics have immunomodulatory activity and when taken chronically reduce exacerbations of COPD. However, chronic use can cause bacterial resistance. EP395 (glasmacinal), a novel macrolide, is being developed as a treatment to reduce exacerbations of COPD without inducing antimicrobial resistance.
METHODS: In this double-blind, placebo-controlled, phase 2a trial (NCT05572333), patients (≥45 years old, diagnosed with COPD for ≥2 years and stable on at least one maintenance inhaled therapy) were randomised (2:1) to EP395 or placebo daily for 12 weeks. The primary objective was safety, with key secondary objectives assessing pharmacodynamic effects of EP395.
RESULTS: A total of 61 patients were randomised (42 EP395, 19 placebo). A 12-week course of EP395 was well tolerated: no serious adverse events were considered related to EP395, and adverse events occurred in similar proportions in both groups (64.3% EP395, 63.2% placebo). Four patients were withdrawn due to adverse events (three EP395, one placebo). Sputum neutrophil elastase and myeloperoxidase, mediators of neutrophil activation, were reduced with EP395 (treatment difference (log scale): neutrophil elastase -0.415 ng·mL[-1], 95% CI -0.787 to -0.043 ng·mL[-1], p=0.030; myeloperoxidase -0.282 ng·mL[-1], 95% CI -0.640 to 0.076 ng·mL[-1], p=0.119). Relative changes in neutrophil elastase and myeloperoxidase from baseline with EP395 were 66% and 75%, respectively, of those observed with placebo. Exploratory 16S rRNA sequencing of sputum showed EP395 had no detectable effect on the lung microbiome, including the proportion of pathogenic Proteobacteria species.
CONCLUSION: In patients with stable COPD, EP395 for 12 weeks was well tolerated, demonstrated selective anti-inflammatory activity and had no detectable effect on the lung microbiome.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Correction: Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework.
Frontiers in immunology, 17:1874174.
[This corrects the article DOI: 10.3389/fimmu.2026.1847027.].
Additional Links: PMID-42206046
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@article {pmid42206046,
year = {2026},
author = {Zhang, W and Yi, J and Li, Z},
title = {Correction: Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1874174},
doi = {10.3389/fimmu.2026.1874174},
pmid = {42206046},
issn = {1664-3224},
mesh = {Humans ; *Microbiota/immunology ; *Idiopathic Pulmonary Fibrosis/immunology/microbiology ; *Immunity, Innate ; Animals ; Inflammasomes/metabolism/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Disease Progression ; Biofilms ; },
abstract = {[This corrects the article DOI: 10.3389/fimmu.2026.1847027.].},
}
MeSH Terms:
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Humans
*Microbiota/immunology
*Idiopathic Pulmonary Fibrosis/immunology/microbiology
*Immunity, Innate
Animals
Inflammasomes/metabolism/immunology
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
Disease Progression
Biofilms
RevDate: 2026-05-28
CmpDate: 2026-05-28
Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework.
Frontiers in immunology, 17:1847027.
Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) remains a major cause of short-term mortality, yet its biological drivers are incompletely understood. Increasing evidence indicates that the distal lung is not sterile and that microbial burden, ecological disruption, and host immune responses may interact within the fibrotic niche. Here, we summarize current evidence and propose a focused, hypothesis-generating framework for microbiome-immune crosstalk in AE-IPF. In this model, pulmonary dysbiosis and persistent microbial stimulation may converge with epithelial injury-derived danger signals to amplify pattern-recognition receptor signaling, reshape macrophage states, and promote injurious neutrophil responses, including excessive neutrophil extracellular trap formation. Emerging data from fibrotic lung disease also raise the possibility that SPP1-associated macrophage programs may contribute to both impaired host defense and maladaptive repair. These observations also support the view that immune-cell state transitions, rather than microbial burden alone, may shape how acute injury is translated into persistent fibroinflammatory remodeling. We also discuss how antimicrobial exposure and resistance-associated persistence traits, including biofilm formation, could contribute to impaired microbial clearance and sustained innate immune activation, while emphasizing that direct in situ evidence in AE-IPF remains limited. Rather than proposing a universal mechanism, this mini review highlights a testable amplification framework that may help refine pathogen-aware stratification, antimicrobial stewardship, and biomarker-guided host-directed strategies in future studies.
Additional Links: PMID-42206055
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@article {pmid42206055,
year = {2026},
author = {Zhang, W and Yi, J and Li, Z},
title = {Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1847027},
pmid = {42206055},
issn = {1664-3224},
mesh = {Humans ; *Idiopathic Pulmonary Fibrosis/immunology/microbiology/pathology/metabolism ; *Microbiota/immunology ; *Immunity, Innate ; Animals ; Disease Progression ; Neutrophils/immunology ; Lung/immunology/microbiology/pathology ; Macrophages/immunology ; Dysbiosis/immunology ; },
abstract = {Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) remains a major cause of short-term mortality, yet its biological drivers are incompletely understood. Increasing evidence indicates that the distal lung is not sterile and that microbial burden, ecological disruption, and host immune responses may interact within the fibrotic niche. Here, we summarize current evidence and propose a focused, hypothesis-generating framework for microbiome-immune crosstalk in AE-IPF. In this model, pulmonary dysbiosis and persistent microbial stimulation may converge with epithelial injury-derived danger signals to amplify pattern-recognition receptor signaling, reshape macrophage states, and promote injurious neutrophil responses, including excessive neutrophil extracellular trap formation. Emerging data from fibrotic lung disease also raise the possibility that SPP1-associated macrophage programs may contribute to both impaired host defense and maladaptive repair. These observations also support the view that immune-cell state transitions, rather than microbial burden alone, may shape how acute injury is translated into persistent fibroinflammatory remodeling. We also discuss how antimicrobial exposure and resistance-associated persistence traits, including biofilm formation, could contribute to impaired microbial clearance and sustained innate immune activation, while emphasizing that direct in situ evidence in AE-IPF remains limited. Rather than proposing a universal mechanism, this mini review highlights a testable amplification framework that may help refine pathogen-aware stratification, antimicrobial stewardship, and biomarker-guided host-directed strategies in future studies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Idiopathic Pulmonary Fibrosis/immunology/microbiology/pathology/metabolism
*Microbiota/immunology
*Immunity, Innate
Animals
Disease Progression
Neutrophils/immunology
Lung/immunology/microbiology/pathology
Macrophages/immunology
Dysbiosis/immunology
RevDate: 2026-05-28
CmpDate: 2026-05-28
Stress accelerates hepatocellular carcinoma progression via a gut microbial-metabolite axis.
Frontiers in immunology, 17:1790214.
BACKGROUND: Hepatocellular carcinoma ranks among the most prevalent malignancies worldwide. While stress can modulate tumor initiation, progression, metastasis, and therapeutic response through diverse mechanisms, its specific role in hepatocellular carcinoma pathobiology remains elusive. This study aimed to elucidate the role of the gut microbiota in stress-promoted hepatocellular carcinoma progression and to uncover the pathways associated with disease progression.
METHODS: Integrating clinical and preclinical models, we delineated stress-induced restructuring of the gut microbiota and functionally restored specific microbial constituents. Mechanistic insights into the microbial metabolite indole-3-propionic acid were derived through in vitro and in vivo interrogations of the hepatocellular carcinoma tumor microenvironment.
RESULTS: Stress profoundly remodels the gut microbiota, with Phocaeicola vulgatus being significantly reduced. Restoration of Phocaeicola vulgatus or administration of its tryptophan-derived metabolite indole-3-propionic acid significantly attenuated hepatocellular carcinoma progression in vivo. Indole-3-propionic acid treatment reduced endothelial JAM2 expression and was associated with reduced JAM2-F11R-mediated endothelial-macrophage crosstalk in hepatocellular carcinoma, which may contribute to suppression of tumor progression.
CONCLUSIONS: These findings support a role for the stress-gut microbiota-metabolite-tumor microenvironment axis in hepatocellular carcinoma progression and suggest potential translational targets for microbiome-based therapeutic strategies.
Additional Links: PMID-42206057
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@article {pmid42206057,
year = {2026},
author = {Hu, Z and Yue, P and Yuan, M and Zhang, Z and Li, Q and Yang, T and Li, Y and Ding, BS and Fan, Z and Yang, B and Cao, Z},
title = {Stress accelerates hepatocellular carcinoma progression via a gut microbial-metabolite axis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1790214},
pmid = {42206057},
issn = {1664-3224},
mesh = {*Liver Neoplasms/pathology/metabolism/microbiology/etiology ; Animals ; *Carcinoma, Hepatocellular/pathology/metabolism/microbiology/etiology ; Humans ; *Gastrointestinal Microbiome ; Indoles/metabolism/pharmacology ; Disease Progression ; Tumor Microenvironment ; *Stress, Physiological ; Mice ; Male ; Cell Line, Tumor ; },
abstract = {BACKGROUND: Hepatocellular carcinoma ranks among the most prevalent malignancies worldwide. While stress can modulate tumor initiation, progression, metastasis, and therapeutic response through diverse mechanisms, its specific role in hepatocellular carcinoma pathobiology remains elusive. This study aimed to elucidate the role of the gut microbiota in stress-promoted hepatocellular carcinoma progression and to uncover the pathways associated with disease progression.
METHODS: Integrating clinical and preclinical models, we delineated stress-induced restructuring of the gut microbiota and functionally restored specific microbial constituents. Mechanistic insights into the microbial metabolite indole-3-propionic acid were derived through in vitro and in vivo interrogations of the hepatocellular carcinoma tumor microenvironment.
RESULTS: Stress profoundly remodels the gut microbiota, with Phocaeicola vulgatus being significantly reduced. Restoration of Phocaeicola vulgatus or administration of its tryptophan-derived metabolite indole-3-propionic acid significantly attenuated hepatocellular carcinoma progression in vivo. Indole-3-propionic acid treatment reduced endothelial JAM2 expression and was associated with reduced JAM2-F11R-mediated endothelial-macrophage crosstalk in hepatocellular carcinoma, which may contribute to suppression of tumor progression.
CONCLUSIONS: These findings support a role for the stress-gut microbiota-metabolite-tumor microenvironment axis in hepatocellular carcinoma progression and suggest potential translational targets for microbiome-based therapeutic strategies.},
}
MeSH Terms:
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hide MeSH Terms
*Liver Neoplasms/pathology/metabolism/microbiology/etiology
Animals
*Carcinoma, Hepatocellular/pathology/metabolism/microbiology/etiology
Humans
*Gastrointestinal Microbiome
Indoles/metabolism/pharmacology
Disease Progression
Tumor Microenvironment
*Stress, Physiological
Mice
Male
Cell Line, Tumor
RevDate: 2026-05-28
CmpDate: 2026-05-28
Multi-metal contamination shapes abundance, co-occurrence, and mobility potential of resistance and virulence genes in mining-impacted soils.
Infectious medicine, 5(2):100260.
BACKGROUND: Antimicrobial resistance is a growing global public health concern, posing a serious threat to human health. This study aimed to characterize the composition and distribution of microbial communities, metal resistance genes (MRGs), antibiotic resistance genes (ARGs), and virulence factor genes (VFGs) under multi-metal stress and assess the impacts of metal and soil properties on the diversity, abundance, carrying rate (proportion of gene carriers), co-occurrence rate (proportion of microorganisms co-carrying multiple gene types), and mobility potential (MP, likelihood of horizontal gene transfer) of these genes.
METHODS: Soil samples were collected from eight sampling sites within a metal mining area (metal-contaminated soil group, MS) and four sites located more than 3 km away from the mining area (control group). Metal concentrations and physicochemical properties of the soils were measured using standard methods. Metagenomic sequencing was performed to characterize the composition and distribution of the microbiome, resistome, and virulome. Statistical modeling was applied to examine the effects of heavy metal content and soil properties on the relative abundance, co-occurrence, and mobilome potential of the three gene types.
RESULTS: Fe, V, Cr, and Cu primarily promoted the diversity, carrying rate, and co-occurrence rate of microbial communities, MRGs, ARGs, and VFGs. In contrast, Ni and Zn exhibited overall inhibitory effects. For every unit increase in Fe and V, the MP of MRGs and VFGs was associated with an increase of 3.0 × 10⁻⁵ and 1.2 × 10⁻⁵, respectively. A per 1 mg/kg increase in Cr and Cu was correlated with a decrease of 4.3 × 10⁻⁵ and 1.1 × 10⁻⁴ in the MP of ARGs and of MRGs, respectively. Positive correlations were found between the MP of plasmid‑mediated ARGs and Cr, and between transposon‑mediated ARGs and Cr/V. The MP of transposon‑mediated MRGs correlated positively with Fe, while Cu correlated negatively with plasmid‑mediated ARGs but positively with insertion sequence‑mediated ARGs. Ni concentration was positively associated with the MP of IS‑mediated VFGs.
CONCLUSIONS: Metals alter the composition and distribution of microbial communities, MRGs, ARGs, and VFGs. A key mechanism underlying this regulation is the modulation of their mobile potential, which either facilitates or restricts horizontal gene transfer.
Additional Links: PMID-42206066
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@article {pmid42206066,
year = {2026},
author = {Zhang, Q and Li, S and Wang, X and Sun, Y and Liu, J and Gao, J and Deng, C and Zhao, W and Ma, Y and Quan, J and Yin, Q and Jian, D and Zhang, R and Qi, R},
title = {Multi-metal contamination shapes abundance, co-occurrence, and mobility potential of resistance and virulence genes in mining-impacted soils.},
journal = {Infectious medicine},
volume = {5},
number = {2},
pages = {100260},
pmid = {42206066},
issn = {2772-431X},
abstract = {BACKGROUND: Antimicrobial resistance is a growing global public health concern, posing a serious threat to human health. This study aimed to characterize the composition and distribution of microbial communities, metal resistance genes (MRGs), antibiotic resistance genes (ARGs), and virulence factor genes (VFGs) under multi-metal stress and assess the impacts of metal and soil properties on the diversity, abundance, carrying rate (proportion of gene carriers), co-occurrence rate (proportion of microorganisms co-carrying multiple gene types), and mobility potential (MP, likelihood of horizontal gene transfer) of these genes.
METHODS: Soil samples were collected from eight sampling sites within a metal mining area (metal-contaminated soil group, MS) and four sites located more than 3 km away from the mining area (control group). Metal concentrations and physicochemical properties of the soils were measured using standard methods. Metagenomic sequencing was performed to characterize the composition and distribution of the microbiome, resistome, and virulome. Statistical modeling was applied to examine the effects of heavy metal content and soil properties on the relative abundance, co-occurrence, and mobilome potential of the three gene types.
RESULTS: Fe, V, Cr, and Cu primarily promoted the diversity, carrying rate, and co-occurrence rate of microbial communities, MRGs, ARGs, and VFGs. In contrast, Ni and Zn exhibited overall inhibitory effects. For every unit increase in Fe and V, the MP of MRGs and VFGs was associated with an increase of 3.0 × 10⁻⁵ and 1.2 × 10⁻⁵, respectively. A per 1 mg/kg increase in Cr and Cu was correlated with a decrease of 4.3 × 10⁻⁵ and 1.1 × 10⁻⁴ in the MP of ARGs and of MRGs, respectively. Positive correlations were found between the MP of plasmid‑mediated ARGs and Cr, and between transposon‑mediated ARGs and Cr/V. The MP of transposon‑mediated MRGs correlated positively with Fe, while Cu correlated negatively with plasmid‑mediated ARGs but positively with insertion sequence‑mediated ARGs. Ni concentration was positively associated with the MP of IS‑mediated VFGs.
CONCLUSIONS: Metals alter the composition and distribution of microbial communities, MRGs, ARGs, and VFGs. A key mechanism underlying this regulation is the modulation of their mobile potential, which either facilitates or restricts horizontal gene transfer.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Relationship between gestational diabetes mellitus and anxiety symptoms and gut microbiome composition in pregnant women.
Open life sciences, 21(1):20251317.
Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy associated with poor outcomes for both mother and baby. An expanding body of research highlights the gut microbiota's influence on host metabolism and neurobehavioral processes, yet how gestational diabetes mellitus, anxiety symptoms, and microbial communities interact is still unclear. To address this gap, we profiled gut-microbiome changes in pregnant women presenting with both GDM and clinically significant anxiety. A total of 120 participants were categorized into four groups: GDM with anxiety (G + A), GDM without anxiety (G + NAF), non-GDM with anxiety (NG + A), and non-GDM without anxiety (NG + NA). Stool specimens were obtained and subjected to 16S rRNA gene profiling of the V3-V4 hypervariable region using Illumina MiSeq sequencing. Results showed significant differences in fasting blood glucose between GDM and non-GDM groups. GDM groups exhibited enrichment of Enterobacteriaceae and reduction of Faecalibacterium, while anxiety groups showed increased Lactococcus and Streptococcus. The dual-exposure group (G + A) demonstrated unique enrichment of oral-derived genera (e.g., Fusobacterium and Actinomyces). Among 963 OTUs identified, 681 were core OTUs shared across groups. GDM and anxiety groups possessed 42 and 32 unique OTUs, respectively, with 26 OTUs specific to the G + A group. LEfSe analysis revealed 16 phylogenetically conserved taxa distinguishing GDM and non-GDM groups, while anxiety-positive groups were characterized by Bacilli and Negativicutes. These findings suggest that GDM and anxiety are associated with distinct gut microbiota profiles, highlighting potential microbial biomarkers for early diagnosis and intervention.
Additional Links: PMID-42206103
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@article {pmid42206103,
year = {2026},
author = {Xu, J and Cai, L and Lu, S and Chen, L and Zhang, T and Wang, J},
title = {Relationship between gestational diabetes mellitus and anxiety symptoms and gut microbiome composition in pregnant women.},
journal = {Open life sciences},
volume = {21},
number = {1},
pages = {20251317},
pmid = {42206103},
issn = {2391-5412},
abstract = {Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy associated with poor outcomes for both mother and baby. An expanding body of research highlights the gut microbiota's influence on host metabolism and neurobehavioral processes, yet how gestational diabetes mellitus, anxiety symptoms, and microbial communities interact is still unclear. To address this gap, we profiled gut-microbiome changes in pregnant women presenting with both GDM and clinically significant anxiety. A total of 120 participants were categorized into four groups: GDM with anxiety (G + A), GDM without anxiety (G + NAF), non-GDM with anxiety (NG + A), and non-GDM without anxiety (NG + NA). Stool specimens were obtained and subjected to 16S rRNA gene profiling of the V3-V4 hypervariable region using Illumina MiSeq sequencing. Results showed significant differences in fasting blood glucose between GDM and non-GDM groups. GDM groups exhibited enrichment of Enterobacteriaceae and reduction of Faecalibacterium, while anxiety groups showed increased Lactococcus and Streptococcus. The dual-exposure group (G + A) demonstrated unique enrichment of oral-derived genera (e.g., Fusobacterium and Actinomyces). Among 963 OTUs identified, 681 were core OTUs shared across groups. GDM and anxiety groups possessed 42 and 32 unique OTUs, respectively, with 26 OTUs specific to the G + A group. LEfSe analysis revealed 16 phylogenetically conserved taxa distinguishing GDM and non-GDM groups, while anxiety-positive groups were characterized by Bacilli and Negativicutes. These findings suggest that GDM and anxiety are associated with distinct gut microbiota profiles, highlighting potential microbial biomarkers for early diagnosis and intervention.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Identifying microbial biomarkers of neurodegeneration: a comparative study in Alzheimer's and Parkinson's disease.
Frontiers in microbiomes, 5:1831956.
INTRODUCTION: Neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD) have been increasingly linked to alterations of the gut microbiota, although reported microbial signatures remain heterogeneous and often lack taxonomic resolution.
METHODS: In the present study, we applied full-length 16S rRNA gene sequencing to characterize gut microbiota composition in 152 individuals, including patients with AD (n = 37), PD (n = 65), and age-matched healthy controls (n = 50), using a unified bioinformatic and statistical framework with adjustment for relevant demographic covariates.
RESULTS: Alzheimer's disease was associated with a modest but significant reduction in microbial richness and Shannon diversity compared with controls, whereas no alpha diversity differences were observed in PD. Beta diversity analyses revealed significant compositional differences across diagnostic groups, driven primarily by PD and modulated by sex but not age. Species-level differential abundance analysis identified a PD-associated microbial signature characterized by reduced abundances of short-chain fatty acid-producing bacteria, including Faecalibacterium prausnitzii, Agathobacter rectalis, Roseburia intestinalis, and Faecalicatena fissicatena, together with increased abundance of Ruminococcus sp. JE7A12. In contrast, AD exhibited minimal species-level changes, with only Bacteroidales bacterium CF showing reduced abundance compared with controls.
DISCUSSION: Overall, these findings indicate that Parkinson's disease is characterized by a targeted disruption of beneficial butyrate-producing bacteria, whereas Alzheimer's disease exhibits subtler and less consistent microbiome alterations. Our results underscore the importance of species-level resolution for identifying disease-associated microbial signatures.
Additional Links: PMID-42206189
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@article {pmid42206189,
year = {2026},
author = {De Jaegher, S and Pinzauti, D and D'Aguanno, M and Parkinson, E and Schofield, J and Strazzeri, F and Skipp, P and Penrice-Randal, R and Kunicki, A and McCausland, B and Kipps, C and Amin, J and Biazzo, M},
title = {Identifying microbial biomarkers of neurodegeneration: a comparative study in Alzheimer's and Parkinson's disease.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1831956},
pmid = {42206189},
issn = {2813-4338},
abstract = {INTRODUCTION: Neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD) have been increasingly linked to alterations of the gut microbiota, although reported microbial signatures remain heterogeneous and often lack taxonomic resolution.
METHODS: In the present study, we applied full-length 16S rRNA gene sequencing to characterize gut microbiota composition in 152 individuals, including patients with AD (n = 37), PD (n = 65), and age-matched healthy controls (n = 50), using a unified bioinformatic and statistical framework with adjustment for relevant demographic covariates.
RESULTS: Alzheimer's disease was associated with a modest but significant reduction in microbial richness and Shannon diversity compared with controls, whereas no alpha diversity differences were observed in PD. Beta diversity analyses revealed significant compositional differences across diagnostic groups, driven primarily by PD and modulated by sex but not age. Species-level differential abundance analysis identified a PD-associated microbial signature characterized by reduced abundances of short-chain fatty acid-producing bacteria, including Faecalibacterium prausnitzii, Agathobacter rectalis, Roseburia intestinalis, and Faecalicatena fissicatena, together with increased abundance of Ruminococcus sp. JE7A12. In contrast, AD exhibited minimal species-level changes, with only Bacteroidales bacterium CF showing reduced abundance compared with controls.
DISCUSSION: Overall, these findings indicate that Parkinson's disease is characterized by a targeted disruption of beneficial butyrate-producing bacteria, whereas Alzheimer's disease exhibits subtler and less consistent microbiome alterations. Our results underscore the importance of species-level resolution for identifying disease-associated microbial signatures.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Host-specific fungal plant pathogens exhibit distinct interactions with the leaf microbiota of wild grasses.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 381(1951):.
The plant's microbiome is influenced by the plant species and biotic factors such as infection by pathogens. Pathogen-microbiome interactions are relevant for disease progression since both can compete within the host. We hypothesize that pathogens specialized to different hosts have distinct, direct and indirect influence on the host microbiome. We focused on the host-specific leaf pathogens Zymoseptoria tritici and Zymoseptoria passerinii. By using microbiome metabarcoding and coculture interactions, we evaluated the influence of virulent (wild host-infecting pathogen) and avirulent (domesticated host-infecting pathogen) Zymoseptoria isolates on the leaf microbiome of the wild grasses Aegilops cylindrica and Hordeum murinum, which are hosts to virulent lineages of Z. tritici and Z. passerinii, respectively. Our microbiome analysis showed that the fungal communities were affected by virulent lineages, while the avirulent lineages had the most negative correlations with bacteria. Both virulent and avirulent pathogens had a similar spectrum of interactions when experimentally cocultured with bacteria. The intensity of pathogen-induced growth enhancement on bacteria differed between Z. tritici isolates. We demonstrated that the pathogen-secreted invertases can be a determinant of bacterial growth enhancement. Our study illustrates the extent of specificity in pathogen-microbe coexistence and suggests an interaction mechanism that may influence in planta interactions. This article is part of the theme issue 'Wild plant pathosystems'.
Additional Links: PMID-42206330
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@article {pmid42206330,
year = {2026},
author = {Flores-Núñez, VM and Dal'Sasso, TCS and Hansen, M and Reinhardt, G and Braun, S and Stukenbrock, EH},
title = {Host-specific fungal plant pathogens exhibit distinct interactions with the leaf microbiota of wild grasses.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1951},
pages = {},
doi = {10.1098/rstb.2025.0112},
pmid = {42206330},
issn = {1471-2970},
support = {//ERC consolidator grant FungalSecrets/ ; },
mesh = {*Ascomycota/physiology/pathogenicity ; *Plant Leaves/microbiology ; *Microbiota ; *Host-Pathogen Interactions ; *Plant Diseases/microbiology ; *Aegilops/microbiology ; *Hordeum/microbiology ; },
abstract = {The plant's microbiome is influenced by the plant species and biotic factors such as infection by pathogens. Pathogen-microbiome interactions are relevant for disease progression since both can compete within the host. We hypothesize that pathogens specialized to different hosts have distinct, direct and indirect influence on the host microbiome. We focused on the host-specific leaf pathogens Zymoseptoria tritici and Zymoseptoria passerinii. By using microbiome metabarcoding and coculture interactions, we evaluated the influence of virulent (wild host-infecting pathogen) and avirulent (domesticated host-infecting pathogen) Zymoseptoria isolates on the leaf microbiome of the wild grasses Aegilops cylindrica and Hordeum murinum, which are hosts to virulent lineages of Z. tritici and Z. passerinii, respectively. Our microbiome analysis showed that the fungal communities were affected by virulent lineages, while the avirulent lineages had the most negative correlations with bacteria. Both virulent and avirulent pathogens had a similar spectrum of interactions when experimentally cocultured with bacteria. The intensity of pathogen-induced growth enhancement on bacteria differed between Z. tritici isolates. We demonstrated that the pathogen-secreted invertases can be a determinant of bacterial growth enhancement. Our study illustrates the extent of specificity in pathogen-microbe coexistence and suggests an interaction mechanism that may influence in planta interactions. This article is part of the theme issue 'Wild plant pathosystems'.},
}
MeSH Terms:
show MeSH Terms
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*Ascomycota/physiology/pathogenicity
*Plant Leaves/microbiology
*Microbiota
*Host-Pathogen Interactions
*Plant Diseases/microbiology
*Aegilops/microbiology
*Hordeum/microbiology
RevDate: 2026-05-28
CmpDate: 2026-05-28
Foliar pathogens and drought drive plant-soil feedback between two co-occurring herbaceous plant species.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 381(1951):.
Plants alter soil biotic and abiotic properties with consequences for plant community dynamics at local and global scales, but how plant-soil interactions are affected by other environmental and biotic interactions remains poorly understood. We performed a fully reciprocal plant-soil feedback (PSF) experiment between two herbaceous plants, Monarda fistulosa and Plantago lanceolata, and tested how PSFs were influenced by drought and foliar powdery mildew pathogen infection. We observed significant negative feedbacks between the two plant species, but only when plants were grown with live soil biota and infected with powdery mildew. The strongest feedback was observed under both foliar infection and drought. High-throughput sequencing of soil fungi and bacteria from the treatment groups with foliar infection and drought revealed that both fungal and bacterial community composition were influenced by soil condition (live versus sterile) and soil training (Monarda versus Plantago). Together, our results indicate that the observed negative PSF was driven by foliar pathogens and plant species-specific soil microbial communities and intensified by drought. Our study suggests that PSF can be sensitive to both aboveground plant-pathogen interactions and climatic factors, improving our understanding of microbial impacts on plant community dynamics. This article is part of the theme issue 'Wild plant pathosystems'.
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@article {pmid42206333,
year = {2026},
author = {Tanford, P and Vargas, RC and Bugay, MJ and Dantas, G and Stein, C and Penczykowski, RM and Mangan, SA},
title = {Foliar pathogens and drought drive plant-soil feedback between two co-occurring herbaceous plant species.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1951},
pages = {},
doi = {10.1098/rstb.2025.0115},
pmid = {42206333},
issn = {1471-2970},
support = {//Washington University in St. Louis InCEES/ ; //Directorate for Biological Sciences/ ; },
mesh = {*Soil Microbiology ; *Droughts ; *Plantago/microbiology/physiology ; *Ascomycota/physiology ; *Plant Diseases/microbiology ; Soil/chemistry ; *Microbiota ; Plant Leaves/microbiology ; *Host-Pathogen Interactions ; },
abstract = {Plants alter soil biotic and abiotic properties with consequences for plant community dynamics at local and global scales, but how plant-soil interactions are affected by other environmental and biotic interactions remains poorly understood. We performed a fully reciprocal plant-soil feedback (PSF) experiment between two herbaceous plants, Monarda fistulosa and Plantago lanceolata, and tested how PSFs were influenced by drought and foliar powdery mildew pathogen infection. We observed significant negative feedbacks between the two plant species, but only when plants were grown with live soil biota and infected with powdery mildew. The strongest feedback was observed under both foliar infection and drought. High-throughput sequencing of soil fungi and bacteria from the treatment groups with foliar infection and drought revealed that both fungal and bacterial community composition were influenced by soil condition (live versus sterile) and soil training (Monarda versus Plantago). Together, our results indicate that the observed negative PSF was driven by foliar pathogens and plant species-specific soil microbial communities and intensified by drought. Our study suggests that PSF can be sensitive to both aboveground plant-pathogen interactions and climatic factors, improving our understanding of microbial impacts on plant community dynamics. This article is part of the theme issue 'Wild plant pathosystems'.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Soil Microbiology
*Droughts
*Plantago/microbiology/physiology
*Ascomycota/physiology
*Plant Diseases/microbiology
Soil/chemistry
*Microbiota
Plant Leaves/microbiology
*Host-Pathogen Interactions
RevDate: 2026-05-28
CmpDate: 2026-05-28
Seasonality, land use and plant community diversity shape microbiome-pathogen interactions in wild populations of Arabidopsis thaliana.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 381(1951):.
The microbiome often protects plants against pathogens, but most findings are limited to controlled experiments in the lab. In the context of wild populations, one key challenge is to understand sources of variation that impact the commensal microbiome, which in turn shapes the degree of protection. Here, we surveyed both disease symptoms and microbiomes from wild populations of Arabidopsis thaliana over four consecutive seasons (Autumn/Spring) across three different land use types. Land use types varied in the extent of anthropogenic influences and included forest meadows, human-impacted fields adjacent to agriculture or municipal parks and highly disturbed habitats near railroad tracks. By building an integrative map of abiotic and biotic variables, we find that a key predictor of disease was biodiversity across ecological scales. Plant communities with higher diversity were associated with increased microbial diversity and reduced disease burden in A. thaliana populations, particularly in the Spring. However, the diversity-microbiome-disease relationships were all sensitive to season and further modulated by land use. Taken together, our work highlights the importance of anthropogenic change reshaping species interactions across ecological scales to impact disease risk in wild plant populations. This article is part of the theme issue 'Wild plant pathosystems'.
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@article {pmid42206334,
year = {2026},
author = {Henry, L and Rat, A and Laderman, E and Lion, R and Mayjonade, B and Team Pathocom, and Roux, F and Weigel, D and Bergelson, J},
title = {Seasonality, land use and plant community diversity shape microbiome-pathogen interactions in wild populations of Arabidopsis thaliana.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1951},
pages = {},
doi = {10.1098/rstb.2025.0116},
pmid = {42206334},
issn = {1471-2970},
support = {//Simons Foundation/ ; /ERC_/European Research Council/International ; //Charles H. Revson Foundation/ ; },
mesh = {*Arabidopsis/microbiology/physiology ; *Microbiota ; Seasons ; *Plant Diseases/microbiology ; *Biodiversity ; *Host-Pathogen Interactions ; },
abstract = {The microbiome often protects plants against pathogens, but most findings are limited to controlled experiments in the lab. In the context of wild populations, one key challenge is to understand sources of variation that impact the commensal microbiome, which in turn shapes the degree of protection. Here, we surveyed both disease symptoms and microbiomes from wild populations of Arabidopsis thaliana over four consecutive seasons (Autumn/Spring) across three different land use types. Land use types varied in the extent of anthropogenic influences and included forest meadows, human-impacted fields adjacent to agriculture or municipal parks and highly disturbed habitats near railroad tracks. By building an integrative map of abiotic and biotic variables, we find that a key predictor of disease was biodiversity across ecological scales. Plant communities with higher diversity were associated with increased microbial diversity and reduced disease burden in A. thaliana populations, particularly in the Spring. However, the diversity-microbiome-disease relationships were all sensitive to season and further modulated by land use. Taken together, our work highlights the importance of anthropogenic change reshaping species interactions across ecological scales to impact disease risk in wild plant populations. This article is part of the theme issue 'Wild plant pathosystems'.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Arabidopsis/microbiology/physiology
*Microbiota
Seasons
*Plant Diseases/microbiology
*Biodiversity
*Host-Pathogen Interactions
RevDate: 2026-05-29
CmpDate: 2026-05-28
Yeast species interactions and composition modulate leaf rust severity in Populus trichocarpa.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 381(1951):.
Plant microbiomes are recognized for increasing defence against pathogens. Yet, identifying the role of beneficial microbes beyond their individual effects remains poorly explored. In a series of in planta greenhouse experiments, we tested the effects of individual foliar yeasts, yeast interactions and the combination of yeast richness and diversity on disease severity caused by the leaf rust pathogen Melampsora × columbiana in the model tree, Populus trichocarpa. We found that single yeasts can either antagonize or facilitate the rust; nevertheless, most yeasts did not modify disease severity. For some individual disease-modifying yeasts, interactions with additional yeasts changed the outcome of disease severity. In one case, a rust facilitator was neutralized by other interacting yeasts; in another, increasing richness in communities containing a rust antagonist was associated with increasing disease severity. However, we did not find evidence for a positive or negative relationship between yeast richness or diversity and disease severity overall. A follow-up in vitro experiment showed strong interspecific competition between yeasts, which might explain changes in disease severity with varying community membership. Our results highlight the role of microbial interactions and composition for plant disease severity, yet caution against interpreting plant microbiome richness or diversity as inherently disease protective. This article is part of the theme issue 'Wild plant pathosystems'.
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@article {pmid42206338,
year = {2026},
author = {Romero-Jiménez, MJ and Pérez-Pazos, E and Leopold, DR and Lebeis, SL and Busby, PE},
title = {Yeast species interactions and composition modulate leaf rust severity in Populus trichocarpa.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1951},
pages = {},
doi = {10.1098/rstb.2025.0121},
pmid = {42206338},
issn = {1471-2970},
support = {//Division of Integrative Organismal Systems/ ; //National Institute of Food and Agriculture/ ; //Agricultural Research Service/ ; },
mesh = {*Populus/microbiology ; *Plant Diseases/microbiology ; *Basidiomycota/physiology ; *Yeasts/physiology ; Plant Leaves/microbiology ; *Microbiota ; *Microbial Interactions ; },
abstract = {Plant microbiomes are recognized for increasing defence against pathogens. Yet, identifying the role of beneficial microbes beyond their individual effects remains poorly explored. In a series of in planta greenhouse experiments, we tested the effects of individual foliar yeasts, yeast interactions and the combination of yeast richness and diversity on disease severity caused by the leaf rust pathogen Melampsora × columbiana in the model tree, Populus trichocarpa. We found that single yeasts can either antagonize or facilitate the rust; nevertheless, most yeasts did not modify disease severity. For some individual disease-modifying yeasts, interactions with additional yeasts changed the outcome of disease severity. In one case, a rust facilitator was neutralized by other interacting yeasts; in another, increasing richness in communities containing a rust antagonist was associated with increasing disease severity. However, we did not find evidence for a positive or negative relationship between yeast richness or diversity and disease severity overall. A follow-up in vitro experiment showed strong interspecific competition between yeasts, which might explain changes in disease severity with varying community membership. Our results highlight the role of microbial interactions and composition for plant disease severity, yet caution against interpreting plant microbiome richness or diversity as inherently disease protective. This article is part of the theme issue 'Wild plant pathosystems'.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Populus/microbiology
*Plant Diseases/microbiology
*Basidiomycota/physiology
*Yeasts/physiology
Plant Leaves/microbiology
*Microbiota
*Microbial Interactions
RevDate: 2026-05-28
Gut Microbiome Differences Between Early Alzheimer Disease and Idiopathic Normal Pressure Hydrocephalus.
Alzheimer disease and associated disorders pii:00002093-990000000-00206 [Epub ahead of print].
BACKGROUND: Alzheimer disease (AD) and idiopathic normal pressure hydrocephalus (iNPH) are neurodegenerative diseases causing memory decline. Previous studies have demonstrated an altered gut microbiome (GM) in both conditions. In this study, we compared the GM composition between the groups to find out how if the GM composition differed between the cognitively healthy individuals (CO) and AD groups, as well as between the AD and iNPH groups.
METHODS: Thirty-seven CO participants, 21 mild AD patients and 10 participants with shunted iNPH gave fecal samples, which were subjected to 16S amplicon sequencing. Then, genus-level differences were analyzed. Information about comorbidities and diet was collected, and cognitive function was evaluated.
RESULTS: Compared with the CO group, Anaerovorax and an unknown genus of the Comamonadaceae family increased, whereas Enterobacter, Absicoccus, Buttiauxella, Raoultella, and Lacticaseibacillus decreased in the AD group. Compared with the iNPH group, Paramuribaculum, an unknown genus of the Desulfovibrionaceae family, Ruficoccus and Mitsuokella increased, whereas Anaeromassilibacillus and Desulfovibrio decreased in the AD group.
CONCLUSIONS: We demonstrated differences in the GM composition between the AD and CO groups, as well as between the AD and iNPH groups. To our knowledge, this is the first report to compare the 2 neurodegenerative diseases and demonstrate GM differences.
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@article {pmid42206504,
year = {2026},
author = {Brandt, E and Koivisto, A and Pereira, P and Mustanoja, E and Auvinen, P and Saari, T and Rusanen, M and Leinonen, V and Scheperjans, F and Kärkkäinen, V},
title = {Gut Microbiome Differences Between Early Alzheimer Disease and Idiopathic Normal Pressure Hydrocephalus.},
journal = {Alzheimer disease and associated disorders},
volume = {},
number = {},
pages = {},
doi = {10.1097/WAD.0000000000000726},
pmid = {42206504},
issn = {1546-4156},
abstract = {BACKGROUND: Alzheimer disease (AD) and idiopathic normal pressure hydrocephalus (iNPH) are neurodegenerative diseases causing memory decline. Previous studies have demonstrated an altered gut microbiome (GM) in both conditions. In this study, we compared the GM composition between the groups to find out how if the GM composition differed between the cognitively healthy individuals (CO) and AD groups, as well as between the AD and iNPH groups.
METHODS: Thirty-seven CO participants, 21 mild AD patients and 10 participants with shunted iNPH gave fecal samples, which were subjected to 16S amplicon sequencing. Then, genus-level differences were analyzed. Information about comorbidities and diet was collected, and cognitive function was evaluated.
RESULTS: Compared with the CO group, Anaerovorax and an unknown genus of the Comamonadaceae family increased, whereas Enterobacter, Absicoccus, Buttiauxella, Raoultella, and Lacticaseibacillus decreased in the AD group. Compared with the iNPH group, Paramuribaculum, an unknown genus of the Desulfovibrionaceae family, Ruficoccus and Mitsuokella increased, whereas Anaeromassilibacillus and Desulfovibrio decreased in the AD group.
CONCLUSIONS: We demonstrated differences in the GM composition between the AD and CO groups, as well as between the AD and iNPH groups. To our knowledge, this is the first report to compare the 2 neurodegenerative diseases and demonstrate GM differences.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Dereplication-assisted culturomics enables strain-level ecological analysis of the human gut microbiome.
Gut microbes, 18(1):2681840.
Recent advances in culturomics have enabled large-scale recovery of microbial isolates from the human gut, generating extensive culture collections that bridge metagenomic predictions and experimental validation. However, these isolate resources remain largely underutilized, as conventional culturomics prioritizes the discovery of novel species while massive collections of commensal isolates persist as unexplored biological datasets. Dereplication, particularly based on MALDI-TOF MS spectral features, has been largely regarded as a logistical tool for managing redundancy rather than an analytical asset. Here, we reposition dereplication as an analytical framework for interpreting large-scale culturomics datasets and resolving strain-level ecological patterns. We applied the SPeDE pipeline to a comprehensive collection of 2,231 isolates, including Bifidobacterium spp. and Enterococcus faecium, recovered from healthy donor feces. Spectrum-derived operational isolation units (OIUs) revealed host-associated strain-level repertoires and lineage-like clustering within species. Notably, distinct spectral clusters observed in E. faecium corresponded to clade-level patterns identified through shotgun metagenomic analysis. These findings demonstrate that dereplication-assisted culturomics can extend beyond redundancy control to enable high-resolution ecological interpretation of cultured microbiome datasets. By reframing dereplication as a bridge between large-scale isolate generation and strain-level microbiome ecology, this study outlines a conceptual and practical direction for the next phase of human microbiome research in the post-culturomics era.
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@article {pmid42206586,
year = {2026},
author = {Yeo, S and Park, H},
title = {Dereplication-assisted culturomics enables strain-level ecological analysis of the human gut microbiome.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2681840},
doi = {10.1080/19490976.2026.2681840},
pmid = {42206586},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; Feces/microbiology ; *Enterococcus faecium/isolation & purification/classification/genetics ; Metagenomics/methods ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; *Bifidobacterium/isolation & purification/classification/genetics ; },
abstract = {Recent advances in culturomics have enabled large-scale recovery of microbial isolates from the human gut, generating extensive culture collections that bridge metagenomic predictions and experimental validation. However, these isolate resources remain largely underutilized, as conventional culturomics prioritizes the discovery of novel species while massive collections of commensal isolates persist as unexplored biological datasets. Dereplication, particularly based on MALDI-TOF MS spectral features, has been largely regarded as a logistical tool for managing redundancy rather than an analytical asset. Here, we reposition dereplication as an analytical framework for interpreting large-scale culturomics datasets and resolving strain-level ecological patterns. We applied the SPeDE pipeline to a comprehensive collection of 2,231 isolates, including Bifidobacterium spp. and Enterococcus faecium, recovered from healthy donor feces. Spectrum-derived operational isolation units (OIUs) revealed host-associated strain-level repertoires and lineage-like clustering within species. Notably, distinct spectral clusters observed in E. faecium corresponded to clade-level patterns identified through shotgun metagenomic analysis. These findings demonstrate that dereplication-assisted culturomics can extend beyond redundancy control to enable high-resolution ecological interpretation of cultured microbiome datasets. By reframing dereplication as a bridge between large-scale isolate generation and strain-level microbiome ecology, this study outlines a conceptual and practical direction for the next phase of human microbiome research in the post-culturomics era.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
Feces/microbiology
*Enterococcus faecium/isolation & purification/classification/genetics
Metagenomics/methods
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
*Bifidobacterium/isolation & purification/classification/genetics
RevDate: 2026-05-28
High-throughput microbiome profiling and co-occurrence with antibiotic resistance genes in Lucilia sericata.
FEMS microbiology letters pii:8697350 [Epub ahead of print].
Blow flies such as Lucilia sericata (Diptera: Calliphoridae) serve important ecological functions as decomposers. However, due to their close association with decaying organic matter, they also play potential roles as reservoirs of pathogenic bacteria and antimicrobial resistance genes (ARGs). In this study, we characterized the bacterial communities and targeted key antibacterial resistance markers of L. sericata specimens using 16S rRNA gene metabarcoding and targeted PCR screening. The microbiome was dominated by Dysgonomonas, Vagococcus, Pseudomonas, Ignatzschineria, and Providencia with geographic variation in community structure. Flies from Chungnam exhibited the lowest microbial diversity, while samples from Jeonnam and Gyeonggi showed greater richness and evenness. Beta diversity analyses confirmed geographic structuring of bacterial communities, with semi-urban and rural locations harboring more diverse taxa. Notably, opportunistic pathogens such as Proteus mirabilis and Providencia were detected alongside a range of ARGs (blaTEM, ermB, sul1, aac(6')-Ib-cr, cat and mecA) and integron elements (intI and intII), suggesting that L. sericata may act as a reservoir of clinically important microbes and resistance genes.
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@article {pmid42206818,
year = {2026},
author = {Shatta, A and Chavarria, X and Choi, JH and Oh, S and Kim, M and Kang, D and Cho, YH and Choi, DY and Yi, MH and Kim, JY},
title = {High-throughput microbiome profiling and co-occurrence with antibiotic resistance genes in Lucilia sericata.},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnag063},
pmid = {42206818},
issn = {1574-6968},
abstract = {Blow flies such as Lucilia sericata (Diptera: Calliphoridae) serve important ecological functions as decomposers. However, due to their close association with decaying organic matter, they also play potential roles as reservoirs of pathogenic bacteria and antimicrobial resistance genes (ARGs). In this study, we characterized the bacterial communities and targeted key antibacterial resistance markers of L. sericata specimens using 16S rRNA gene metabarcoding and targeted PCR screening. The microbiome was dominated by Dysgonomonas, Vagococcus, Pseudomonas, Ignatzschineria, and Providencia with geographic variation in community structure. Flies from Chungnam exhibited the lowest microbial diversity, while samples from Jeonnam and Gyeonggi showed greater richness and evenness. Beta diversity analyses confirmed geographic structuring of bacterial communities, with semi-urban and rural locations harboring more diverse taxa. Notably, opportunistic pathogens such as Proteus mirabilis and Providencia were detected alongside a range of ARGs (blaTEM, ermB, sul1, aac(6')-Ib-cr, cat and mecA) and integron elements (intI and intII), suggesting that L. sericata may act as a reservoir of clinically important microbes and resistance genes.},
}
RevDate: 2026-05-28
Early-life proteomic and microbiome features signal obesity risk across 26 years of follow-up.
mSystems [Epub ahead of print].
UNLABELLED: Childhood obesity is rising globally. Yet, few studies have examined the microbiome and proteome in early childhood in relation to this outcome, and most are cross-sectional by design. Early-life factors in the ABIS birth cohort (n = 16,683) were associated with obesity up to age 26 (mean follow-up 25.3 years, range 23.7-26.5 years): psychosocial stressors, smoking, infections, and diet in the first year. We assessed biomarkers, including cord blood metabolome (n = 290) and proteome (n = 358), by liquid chromatography, mass spectrometry, and Olink. Gut microbial composition at age one (n = 1,743) was assessed using stool samples and 16S rRNA sequencing. In this prospective longitudinal cohort study, significant differences were found in infants with future obesity, including elevated angiopoietin-like 4 (ANGPTL4), follistatin, and hepatocyte growth factor (independently of maternal weight) and reduced isocaproic acid, tryptophan, and oleic acid, with prenatal mediation. Akkermansia, asaccharolytic bacteria (Phascolarctobacterium and Senegalimassiliensia), and equol-producers (Adlercreutzia and Slackia) were depleted. Machine learning models selecting 40 most predictive features showed long-term prediction from birth proteomics and bacterial taxa at age one (area under the curve [AUC] = 0.83 ± .05, n = 1,877) and additional metrics, for example, parental and child body mass index in the first 8 years (AUC = 0.89 ± .02, n = 1,877), suggesting durable biological encoding. Proteomic markers across folds included fibroblast growth factor 19, ANGPTL4, sulfotransferase family 2A member 1, and interleukin 20. These findings suggest clinically relevant biomarkers indicating early-life regulation of bile acid metabolism, lipid storage vs. oxidation, and immune-metabolic signaling and pathways to prospectively prevent childhood- and adult-onset obesity across a 26-year predictive gap.
IMPORTANCE: Understanding the origins of obesity is critical for developing preventive strategies, and early life represents a particularly sensitive window. This study leverages a large, general-population cohort with prospectively collected data, including parental body mass index (BMI), cord blood proteomics, and the gut microbiome at age one, linked to obesity outcomes over 26 years. Using integrated machine learning models, we show that in addition to parental BMI, specific proteomic and microbial markers present in infancy can predict long-term obesity risk, highlighting the role of early metabolic programming. Several key markers point to bile acid signaling as a mechanism connecting early microbiome development with fat accumulation and insulin regulation. By identifying these early-life predictors long before obesity manifests, these results provide new insights into intergenerational risk and suggest measurable targets for preventing obesity and related metabolic disorders from the earliest stages of life.
Additional Links: PMID-42206849
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@article {pmid42206849,
year = {2026},
author = {Ahrens, AP and Dias, R and Hyötyläinen, T and White, PA and Orešič, M and Triplett, EW and Ludvigsson, J},
title = {Early-life proteomic and microbiome features signal obesity risk across 26 years of follow-up.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0142425},
doi = {10.1128/msystems.01424-25},
pmid = {42206849},
issn = {2379-5077},
abstract = {UNLABELLED: Childhood obesity is rising globally. Yet, few studies have examined the microbiome and proteome in early childhood in relation to this outcome, and most are cross-sectional by design. Early-life factors in the ABIS birth cohort (n = 16,683) were associated with obesity up to age 26 (mean follow-up 25.3 years, range 23.7-26.5 years): psychosocial stressors, smoking, infections, and diet in the first year. We assessed biomarkers, including cord blood metabolome (n = 290) and proteome (n = 358), by liquid chromatography, mass spectrometry, and Olink. Gut microbial composition at age one (n = 1,743) was assessed using stool samples and 16S rRNA sequencing. In this prospective longitudinal cohort study, significant differences were found in infants with future obesity, including elevated angiopoietin-like 4 (ANGPTL4), follistatin, and hepatocyte growth factor (independently of maternal weight) and reduced isocaproic acid, tryptophan, and oleic acid, with prenatal mediation. Akkermansia, asaccharolytic bacteria (Phascolarctobacterium and Senegalimassiliensia), and equol-producers (Adlercreutzia and Slackia) were depleted. Machine learning models selecting 40 most predictive features showed long-term prediction from birth proteomics and bacterial taxa at age one (area under the curve [AUC] = 0.83 ± .05, n = 1,877) and additional metrics, for example, parental and child body mass index in the first 8 years (AUC = 0.89 ± .02, n = 1,877), suggesting durable biological encoding. Proteomic markers across folds included fibroblast growth factor 19, ANGPTL4, sulfotransferase family 2A member 1, and interleukin 20. These findings suggest clinically relevant biomarkers indicating early-life regulation of bile acid metabolism, lipid storage vs. oxidation, and immune-metabolic signaling and pathways to prospectively prevent childhood- and adult-onset obesity across a 26-year predictive gap.
IMPORTANCE: Understanding the origins of obesity is critical for developing preventive strategies, and early life represents a particularly sensitive window. This study leverages a large, general-population cohort with prospectively collected data, including parental body mass index (BMI), cord blood proteomics, and the gut microbiome at age one, linked to obesity outcomes over 26 years. Using integrated machine learning models, we show that in addition to parental BMI, specific proteomic and microbial markers present in infancy can predict long-term obesity risk, highlighting the role of early metabolic programming. Several key markers point to bile acid signaling as a mechanism connecting early microbiome development with fat accumulation and insulin regulation. By identifying these early-life predictors long before obesity manifests, these results provide new insights into intergenerational risk and suggest measurable targets for preventing obesity and related metabolic disorders from the earliest stages of life.},
}
RevDate: 2026-05-28
Shotgun metagenomics and metatranscriptomics of soil microbial communities under monoculture and polyculture cover crops.
Microbiology resource announcements [Epub ahead of print].
Here, we present 30 metagenomes, 21 metatranscriptomes, and 334 metagenome-assembled genomes collected from soils under different cover crop species. This data set will be useful for studying microbial interactions, especially functional redundancy, with relevance to agricultural management and sustainability.
Additional Links: PMID-42207032
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@article {pmid42207032,
year = {2026},
author = {Giani, N and John, J and Campbell, B},
title = {Shotgun metagenomics and metatranscriptomics of soil microbial communities under monoculture and polyculture cover crops.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0030926},
doi = {10.1128/mra.00309-26},
pmid = {42207032},
issn = {2576-098X},
abstract = {Here, we present 30 metagenomes, 21 metatranscriptomes, and 334 metagenome-assembled genomes collected from soils under different cover crop species. This data set will be useful for studying microbial interactions, especially functional redundancy, with relevance to agricultural management and sustainability.},
}
RevDate: 2026-05-28
CHD-18g-modulated Pseudomonas taxa support poplar salt tolerance.
The ISME journal pii:8697384 [Epub ahead of print].
Against the background of global climate change, soil salinization has emerged as a major abiotic stressor constraining agroforestry productivity worldwide. Root-recruited microbes enhance plant stress resilience, and host-microbe interactions depend on plant root metabolism. Stress-tolerant plant genotypes exhibit a marked capacity to enrich beneficial root-associated microbes through specialized metabolic responses, thereby facilitating phenotypic plasticity. However, the molecular mechanisms underlying these plant-microbe interactions remain unclear. In this study, we compared salt tolerance among three poplar varieties under aseptic and non-aseptic conditions, and analyzed their rhizosphere bacterial community responses to salt stress. We found that microbial inoculation modulated poplar salt tolerance, and poplar shaped rhizosphere bacterial communities in a genotype-dependent manner. Transcriptome sequencing and targeted metabolomic analysis indicated that salt-tolerant poplar plants preferentially activate the phenylpropanoid biosynthesis pathway, accompanied by the enhanced root secretion of benzoic acid (BA) and salicylic acid (SA) and up-regulation of CHD-18g encoding cinnamoyl-CoA hydratase/dehydrogenase. Overexpression of CHD-18g increased rhizosphere Pseudomonas abundance by enhancing BA and SA biosynthesis. Binary interaction assays further showed that the BA-induced Pseudomonas taxa mitigated salt stress and promoted poplar growth under salt stress. Our findings propose a framework linking host gene expression, root metabolism, and key microbial taxa in conferring salt tolerance. This work uncovers a metabolic signaling mechanism by which trees shape their root microbiome to enhance stress adaptation, offering actionable genetic and ecological strategies for improving tree resilience in sustainable agroforestry systems.
Additional Links: PMID-42207174
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PubMed:
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@article {pmid42207174,
year = {2026},
author = {Liao, Y and Zhang, Q and Zheng, J and Zhang, J and Dai, T and Zhu, F and Carrión, VJ and Delgado-Baquerizo, M and Sonne, C and Cao, F and Li, X},
title = {CHD-18g-modulated Pseudomonas taxa support poplar salt tolerance.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag138},
pmid = {42207174},
issn = {1751-7370},
abstract = {Against the background of global climate change, soil salinization has emerged as a major abiotic stressor constraining agroforestry productivity worldwide. Root-recruited microbes enhance plant stress resilience, and host-microbe interactions depend on plant root metabolism. Stress-tolerant plant genotypes exhibit a marked capacity to enrich beneficial root-associated microbes through specialized metabolic responses, thereby facilitating phenotypic plasticity. However, the molecular mechanisms underlying these plant-microbe interactions remain unclear. In this study, we compared salt tolerance among three poplar varieties under aseptic and non-aseptic conditions, and analyzed their rhizosphere bacterial community responses to salt stress. We found that microbial inoculation modulated poplar salt tolerance, and poplar shaped rhizosphere bacterial communities in a genotype-dependent manner. Transcriptome sequencing and targeted metabolomic analysis indicated that salt-tolerant poplar plants preferentially activate the phenylpropanoid biosynthesis pathway, accompanied by the enhanced root secretion of benzoic acid (BA) and salicylic acid (SA) and up-regulation of CHD-18g encoding cinnamoyl-CoA hydratase/dehydrogenase. Overexpression of CHD-18g increased rhizosphere Pseudomonas abundance by enhancing BA and SA biosynthesis. Binary interaction assays further showed that the BA-induced Pseudomonas taxa mitigated salt stress and promoted poplar growth under salt stress. Our findings propose a framework linking host gene expression, root metabolism, and key microbial taxa in conferring salt tolerance. This work uncovers a metabolic signaling mechanism by which trees shape their root microbiome to enhance stress adaptation, offering actionable genetic and ecological strategies for improving tree resilience in sustainable agroforestry systems.},
}
RevDate: 2026-05-28
CmpDate: 2026-05-28
Intestinal microbiome in necrotic enteritis infection of broiler and comparison of treatment alternatives.
Tropical animal health and production, 58(5):.
Clostridium perfringens is the primary causative agent of necrotic enteritis (NE), a gastrointestinal disease that leads to substantial economic losses in poultry. This study aims to characterize the intestinal microbiome of chickens and assess the effects of Bacillus velezensis on gut microbiota and recovery from necrotic enteritis, comparing its efficacy to antibiotic treatment. The experiment involved five groups, each consisting of 16 chickens. The first group, the start-of-challenge (DB) group, included day-old chicks. The second group, the post-challenge control (DS) group, was reared until the end of the trial. The third group was infected with C. perfringens (NE group). The fourth group received both C. perfringens and B. velezensis (BV group), while the fifth group was treated with C. perfringens and amoxicillin (AB group). All chickens were euthanized via cervical dislocation following the experimental infection. Fecal samples collected from the cecum underwent 16 S rRNA gene-based metagenomic analysis, and the resulting data were statistically evaluated. Macroscopic examination after euthanasia revealed pathological changes in the intestines of chickens in the NE group, which had received only C. perfringens. Their intestines appeared swollen, with slight mild mucosal hemorrhage. In contrast, no macroscopic lesions were observed in the DB, DS, BV, or AB groups. Microbiome analysis showed a decline in microbial diversity within the NE group. The BV group exhibited a microbial composition most similar to that of healthy animals, followed by the AB group. The study concludes that B. velezensis could serve as an alternative to prophylactic antibiotics in mitigating the adverse effects of necrotic enteritis on the gut microbiome.
Additional Links: PMID-42207344
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@article {pmid42207344,
year = {2026},
author = {Cagirgan, OY and Korkmaz, S and Diker, KS},
title = {Intestinal microbiome in necrotic enteritis infection of broiler and comparison of treatment alternatives.},
journal = {Tropical animal health and production},
volume = {58},
number = {5},
pages = {},
pmid = {42207344},
issn = {1573-7438},
support = {VTF-190002//Bilimsel Araştırma Projeleri Birimi, Aydın Adnan Menderes Üniversitesi/ ; },
mesh = {Animals ; *Chickens/microbiology ; *Clostridium Infections/veterinary/microbiology/drug therapy ; *Poultry Diseases/microbiology/drug therapy ; *Enteritis/veterinary/microbiology/drug therapy ; Clostridium perfringens/physiology ; Anti-Bacterial Agents/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; *Bacillus/physiology ; *Probiotics/administration & dosage ; Amoxicillin/therapeutic use/administration & dosage ; Necrosis/veterinary/microbiology ; Male ; },
abstract = {Clostridium perfringens is the primary causative agent of necrotic enteritis (NE), a gastrointestinal disease that leads to substantial economic losses in poultry. This study aims to characterize the intestinal microbiome of chickens and assess the effects of Bacillus velezensis on gut microbiota and recovery from necrotic enteritis, comparing its efficacy to antibiotic treatment. The experiment involved five groups, each consisting of 16 chickens. The first group, the start-of-challenge (DB) group, included day-old chicks. The second group, the post-challenge control (DS) group, was reared until the end of the trial. The third group was infected with C. perfringens (NE group). The fourth group received both C. perfringens and B. velezensis (BV group), while the fifth group was treated with C. perfringens and amoxicillin (AB group). All chickens were euthanized via cervical dislocation following the experimental infection. Fecal samples collected from the cecum underwent 16 S rRNA gene-based metagenomic analysis, and the resulting data were statistically evaluated. Macroscopic examination after euthanasia revealed pathological changes in the intestines of chickens in the NE group, which had received only C. perfringens. Their intestines appeared swollen, with slight mild mucosal hemorrhage. In contrast, no macroscopic lesions were observed in the DB, DS, BV, or AB groups. Microbiome analysis showed a decline in microbial diversity within the NE group. The BV group exhibited a microbial composition most similar to that of healthy animals, followed by the AB group. The study concludes that B. velezensis could serve as an alternative to prophylactic antibiotics in mitigating the adverse effects of necrotic enteritis on the gut microbiome.},
}
MeSH Terms:
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Animals
*Chickens/microbiology
*Clostridium Infections/veterinary/microbiology/drug therapy
*Poultry Diseases/microbiology/drug therapy
*Enteritis/veterinary/microbiology/drug therapy
Clostridium perfringens/physiology
Anti-Bacterial Agents/therapeutic use
*Gastrointestinal Microbiome/drug effects
*Bacillus/physiology
*Probiotics/administration & dosage
Amoxicillin/therapeutic use/administration & dosage
Necrosis/veterinary/microbiology
Male
RevDate: 2026-05-28
CmpDate: 2026-05-28
Targeting Gut Microbiota by DPP-4 Inhibitors in Obesity: Mechanistic Insights and Therapeutic Implications.
Current nutrition reports, 15(1):.
PURPOSE OF REVIEW: Obesity is a complex metabolic disorder driven by factors such as chronic inflammation, insulin resistance, and significant alterations in the gut microbiota. Dipeptidyl peptidase-4 (DPP-4), an enzyme primarily known for inactivating incretin hormones like glucagon-like peptide-1 (GLP-1), is now recognized as a critical link between metabolic dysfunction and gut microbiome dysbiosis. This review aims to examine the mechanistic role of DPP-4 and its inhibitors in obesity, specifically focusing on how they modulate the gut microbiome to influence host energy balance and metabolic health.
RECENT FINDINGS: Recent experimental and clinical evidence indicates that DPP-4 activity contributes to obesity by influencing microbial composition, diversity, and function. Studies demonstrate that DPP-4 inhibitors can reshape the gut microbiota by reducing dysbiosis, decreasing the Firmicutes-to-Bacteroidetes ratio, and enhancing the production of short-chain fatty acids (SCFAs). Furthermore, these inhibitors improve gut barrier integrity and regulate bile acid metabolism, which helps attenuate systemic inflammation and restore insulin sensitivity. While DPP-4 inhibitors are often weight-neutral in clinical settings, they appear to assist in maintaining metabolic stability by enhancing central satiety signaling and reducing neuroinflammation. The gut microbiome acts as a key intermediary in the metabolic regulation managed by DPP-4. By restoring microbial balance and promoting beneficial metabolites, DPP-4 inhibitors offer therapeutic advantages that extend beyond traditional glycemic control to include improved energy equilibrium and reduced adiposity. Targeting the interactions between DPP-4 and the microbiota represents a promising future therapeutic strategy for managing obesity and its associated metabolic complications.
Additional Links: PMID-42207404
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Citation:
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@article {pmid42207404,
year = {2026},
author = {Alanazi, M and Al-Kuraishy, HM and Mohamed, AA and Abass, SA and Shokr, MM and Alruwaili, M and Batiha, GE},
title = {Targeting Gut Microbiota by DPP-4 Inhibitors in Obesity: Mechanistic Insights and Therapeutic Implications.},
journal = {Current nutrition reports},
volume = {15},
number = {1},
pages = {},
pmid = {42207404},
issn = {2161-3311},
mesh = {Humans ; *Obesity/drug therapy/microbiology ; *Dipeptidyl-Peptidase IV Inhibitors/pharmacology/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; Animals ; Dysbiosis/drug therapy ; *Dipeptidyl Peptidase 4/metabolism ; Energy Metabolism/drug effects ; Insulin Resistance ; },
abstract = {PURPOSE OF REVIEW: Obesity is a complex metabolic disorder driven by factors such as chronic inflammation, insulin resistance, and significant alterations in the gut microbiota. Dipeptidyl peptidase-4 (DPP-4), an enzyme primarily known for inactivating incretin hormones like glucagon-like peptide-1 (GLP-1), is now recognized as a critical link between metabolic dysfunction and gut microbiome dysbiosis. This review aims to examine the mechanistic role of DPP-4 and its inhibitors in obesity, specifically focusing on how they modulate the gut microbiome to influence host energy balance and metabolic health.
RECENT FINDINGS: Recent experimental and clinical evidence indicates that DPP-4 activity contributes to obesity by influencing microbial composition, diversity, and function. Studies demonstrate that DPP-4 inhibitors can reshape the gut microbiota by reducing dysbiosis, decreasing the Firmicutes-to-Bacteroidetes ratio, and enhancing the production of short-chain fatty acids (SCFAs). Furthermore, these inhibitors improve gut barrier integrity and regulate bile acid metabolism, which helps attenuate systemic inflammation and restore insulin sensitivity. While DPP-4 inhibitors are often weight-neutral in clinical settings, they appear to assist in maintaining metabolic stability by enhancing central satiety signaling and reducing neuroinflammation. The gut microbiome acts as a key intermediary in the metabolic regulation managed by DPP-4. By restoring microbial balance and promoting beneficial metabolites, DPP-4 inhibitors offer therapeutic advantages that extend beyond traditional glycemic control to include improved energy equilibrium and reduced adiposity. Targeting the interactions between DPP-4 and the microbiota represents a promising future therapeutic strategy for managing obesity and its associated metabolic complications.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Obesity/drug therapy/microbiology
*Dipeptidyl-Peptidase IV Inhibitors/pharmacology/therapeutic use
*Gastrointestinal Microbiome/drug effects
Animals
Dysbiosis/drug therapy
*Dipeptidyl Peptidase 4/metabolism
Energy Metabolism/drug effects
Insulin Resistance
RevDate: 2026-05-28
CmpDate: 2026-05-28
Response of microbial community in the soil plastisphere of polypropylene microplastics to the stress of phenanthrene pollution: Microbial composition, function, and network.
World journal of microbiology & biotechnology, 42(6):.
Microplastics (MPs) accumulate in soils, forming microbial habitats termed the "plastisphere", which can concentrate hydrophobic pollutants like phenanthrene (PHE). This study investigated how PHE stress influences the microbial community in the polypropylene-amended soil plastisphere compared to bulk soil, revealing its "microbial refuge" function. Significant differences in microbial composition were observed. Under PHE stress, the number of unique genera in the plastisphere increased from 4 (without PHE) to 9, and the composition of significantly enriched genera changed substantially, with only 1 out of 6 enriched genera shared between PHE-stressed and non-stressed conditions. In contrast, the depleted genera remained largely consistent. Functional prediction indicated that PHE stress was associated with reduced health risks in the plastisphere relative to bulk soil. Carbon and methane metabolism pathways were significantly enriched in the plastisphere regardless of PHE stress. In contrast, nitrogen metabolism, aromatic compound degradation, and PAH degradation pathways did not differ significantly between the plastisphere and soil. Although several pathways reached statistical significance, fewer than 8.33% exhibited an absolute log2FC > 1. This discrepancy indicates that microplastics exert a limited biological impact on the overall metabolic potential of the soil microbiome, irrespective of PHE contamination. Microbial co-occurrence networks initially showed similar complexity between plastisphere and soil. However, PHE stress markedly reduced network complexity (degree) in the plastisphere and increased the proportion of negative correlations (indicating competition/antagonism) from ~ 60% to ~ 50% in both habitats. This study advances the mechanistic understanding of pollutant-driven microbial responses in soil plastispheres, with a focus on how this unique plastic-associated microbial niche mediates microbial composition, function, and network under PAH stress, thereby informing targeted bioremediation and ecological risk models for microplastic-organic co-contaminated environments.
Additional Links: PMID-42207427
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@article {pmid42207427,
year = {2026},
author = {Li, Q and Zhang, L and Qin, Y and Mei, W},
title = {Response of microbial community in the soil plastisphere of polypropylene microplastics to the stress of phenanthrene pollution: Microbial composition, function, and network.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {6},
pages = {},
pmid = {42207427},
issn = {1573-0972},
support = {32560012//National Natural Science Foundation of China/ ; 2023GXNSFBA026331//Natural Science Foundation of Guangxi Zhuang Autonomous Region/ ; },
mesh = {*Phenanthrenes/metabolism/analysis ; *Soil Microbiology ; *Soil Pollutants/metabolism ; Bacteria/classification/metabolism/genetics/drug effects/isolation & purification ; *Microplastics/metabolism ; *Polypropylenes ; Biodegradation, Environmental ; Soil/chemistry ; *Microbiota/drug effects ; RNA, Ribosomal, 16S/genetics ; Carbon/metabolism ; },
abstract = {Microplastics (MPs) accumulate in soils, forming microbial habitats termed the "plastisphere", which can concentrate hydrophobic pollutants like phenanthrene (PHE). This study investigated how PHE stress influences the microbial community in the polypropylene-amended soil plastisphere compared to bulk soil, revealing its "microbial refuge" function. Significant differences in microbial composition were observed. Under PHE stress, the number of unique genera in the plastisphere increased from 4 (without PHE) to 9, and the composition of significantly enriched genera changed substantially, with only 1 out of 6 enriched genera shared between PHE-stressed and non-stressed conditions. In contrast, the depleted genera remained largely consistent. Functional prediction indicated that PHE stress was associated with reduced health risks in the plastisphere relative to bulk soil. Carbon and methane metabolism pathways were significantly enriched in the plastisphere regardless of PHE stress. In contrast, nitrogen metabolism, aromatic compound degradation, and PAH degradation pathways did not differ significantly between the plastisphere and soil. Although several pathways reached statistical significance, fewer than 8.33% exhibited an absolute log2FC > 1. This discrepancy indicates that microplastics exert a limited biological impact on the overall metabolic potential of the soil microbiome, irrespective of PHE contamination. Microbial co-occurrence networks initially showed similar complexity between plastisphere and soil. However, PHE stress markedly reduced network complexity (degree) in the plastisphere and increased the proportion of negative correlations (indicating competition/antagonism) from ~ 60% to ~ 50% in both habitats. This study advances the mechanistic understanding of pollutant-driven microbial responses in soil plastispheres, with a focus on how this unique plastic-associated microbial niche mediates microbial composition, function, and network under PAH stress, thereby informing targeted bioremediation and ecological risk models for microplastic-organic co-contaminated environments.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Phenanthrenes/metabolism/analysis
*Soil Microbiology
*Soil Pollutants/metabolism
Bacteria/classification/metabolism/genetics/drug effects/isolation & purification
*Microplastics/metabolism
*Polypropylenes
Biodegradation, Environmental
Soil/chemistry
*Microbiota/drug effects
RNA, Ribosomal, 16S/genetics
Carbon/metabolism
RevDate: 2026-05-28
CmpDate: 2026-05-28
The impact of gut microbiota and metabolite-driven immune cell spatiotemporal dynamics on tumors.
Gut microbes, 18(1):2681842.
Cancer poses a significant threat to human health. The immune response plays a pivotal role in tumor cell elimination, with increasing attention given to the spatiotemporal dynamics of immune cells across temporal, spatial, and functional dimensions. The gut microbiota, which constitutes the majority of the human microbiome, contributes to tumor initiation and progression. The tumor microenvironment (TME) serves as the primary site for immune cell-mediated anti-tumor responses, with the gut microbiota and its metabolites driving immune cell activation and spatiotemporal remodeling. This review explores the mechanisms by which the gut microbiota and its metabolites influence anti-tumor immunity, alongside the impact of immune cell dynamics on tumors. Furthermore, it proposes novel research strategies, including the "gut microbiota-immune cell dynamic monitoring model" and the "organoid-microbe co-culture platform." This work lays a theoretical foundation for advancing our understanding of the underlying mechanisms and developing innovative therapeutic approaches.
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@article {pmid42207498,
year = {2026},
author = {Ding, JB and Lin, MX and Zang, D and Chen, J},
title = {The impact of gut microbiota and metabolite-driven immune cell spatiotemporal dynamics on tumors.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2681842},
doi = {10.1080/19490976.2026.2681842},
pmid = {42207498},
issn = {1949-0984},
mesh = {Humans ; *Tumor Microenvironment/immunology ; *Gastrointestinal Microbiome/immunology ; *Neoplasms/immunology/microbiology ; Animals ; },
abstract = {Cancer poses a significant threat to human health. The immune response plays a pivotal role in tumor cell elimination, with increasing attention given to the spatiotemporal dynamics of immune cells across temporal, spatial, and functional dimensions. The gut microbiota, which constitutes the majority of the human microbiome, contributes to tumor initiation and progression. The tumor microenvironment (TME) serves as the primary site for immune cell-mediated anti-tumor responses, with the gut microbiota and its metabolites driving immune cell activation and spatiotemporal remodeling. This review explores the mechanisms by which the gut microbiota and its metabolites influence anti-tumor immunity, alongside the impact of immune cell dynamics on tumors. Furthermore, it proposes novel research strategies, including the "gut microbiota-immune cell dynamic monitoring model" and the "organoid-microbe co-culture platform." This work lays a theoretical foundation for advancing our understanding of the underlying mechanisms and developing innovative therapeutic approaches.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Tumor Microenvironment/immunology
*Gastrointestinal Microbiome/immunology
*Neoplasms/immunology/microbiology
Animals
RevDate: 2026-05-28
Immune System Development-Pro Tips for Paediatricians.
Acta paediatrica (Oslo, Norway : 1992) [Epub ahead of print].
There are many misconceptions about the immune system in children, its impact on infectious disease susceptibility and its role in the rapidly increasing rates of immune mediated diseases in industrialized societies. In this mini review, I will discuss common believes and the data supporting or countering such believes, with a focus on clinically relevant topics of relevance to trainees and practicing paediatricians. I will emphasize data from studies performed in humans rather than reductionist mouse models. I discuss open questions requiring further investigation and end with a discussion on clinical observations of particular concern which paediatricians should consider when caring for children in their practices. Immune development is increasingly recognized as an important determinant of health, not just early in life, but also long term and all of us caring for children should know more about it.
Additional Links: PMID-42207652
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@article {pmid42207652,
year = {2026},
author = {Brodin, P},
title = {Immune System Development-Pro Tips for Paediatricians.},
journal = {Acta paediatrica (Oslo, Norway : 1992)},
volume = {},
number = {},
pages = {},
doi = {10.1111/apa.70627},
pmid = {42207652},
issn = {1651-2227},
abstract = {There are many misconceptions about the immune system in children, its impact on infectious disease susceptibility and its role in the rapidly increasing rates of immune mediated diseases in industrialized societies. In this mini review, I will discuss common believes and the data supporting or countering such believes, with a focus on clinically relevant topics of relevance to trainees and practicing paediatricians. I will emphasize data from studies performed in humans rather than reductionist mouse models. I discuss open questions requiring further investigation and end with a discussion on clinical observations of particular concern which paediatricians should consider when caring for children in their practices. Immune development is increasingly recognized as an important determinant of health, not just early in life, but also long term and all of us caring for children should know more about it.},
}
RevDate: 2026-05-28
TIPP-SD: A new method for species detection in microbiomes.
PLoS computational biology, 22(5):e1014347 pii:PCOMPBIOL-D-25-01774 [Epub ahead of print].
In this study, we present TIPP-SD (i.e., TIPP for Species Detection), a new technique for species detection in a microbiome sample. TIPP-SD uses a substantially modified version of TIPP3, which is a recently developed abundance profiling tool based on maximum likelihood phylogenetic placement into marker gene taxonomies. TIPP-SD depends on a parameter (i.e., "threshold") for the required support for species detection, thus allowing us to compute a precision-recall curve as we vary this parameter. In comparing the precision-recall curves for TIPP-SD, TIPP3, Kraken2, Bracken, Metabuli, and Metapresence, we find that TIPP-SD improves on the other methods with respect to accuracy under conditions where there is a highly variable distribution of species abundance or where there is sequencing error. Under other conditions, TIPP-SD is close to the best of these methods. Finally, although TIPP-SD is slower than the other methods, it is still fast enough to be used on large datasets. TIPP-SD is available in github as part of the TIPP3 software package.
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@article {pmid42207845,
year = {2026},
author = {Shen, C and Wedell, E and Pop, M and Warnow, T},
title = {TIPP-SD: A new method for species detection in microbiomes.},
journal = {PLoS computational biology},
volume = {22},
number = {5},
pages = {e1014347},
doi = {10.1371/journal.pcbi.1014347},
pmid = {42207845},
issn = {1553-7358},
abstract = {In this study, we present TIPP-SD (i.e., TIPP for Species Detection), a new technique for species detection in a microbiome sample. TIPP-SD uses a substantially modified version of TIPP3, which is a recently developed abundance profiling tool based on maximum likelihood phylogenetic placement into marker gene taxonomies. TIPP-SD depends on a parameter (i.e., "threshold") for the required support for species detection, thus allowing us to compute a precision-recall curve as we vary this parameter. In comparing the precision-recall curves for TIPP-SD, TIPP3, Kraken2, Bracken, Metabuli, and Metapresence, we find that TIPP-SD improves on the other methods with respect to accuracy under conditions where there is a highly variable distribution of species abundance or where there is sequencing error. Under other conditions, TIPP-SD is close to the best of these methods. Finally, although TIPP-SD is slower than the other methods, it is still fast enough to be used on large datasets. TIPP-SD is available in github as part of the TIPP3 software package.},
}
RevDate: 2026-05-28
Plant-driven assembly and maintenance of disease-suppressive soil microbiomes in a changing climate.
Microbiological research, 310:128557 pii:S0944-5013(26)00121-7 [Epub ahead of print].
Disease-suppressive soils are a fundamental aspect of sustainable agriculture, where native microbiomes help control soilborne pathogens through antagonistic interactions, protecting plant health even in favorable environmental conditions. This review synthesizes the current understanding of how plants actively assemble and maintain protective root microbiomes, a process that initiates and sustains this suppressiveness. The mechanistic depth of this synthesis is anchored primarily in annual cereal and vegetable crop systems, where the genetic, chemical, and ecological bases of plant-driven suppression have been most extensively characterized. While illustrative examples from perennial and woody systems are included to highlight specific principles, a comprehensive treatment of their distinct assembly dynamics, shaped by root persistence and long-term legacy accumulation, lies beyond the scope of this review. We detail how plants recruit beneficial microbes through a dynamic dialogue involving root exudates and immune system modulation, creating rhizosphere hotspots that enrich for protective consortia. This assembly is governed by host genetics, which shapes microbial recruitment and the plant's responsiveness to beneficial feedback. Critically, these interactions foster self-reinforcing legacies, where pathogen-induced stress reprograms exudate profiles to recruit suppressors, establishing durable microbiome shifts that confer intergenerational protection. However, escalating climate change threatens this equilibrium by perturbing microbial community structure, reducing beneficial diversity, favoring opportunistic pathogens, and eroding suppression efficacy. By integrating plant-microbe communication with soil-borne disease ecology, this perspective illuminates strategies for breeding crops and engineering soils to harness protective feedbacks for sustainable, microbiome-mediated disease management.
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@article {pmid42208156,
year = {2026},
author = {Asif, M and Chen, Y and Bian, BR and Huang, J and Ahmad, K and Dong, L and Li, WJ},
title = {Plant-driven assembly and maintenance of disease-suppressive soil microbiomes in a changing climate.},
journal = {Microbiological research},
volume = {310},
number = {},
pages = {128557},
doi = {10.1016/j.micres.2026.128557},
pmid = {42208156},
issn = {1618-0623},
abstract = {Disease-suppressive soils are a fundamental aspect of sustainable agriculture, where native microbiomes help control soilborne pathogens through antagonistic interactions, protecting plant health even in favorable environmental conditions. This review synthesizes the current understanding of how plants actively assemble and maintain protective root microbiomes, a process that initiates and sustains this suppressiveness. The mechanistic depth of this synthesis is anchored primarily in annual cereal and vegetable crop systems, where the genetic, chemical, and ecological bases of plant-driven suppression have been most extensively characterized. While illustrative examples from perennial and woody systems are included to highlight specific principles, a comprehensive treatment of their distinct assembly dynamics, shaped by root persistence and long-term legacy accumulation, lies beyond the scope of this review. We detail how plants recruit beneficial microbes through a dynamic dialogue involving root exudates and immune system modulation, creating rhizosphere hotspots that enrich for protective consortia. This assembly is governed by host genetics, which shapes microbial recruitment and the plant's responsiveness to beneficial feedback. Critically, these interactions foster self-reinforcing legacies, where pathogen-induced stress reprograms exudate profiles to recruit suppressors, establishing durable microbiome shifts that confer intergenerational protection. However, escalating climate change threatens this equilibrium by perturbing microbial community structure, reducing beneficial diversity, favoring opportunistic pathogens, and eroding suppression efficacy. By integrating plant-microbe communication with soil-borne disease ecology, this perspective illuminates strategies for breeding crops and engineering soils to harness protective feedbacks for sustainable, microbiome-mediated disease management.},
}
RevDate: 2026-05-28
Alopecia areata: Mechanisms, targeted therapies, and translational challenges.
Current opinion in pharmacology, 89:102635 pii:S1471-4892(26)00031-7 [Epub ahead of print].
Alopecia areata (AA) is an immune-mediated disorder characterized by non-scarring hair loss and substantial psychosocial burden. Although recent advances have clarified key pathogenic mechanisms and expanded therapeutic options, important uncertainties persist regarding disease heterogeneity, treatment durability, and long-term safety. Central to AA pathogenesis is the collapse of hair follicle immune privilege, driven primarily by cytotoxic CD8[+] NKG2D[+] T-cells and sustained by interferon-γ-dependent Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling. However, emerging evidence indicates immunological variability across patient subsets, including inconsistent contributions from T helper cell pathways and regulatory immune dysfunction. The clinical approval of JAK inhibitors-baricitinib, ritlecitinib, and deuruxolitinib-represents a major therapeutic milestone, validating targeted immune modulation as an effective strategy for moderate-to-severe AA. Nevertheless, relapse following treatment discontinuation, interindividual variability in response, and unresolved long-term safety considerations highlight the limitations of current approaches. In parallel, regenerative therapies, microbiome-based interventions, gene-targeted strategies, and device-assisted technologies are under investigation, yet most face substantial translational, regulatory, and scalability challenges. This review critically synthesizes current evidence on AA pathogenesis and therapy, with particular emphasis on unresolved controversies, translational barriers, and clinical implications. By integrating mechanistic insights with emerging clinical data, the article highlights priorities for future research, including biomarker development, precision medicine approaches, and strategies aimed at achieving durable disease control rather than transient immune suppression.
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@article {pmid42208158,
year = {2026},
author = {Kumar, V and Sahoo, S and Kumar, P},
title = {Alopecia areata: Mechanisms, targeted therapies, and translational challenges.},
journal = {Current opinion in pharmacology},
volume = {89},
number = {},
pages = {102635},
doi = {10.1016/j.coph.2026.102635},
pmid = {42208158},
issn = {1471-4973},
abstract = {Alopecia areata (AA) is an immune-mediated disorder characterized by non-scarring hair loss and substantial psychosocial burden. Although recent advances have clarified key pathogenic mechanisms and expanded therapeutic options, important uncertainties persist regarding disease heterogeneity, treatment durability, and long-term safety. Central to AA pathogenesis is the collapse of hair follicle immune privilege, driven primarily by cytotoxic CD8[+] NKG2D[+] T-cells and sustained by interferon-γ-dependent Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling. However, emerging evidence indicates immunological variability across patient subsets, including inconsistent contributions from T helper cell pathways and regulatory immune dysfunction. The clinical approval of JAK inhibitors-baricitinib, ritlecitinib, and deuruxolitinib-represents a major therapeutic milestone, validating targeted immune modulation as an effective strategy for moderate-to-severe AA. Nevertheless, relapse following treatment discontinuation, interindividual variability in response, and unresolved long-term safety considerations highlight the limitations of current approaches. In parallel, regenerative therapies, microbiome-based interventions, gene-targeted strategies, and device-assisted technologies are under investigation, yet most face substantial translational, regulatory, and scalability challenges. This review critically synthesizes current evidence on AA pathogenesis and therapy, with particular emphasis on unresolved controversies, translational barriers, and clinical implications. By integrating mechanistic insights with emerging clinical data, the article highlights priorities for future research, including biomarker development, precision medicine approaches, and strategies aimed at achieving durable disease control rather than transient immune suppression.},
}
RevDate: 2026-05-28
Wastewater-impacted Skagerrak Sea microbiomes anaerobically demethylate micropollutants.
Water research, 302:126138 pii:S0043-1354(26)00818-3 [Epub ahead of print].
Methylated micropollutants such as naproxen and caffeine persist in wastewater effluents and accumulate in coastal sediments, including Hakefjorden, Skagerrak Sea, yet their anaerobic fate and role in methane emissions remain unresolved. In particular, it is unclear whether pollutant-derived methyl groups are routed mainly to CO2 or can be transformed into CH4 in sulfate-rich coastal sediments. Our primary objective was to resolve this routing by tracing the fate and microbiome responses to [13]C-labeled naproxen and caffeine in sediment microcosms. We show that naproxen underwent rapid O-demethylation to desmethylnaproxen, with 90% ± 15.5% removed within 25 days, producing primarily [13]CO2 and some [13]CH4. Naproxen enriched methylotrophic and hydrogenotrophic Methanomicrobia, alongside Lokiarchaeia, Bathyarchaeia, and bacterial taxa like Eubacterium (Alkalibaculum A sporogenes) and Syntrophomonadaceae. Metagenomics revealed O-demethylation genes in enriched bacterial MAGs affiliated with uncultured Thermoanaerobaculia, indicating a bacterial demethylation potential. In contrast, caffeine was largely recalcitrant to degradation (∼85% ± 5% remaining), yet its [13]C-labeled N-methyl groups fueled trace [13]CH4 production. These results show that methylated micropollutants can activate both bacterial and archaeal demethylation pathways in coastal sediment microbiomes.
Additional Links: PMID-42208188
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@article {pmid42208188,
year = {2026},
author = {Gilevska, T and Rotaru, AE and Anestis, K and Fonseca, A and Kümmel, S and Krauss, M and Inostroza, PA and Bonaglia, S},
title = {Wastewater-impacted Skagerrak Sea microbiomes anaerobically demethylate micropollutants.},
journal = {Water research},
volume = {302},
number = {},
pages = {126138},
doi = {10.1016/j.watres.2026.126138},
pmid = {42208188},
issn = {1879-2448},
abstract = {Methylated micropollutants such as naproxen and caffeine persist in wastewater effluents and accumulate in coastal sediments, including Hakefjorden, Skagerrak Sea, yet their anaerobic fate and role in methane emissions remain unresolved. In particular, it is unclear whether pollutant-derived methyl groups are routed mainly to CO2 or can be transformed into CH4 in sulfate-rich coastal sediments. Our primary objective was to resolve this routing by tracing the fate and microbiome responses to [13]C-labeled naproxen and caffeine in sediment microcosms. We show that naproxen underwent rapid O-demethylation to desmethylnaproxen, with 90% ± 15.5% removed within 25 days, producing primarily [13]CO2 and some [13]CH4. Naproxen enriched methylotrophic and hydrogenotrophic Methanomicrobia, alongside Lokiarchaeia, Bathyarchaeia, and bacterial taxa like Eubacterium (Alkalibaculum A sporogenes) and Syntrophomonadaceae. Metagenomics revealed O-demethylation genes in enriched bacterial MAGs affiliated with uncultured Thermoanaerobaculia, indicating a bacterial demethylation potential. In contrast, caffeine was largely recalcitrant to degradation (∼85% ± 5% remaining), yet its [13]C-labeled N-methyl groups fueled trace [13]CH4 production. These results show that methylated micropollutants can activate both bacterial and archaeal demethylation pathways in coastal sediment microbiomes.},
}
RevDate: 2026-05-28
Th17/Treg imbalance: a key driver of neutrophilic inflammation in severe asthma.
International immunopharmacology, 184:116920 pii:S1567-5769(26)00766-6 [Epub ahead of print].
Severe asthma, characterized by neutrophilic airway inflammation, poses a significant clinical obstacle, primarily due to its frequent association with glucocorticoid resistance. This review provides a systematic analysis of how the imbalance between T helper 17 (Th17) cells and regulatory T (Treg) cells contributes to this glucocorticoid-resistant phenotype. We emphasize three interconnected mechanisms that transcend traditional cytokine networks: immunometabolic reprogramming, which promotes glycolytic adaptation in Th17 cells while simultaneously impairing oxidative metabolism in Tregs; microbiome dysregulation, acting via the "gut-lung axis", which disrupts local and systemic immune tolerance; and Treg plasticity, wherein inflammatory signals transform suppressive Tregs into pro-inflammatory Th17-like cells, thereby exacerbating immune imbalance. Consequently, these processes establish a self-perpetuating inflammatory environment that sustains neutrophilic infiltration and impairs glucocorticoid sensitivity. On this basis, we evaluate emerging therapeutic strategies targeting the Th17/Treg axis, including Interleukin-17/Interleukin-23 (IL-17/IL-23) blockade, Janus kinase inhibitors, and Treg-enhancing approaches. We conclude that biomarker-guided patient stratification, rather than a "one-size-fits-all" strategy, will be essential to translate these mechanistic insights into effective precision immunotherapy for severe neutrophilic asthma.
Additional Links: PMID-42208332
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@article {pmid42208332,
year = {2026},
author = {Yao, B and Song, C and Li, S and Ran, Z and Wang, C and Wu, M and Yuan, Q},
title = {Th17/Treg imbalance: a key driver of neutrophilic inflammation in severe asthma.},
journal = {International immunopharmacology},
volume = {184},
number = {},
pages = {116920},
doi = {10.1016/j.intimp.2026.116920},
pmid = {42208332},
issn = {1878-1705},
abstract = {Severe asthma, characterized by neutrophilic airway inflammation, poses a significant clinical obstacle, primarily due to its frequent association with glucocorticoid resistance. This review provides a systematic analysis of how the imbalance between T helper 17 (Th17) cells and regulatory T (Treg) cells contributes to this glucocorticoid-resistant phenotype. We emphasize three interconnected mechanisms that transcend traditional cytokine networks: immunometabolic reprogramming, which promotes glycolytic adaptation in Th17 cells while simultaneously impairing oxidative metabolism in Tregs; microbiome dysregulation, acting via the "gut-lung axis", which disrupts local and systemic immune tolerance; and Treg plasticity, wherein inflammatory signals transform suppressive Tregs into pro-inflammatory Th17-like cells, thereby exacerbating immune imbalance. Consequently, these processes establish a self-perpetuating inflammatory environment that sustains neutrophilic infiltration and impairs glucocorticoid sensitivity. On this basis, we evaluate emerging therapeutic strategies targeting the Th17/Treg axis, including Interleukin-17/Interleukin-23 (IL-17/IL-23) blockade, Janus kinase inhibitors, and Treg-enhancing approaches. We conclude that biomarker-guided patient stratification, rather than a "one-size-fits-all" strategy, will be essential to translate these mechanistic insights into effective precision immunotherapy for severe neutrophilic asthma.},
}
RevDate: 2026-05-28
Kidney dysfunction regulates gut transporters.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 200:119581 pii:S0753-3322(26)00617-7 [Epub ahead of print].
BACKGROUND: The gut-kidney axis is crucial in chronic kidney disease (CKD). As kidney function declines, uremic toxins accumulate in plasma, and gut dysbiosis, oxidative stress, and inflammation arise, potentially affecting the expression of proteins involved in absorption, distribution, metabolism, and excretion (ADME). We aimed to determine the colonic expression of ADME proteins in CKD and explore modulatory mechanisms.
METHODS: RNA and protein expression of key gut transporters, enzymes and receptors were determined in colon biopsies from 17 patients with CKD and 12 healthy volunteers using RNA sequencing and targeted mass spectrometry. In parallel, we induced CKD in rats by 5/6th nephrectomy, and we administered an antibiotic cocktail to assess differences when depleting the gut microbiome. Caco-2 cells exposed to human serum or fecal water derived from CKD patients were used to elucidate modulatory mechanisms.
RESULTS: CKD downregulated the colon efflux transporter proteins P-gp (apical), MRP3 (basolateral) and BCRP (apical) (BCRP only in patients not undergoing hemodialysis). P-gp downregulation was mediated by aromatic gut microbiome-derived uremic toxins in patients, consistently with in vitro observation that P-gp was downregulated in Caco-2 cells exposed to CKD serum. In CKD rats' colon, Mdr1a was downregulated, and Bcrp was upregulated only when antibiotics were administered, indicating the gut microbiome influences P-gp and BCRP in CKD.
CONCLUSIONS: We confirmed kidney-gut crosstalk, highlighting how uremic environment and gut dysbiosis consequent to CKD impact gut transport physiology. P-gp and BCRP can be downregulated via gut microbiome metabolites, thus shedding light on the importance of therapies targeting microbial activity.
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@article {pmid42208345,
year = {2026},
author = {Lauriola, M and Dejongh, S and Steigert, S and Zadora, W and Valkenburg, S and Augustijns, P and Glorieux, G and Oswald, S and Farré, R and Meijers, B},
title = {Kidney dysfunction regulates gut transporters.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {200},
number = {},
pages = {119581},
doi = {10.1016/j.biopha.2026.119581},
pmid = {42208345},
issn = {1950-6007},
abstract = {BACKGROUND: The gut-kidney axis is crucial in chronic kidney disease (CKD). As kidney function declines, uremic toxins accumulate in plasma, and gut dysbiosis, oxidative stress, and inflammation arise, potentially affecting the expression of proteins involved in absorption, distribution, metabolism, and excretion (ADME). We aimed to determine the colonic expression of ADME proteins in CKD and explore modulatory mechanisms.
METHODS: RNA and protein expression of key gut transporters, enzymes and receptors were determined in colon biopsies from 17 patients with CKD and 12 healthy volunteers using RNA sequencing and targeted mass spectrometry. In parallel, we induced CKD in rats by 5/6th nephrectomy, and we administered an antibiotic cocktail to assess differences when depleting the gut microbiome. Caco-2 cells exposed to human serum or fecal water derived from CKD patients were used to elucidate modulatory mechanisms.
RESULTS: CKD downregulated the colon efflux transporter proteins P-gp (apical), MRP3 (basolateral) and BCRP (apical) (BCRP only in patients not undergoing hemodialysis). P-gp downregulation was mediated by aromatic gut microbiome-derived uremic toxins in patients, consistently with in vitro observation that P-gp was downregulated in Caco-2 cells exposed to CKD serum. In CKD rats' colon, Mdr1a was downregulated, and Bcrp was upregulated only when antibiotics were administered, indicating the gut microbiome influences P-gp and BCRP in CKD.
CONCLUSIONS: We confirmed kidney-gut crosstalk, highlighting how uremic environment and gut dysbiosis consequent to CKD impact gut transport physiology. P-gp and BCRP can be downregulated via gut microbiome metabolites, thus shedding light on the importance of therapies targeting microbial activity.},
}
RevDate: 2026-05-28
Reduced nitrogen fertilization combined with microbial bio-inputs restores soil bacterial functional profiles and sustains wheat performance.
The Science of the total environment, 1040:181886 pii:S0048-9697(26)00550-4 [Epub ahead of print].
Nitrogen (N) fertilization is a major driver of wheat productivity but also entails significant environmental costs, underscoring the need for strategies that reduce N inputs without compromising yield. Microbial bio-inputs are increasingly proposed as complementary tools to improve N use efficiency, yet their effects on soil microbial communities and functions under reduced N fertilization remain poorly documented in wheat agrosystems. In this study, we investigated the effects of two microbial bio-inputs, Sphingomonas sediminicola Dae20 and the cell-free supernatant of Bacillus velezensis GA1, applied alone or in combination under reduced N fertilization, on wheat performance, soil microbial functioning and bacterial community structure. A field experiment was conducted with five management treatments, including conventional or reduced N fertilization and reduced N combined with each bio-input or their combination. Grain yield and quality were measured, alongside soil microbial metabolic activity, functional richness, and bacterial community structure at tillering, stem elongation and ripening. Reducing N fertilization resulted in a yield decrease of approximately 20%, while grain quality remained unaffected. Both bio-inputs partially compensated for yield losses, and their combined application restored yields obtained under conventional fertilization, without increasing grain N and protein concentrations. Bio-input effects were mainly functional, as bacterial diversity remained stable across treatments. In contrast, microbial metabolic activity and functional richness declined sharply at the end of the crop cycle in untreated soils but were maintained in bio-input-treated soils. These late-season effects coincided with wheat senescence, suggesting that bio-inputs stabilize microbial functioning when rhizosphere resources become limiting. Together, our results indicate that microbial bio-inputs do not reshape soil bacterial diversity but act as functional buffers of the soil microbiome, contributing to improved crop performance under reduced N fertilization and highlighting the importance of integrating functional and temporal indicators when evaluating bio-input strategies for sustainable agroecosystems.
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@article {pmid42208480,
year = {2026},
author = {Pecourt, A and Bertrand, A and Catterou, M and Rochex, A and Arnauld, S and Lacoux, J and Sarazin, V and Leclère, V and Dubois, F and Duclercq, J},
title = {Reduced nitrogen fertilization combined with microbial bio-inputs restores soil bacterial functional profiles and sustains wheat performance.},
journal = {The Science of the total environment},
volume = {1040},
number = {},
pages = {181886},
doi = {10.1016/j.scitotenv.2026.181886},
pmid = {42208480},
issn = {1879-1026},
abstract = {Nitrogen (N) fertilization is a major driver of wheat productivity but also entails significant environmental costs, underscoring the need for strategies that reduce N inputs without compromising yield. Microbial bio-inputs are increasingly proposed as complementary tools to improve N use efficiency, yet their effects on soil microbial communities and functions under reduced N fertilization remain poorly documented in wheat agrosystems. In this study, we investigated the effects of two microbial bio-inputs, Sphingomonas sediminicola Dae20 and the cell-free supernatant of Bacillus velezensis GA1, applied alone or in combination under reduced N fertilization, on wheat performance, soil microbial functioning and bacterial community structure. A field experiment was conducted with five management treatments, including conventional or reduced N fertilization and reduced N combined with each bio-input or their combination. Grain yield and quality were measured, alongside soil microbial metabolic activity, functional richness, and bacterial community structure at tillering, stem elongation and ripening. Reducing N fertilization resulted in a yield decrease of approximately 20%, while grain quality remained unaffected. Both bio-inputs partially compensated for yield losses, and their combined application restored yields obtained under conventional fertilization, without increasing grain N and protein concentrations. Bio-input effects were mainly functional, as bacterial diversity remained stable across treatments. In contrast, microbial metabolic activity and functional richness declined sharply at the end of the crop cycle in untreated soils but were maintained in bio-input-treated soils. These late-season effects coincided with wheat senescence, suggesting that bio-inputs stabilize microbial functioning when rhizosphere resources become limiting. Together, our results indicate that microbial bio-inputs do not reshape soil bacterial diversity but act as functional buffers of the soil microbiome, contributing to improved crop performance under reduced N fertilization and highlighting the importance of integrating functional and temporal indicators when evaluating bio-input strategies for sustainable agroecosystems.},
}
RevDate: 2026-05-28
Beyond survival: What drives senescence in trauma, shock and sepsis?.
Injury, 57(7):113395 pii:S0020-1383(26)00380-3 [Epub ahead of print].
Cellular senescence is a conserved stress response characterized by stable growth arrest, resistance to apoptosis, and a pro-inflammatory secretome that shapes tissue repair, tumor suppression, and aging. In this review, senescence is framed in the context of trauma, hemorrhagic shock, and sepsis. Severe injuries to brain, lung, abdomen, and bone, as well as ischemia-reperfusion and hemorrhagic shock, rapidly induce p21- and p16-governed senescence-like programs that modulate neurodegeneration, fibrosis, fracture healing, and organ dysfunction. In sepsis, senescence extends beyond immunosenescence to endothelial, epithelial, and stromal compartments, intersecting with ferroptosis, mitochondrial failure, and microbiome dysbiosis, and contributing to post-sepsis syndrome. Integrating mechanistic data with high-dimensional profiling and early interventional studies, this review proposes a context- and time-dependent model in which acute "pseudosenescence" may be organ-protective, whereas persistent senescent reservoirs fuel inflammaging and chronic pathology. Future translational studies are required to define the clinical rationale for phase-specific senotherapeutic interventions in trauma, shock, and sepsis, particularly with respect to long-term outcomes beyond survival.
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@article {pmid42208489,
year = {2026},
author = {Mösenlechner, M and Ignatius, A and Haffner-Luntzer, M and Halbgebauer, R and Huber-Lang, MS},
title = {Beyond survival: What drives senescence in trauma, shock and sepsis?.},
journal = {Injury},
volume = {57},
number = {7},
pages = {113395},
doi = {10.1016/j.injury.2026.113395},
pmid = {42208489},
issn = {1879-0267},
abstract = {Cellular senescence is a conserved stress response characterized by stable growth arrest, resistance to apoptosis, and a pro-inflammatory secretome that shapes tissue repair, tumor suppression, and aging. In this review, senescence is framed in the context of trauma, hemorrhagic shock, and sepsis. Severe injuries to brain, lung, abdomen, and bone, as well as ischemia-reperfusion and hemorrhagic shock, rapidly induce p21- and p16-governed senescence-like programs that modulate neurodegeneration, fibrosis, fracture healing, and organ dysfunction. In sepsis, senescence extends beyond immunosenescence to endothelial, epithelial, and stromal compartments, intersecting with ferroptosis, mitochondrial failure, and microbiome dysbiosis, and contributing to post-sepsis syndrome. Integrating mechanistic data with high-dimensional profiling and early interventional studies, this review proposes a context- and time-dependent model in which acute "pseudosenescence" may be organ-protective, whereas persistent senescent reservoirs fuel inflammaging and chronic pathology. Future translational studies are required to define the clinical rationale for phase-specific senotherapeutic interventions in trauma, shock, and sepsis, particularly with respect to long-term outcomes beyond survival.},
}
RevDate: 2026-05-28
Cross-kingdom metabolic interactions govern Candida albicans overgrowth and colitis progression.
Cell host & microbe pii:S1931-3128(26)00176-9 [Epub ahead of print].
Inflammatory bowel disease is shaped by complex microbial communities, yet the contribution of fungal-bacterial interactions to disease progression remains poorly defined. Here, we identify Cladosporium tenuissimum (C. tenuissimum) as a gut fungus with potent colitis-alleviating activity. Mechanistically, C. tenuissimum restrains Candida albicans (C. albicans) overgrowth through nutrient competition, particularly via the utilization and subsequent limitation of the amino acid ornithine. C. albicans can evade this suppression and potentiate intestinal inflammation through nutrient escape by preferentially exploiting specific amino acids, such as threonine. We further reveal a bacterial-fungal metabolic axis in which threonine-producing Bacteroides fragilis facilitates C. albicans escape from gut microbiome-mediated fungal control, thereby exacerbating colitis. Notably, dietary threonine restriction markedly attenuates C. albicans-driven colitis in mice. Together, our findings uncover a cross-kingdom metabolic network that determines C. albicans homeostasis and, in turn, governs intestinal inflammatory outcomes, offering new conceptual and therapeutic avenues for IBD.
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@article {pmid42208527,
year = {2026},
author = {Zhou, Y and Ding, J and Ning, L and Xu, X and Dou, L and Shen, J and Xuan, B and Wang, Z and Jiang, Y and Zhao, Y and Zhang, Y and Huang, X and Hu, M and Shao, Y and Li, L and Chen, C and Li, M and Fang, JY and Shen, N and Liu, NN and Chen, H and Sheng, C and Hong, J},
title = {Cross-kingdom metabolic interactions govern Candida albicans overgrowth and colitis progression.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.04.020},
pmid = {42208527},
issn = {1934-6069},
abstract = {Inflammatory bowel disease is shaped by complex microbial communities, yet the contribution of fungal-bacterial interactions to disease progression remains poorly defined. Here, we identify Cladosporium tenuissimum (C. tenuissimum) as a gut fungus with potent colitis-alleviating activity. Mechanistically, C. tenuissimum restrains Candida albicans (C. albicans) overgrowth through nutrient competition, particularly via the utilization and subsequent limitation of the amino acid ornithine. C. albicans can evade this suppression and potentiate intestinal inflammation through nutrient escape by preferentially exploiting specific amino acids, such as threonine. We further reveal a bacterial-fungal metabolic axis in which threonine-producing Bacteroides fragilis facilitates C. albicans escape from gut microbiome-mediated fungal control, thereby exacerbating colitis. Notably, dietary threonine restriction markedly attenuates C. albicans-driven colitis in mice. Together, our findings uncover a cross-kingdom metabolic network that determines C. albicans homeostasis and, in turn, governs intestinal inflammatory outcomes, offering new conceptual and therapeutic avenues for IBD.},
}
RevDate: 2026-05-28
Distinct Cutaneous Microbial Community Signatures Across Keloids, Surgical Scars, and Healthy Skin.
Journal of the American Academy of Dermatology pii:S0190-9622(26)02769-6 [Epub ahead of print].
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@article {pmid42208622,
year = {2026},
author = {Geng, BJ and Wei, GX and Niu, XL and Tang, MR and Zhang, YJ},
title = {Distinct Cutaneous Microbial Community Signatures Across Keloids, Surgical Scars, and Healthy Skin.},
journal = {Journal of the American Academy of Dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaad.2026.05.069},
pmid = {42208622},
issn = {1097-6787},
}
RevDate: 2026-05-28
Targeting the Microbiome-NLRP3-Ferroptosis Axis in Multiple Sclerosis: Neuropharmacological Implications for Microglial Dysfunction and Demyelination.
Neuropharmacology pii:S0028-3908(26)00215-7 [Epub ahead of print].
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) characterized by neuroinflammation, demyelination, and neurodegeneration. Recent evidence has established a mechanistic connection between gut microbial dysbiosis, the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, and ferroptosis, an iron-dependent regulated cell death marked by lipid peroxidation. This review synthesizes current understanding of how alterations in the gut microbiome disrupt the gut-brain axis and compromise the blood-brain barrier (BBB), thereby promoting the activation of the microglial NLRP3 inflammasome in the central nervous system. The resulting neuroinflammatory milieu, marked by oxidative stress and iron dysregulation, renders oligodendrocytes and neurons susceptible to ferroptosis via essential enzymes like ACSL4 and ALOX15. We examine the reciprocal relationship between NLRP3-induced inflammation and ferroptotic cell death, emphasizing microglia as crucial mediators of this detrimental cycle. We explore innovative neuropharmacological strategies targeting the gut microbiota, NLRP3 inhibition, and ferroptosis pathways (e.g., ACSL4/ALOX15 inhibitors) to achieve neuroprotection and reduce disease progression. This extensive perspective enhances understanding of MS pathophysiology and identifies actionable therapeutic targets within the microbiome-inflammasome-ferroptosis axis for the development of mechanism-based therapies.
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@article {pmid42208757,
year = {2026},
author = {Fawzy, MN and Abdelaziz, AM and Shokr, MM and Fathy, MK},
title = {Targeting the Microbiome-NLRP3-Ferroptosis Axis in Multiple Sclerosis: Neuropharmacological Implications for Microglial Dysfunction and Demyelination.},
journal = {Neuropharmacology},
volume = {},
number = {},
pages = {111042},
doi = {10.1016/j.neuropharm.2026.111042},
pmid = {42208757},
issn = {1873-7064},
abstract = {Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) characterized by neuroinflammation, demyelination, and neurodegeneration. Recent evidence has established a mechanistic connection between gut microbial dysbiosis, the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, and ferroptosis, an iron-dependent regulated cell death marked by lipid peroxidation. This review synthesizes current understanding of how alterations in the gut microbiome disrupt the gut-brain axis and compromise the blood-brain barrier (BBB), thereby promoting the activation of the microglial NLRP3 inflammasome in the central nervous system. The resulting neuroinflammatory milieu, marked by oxidative stress and iron dysregulation, renders oligodendrocytes and neurons susceptible to ferroptosis via essential enzymes like ACSL4 and ALOX15. We examine the reciprocal relationship between NLRP3-induced inflammation and ferroptotic cell death, emphasizing microglia as crucial mediators of this detrimental cycle. We explore innovative neuropharmacological strategies targeting the gut microbiota, NLRP3 inhibition, and ferroptosis pathways (e.g., ACSL4/ALOX15 inhibitors) to achieve neuroprotection and reduce disease progression. This extensive perspective enhances understanding of MS pathophysiology and identifies actionable therapeutic targets within the microbiome-inflammasome-ferroptosis axis for the development of mechanism-based therapies.},
}
RevDate: 2026-05-28
IL23R genetic variants associate with Crohn's disease risk and microbiome changes in healthy first-degree relatives.
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association pii:S1542-3565(26)00390-3 [Epub ahead of print].
BACKGROUND AND AIMS: Single nucleotide polymorphisms (SNPs) in the Interleukin-23 receptor (IL23-R) gene are associated with Crohn's disease (CD), suggesting a role in pathogenesis and several biologic agents targeting this pathway are now established therapies. IL-23 has been suggested to be involved in regulation of intestinal barrier function and may impact gut microbial composition. We investigated whether IL23-R genetic variants predict CD risk and influence gut barrier function and microbiome composition in healthy first-degree relatives (FDRs).
METHODS: 3,055 healthy FDRs with genotypic data from the Genetic Environmental Microbial (CCC-GEM) cohort were included. A weighted IL23R genetic risk score (IL23R-GRS) was generated from seven CD-associated IL23R SNPs and dichotomized as High (top quintile) vs. Low IL23R-GRS. A subset of this cohort was assessed for intestinal permeability (n=1,698) and microbiome profiling (n=2,523). Cox proportional-hazards models evaluated CD onset risk.
RESULTS: High IL23R-GRS was associated with increased CD risk (hazard ratio 1.67, 95% confidence interval 1.01-2.75, p=0.044). This association remained significant after adjusting for fecal calprotectin, indicating genetic risk independent of subclinical inflammation. High IL23R-GRS was not associated with intestinal permeability (p=0.84) but was associated with differences in 15 genera, including decreased Faecalibacterium and increased Akkermansia (q<0.1).
CONCLUSION: High IL23R-GRS was associated with increased CD risk in healthy FDRs and was associated with microbial differences, but not with intestinal permeability. These findings suggest potential clinical applications for IL23R-GRS in identifying high-risk individuals who may benefit from closer monitoring or future IL-23 pathway-targeted preventive interventions.
Additional Links: PMID-42208782
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@article {pmid42208782,
year = {2026},
author = {Leibovitzh, H and Neustaeter, A and Lee, SH and Xue, M and Espin-Garcia, O and Olivera, PA and Huynh, HQ and Griffiths, AM and Turner, D and Madsen, KL and Silverberg, MS and Steinhart, AH and Mack, DR and Jacobson, K and Moayyedi, P and Aumais, G and Bernstein, CN and Marshall, JK and Panaccione, R and Xu, W and , and Turpin, W and Croitoru, K},
title = {IL23R genetic variants associate with Crohn's disease risk and microbiome changes in healthy first-degree relatives.},
journal = {Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cgh.2026.05.011},
pmid = {42208782},
issn = {1542-7714},
abstract = {BACKGROUND AND AIMS: Single nucleotide polymorphisms (SNPs) in the Interleukin-23 receptor (IL23-R) gene are associated with Crohn's disease (CD), suggesting a role in pathogenesis and several biologic agents targeting this pathway are now established therapies. IL-23 has been suggested to be involved in regulation of intestinal barrier function and may impact gut microbial composition. We investigated whether IL23-R genetic variants predict CD risk and influence gut barrier function and microbiome composition in healthy first-degree relatives (FDRs).
METHODS: 3,055 healthy FDRs with genotypic data from the Genetic Environmental Microbial (CCC-GEM) cohort were included. A weighted IL23R genetic risk score (IL23R-GRS) was generated from seven CD-associated IL23R SNPs and dichotomized as High (top quintile) vs. Low IL23R-GRS. A subset of this cohort was assessed for intestinal permeability (n=1,698) and microbiome profiling (n=2,523). Cox proportional-hazards models evaluated CD onset risk.
RESULTS: High IL23R-GRS was associated with increased CD risk (hazard ratio 1.67, 95% confidence interval 1.01-2.75, p=0.044). This association remained significant after adjusting for fecal calprotectin, indicating genetic risk independent of subclinical inflammation. High IL23R-GRS was not associated with intestinal permeability (p=0.84) but was associated with differences in 15 genera, including decreased Faecalibacterium and increased Akkermansia (q<0.1).
CONCLUSION: High IL23R-GRS was associated with increased CD risk in healthy FDRs and was associated with microbial differences, but not with intestinal permeability. These findings suggest potential clinical applications for IL23R-GRS in identifying high-risk individuals who may benefit from closer monitoring or future IL-23 pathway-targeted preventive interventions.},
}
RevDate: 2026-05-28
Exposure to antibiotics with anaerobe coverage in later life is associated with higher enteric pathobiont carriage.
The Journal of infection pii:S0163-4453(26)00099-X [Epub ahead of print].
OBJECTIVES: Infections involving enteric bacteria commonly cause hospitalisation and death in long-term residential aged care (LTC) populations. The risk of such infections has been linked with antibiotic-associated depletion of gut anaerobic commensals and the resulting increase in asymptomatic carriage of gut pathobionts. We sought to determine how antibiotic characteristics, particularly activity against anaerobes, influence pathobiont prevalence in LTC residents.
METHODS: Stool samples from 164 LTC residents (median age: 87.9 years, interquartile range: 81.3-93.0 years) underwent metagenomic analysis. Associations between prior antibiotic exposures (categorised according to anaerobe coverage and type) and gut microbiome characteristics were explored using multivariable models.
RESULTS: Of the 164 participants, 138 (84.1%) carried at least one enteric pathobiont. Compared to those with no prior antibiotic exposure, treatment with anaerobe covering (EAC) antibiotics was associated with higher rates of pathobiont carriage (β=1.36, P=0.010) and higher overall pathobiont relative abundance (β=3.53, P=0.013). In contrast, exposure to antibiotics with limited anaerobe coverage (LAC) showed no such associations. Investigation of commonly prescribed EAC and LAC antibiotics (amoxicillin-clavulanate and cefalexin, respectively) were consistent with these findings, with higher detection (β=1.60, P=0.007) and relative abundance (β=3.32, P=0.039) of pathobiont species in amoxicillin-clavulanate recipients. Pathobionts with greater representation included both species with inherent resistance (i.e. Enterococcus faecium) and sensitivity (i.e. Klebsiella pneumoniae) to amoxicillin-clavulanate.
CONCLUSIONS: Antibiotics that deplete commensal anaerobes are associated with pathobiont prevalence in the gut, even where pathobiont species are sensitive to the administered antibiotic. Off-target disruption of commensal anaerobes should be considered when selecting antibiotic treatments, particularly for LTC individuals.
Additional Links: PMID-42208810
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@article {pmid42208810,
year = {2026},
author = {Vasil, E and Papanicolas, LE and Miller, SJ and Shoubridge, AP and Taylor, SL and Rogers, GB},
title = {Exposure to antibiotics with anaerobe coverage in later life is associated with higher enteric pathobiont carriage.},
journal = {The Journal of infection},
volume = {},
number = {},
pages = {106774},
doi = {10.1016/j.jinf.2026.106774},
pmid = {42208810},
issn = {1532-2742},
abstract = {OBJECTIVES: Infections involving enteric bacteria commonly cause hospitalisation and death in long-term residential aged care (LTC) populations. The risk of such infections has been linked with antibiotic-associated depletion of gut anaerobic commensals and the resulting increase in asymptomatic carriage of gut pathobionts. We sought to determine how antibiotic characteristics, particularly activity against anaerobes, influence pathobiont prevalence in LTC residents.
METHODS: Stool samples from 164 LTC residents (median age: 87.9 years, interquartile range: 81.3-93.0 years) underwent metagenomic analysis. Associations between prior antibiotic exposures (categorised according to anaerobe coverage and type) and gut microbiome characteristics were explored using multivariable models.
RESULTS: Of the 164 participants, 138 (84.1%) carried at least one enteric pathobiont. Compared to those with no prior antibiotic exposure, treatment with anaerobe covering (EAC) antibiotics was associated with higher rates of pathobiont carriage (β=1.36, P=0.010) and higher overall pathobiont relative abundance (β=3.53, P=0.013). In contrast, exposure to antibiotics with limited anaerobe coverage (LAC) showed no such associations. Investigation of commonly prescribed EAC and LAC antibiotics (amoxicillin-clavulanate and cefalexin, respectively) were consistent with these findings, with higher detection (β=1.60, P=0.007) and relative abundance (β=3.32, P=0.039) of pathobiont species in amoxicillin-clavulanate recipients. Pathobionts with greater representation included both species with inherent resistance (i.e. Enterococcus faecium) and sensitivity (i.e. Klebsiella pneumoniae) to amoxicillin-clavulanate.
CONCLUSIONS: Antibiotics that deplete commensal anaerobes are associated with pathobiont prevalence in the gut, even where pathobiont species are sensitive to the administered antibiotic. Off-target disruption of commensal anaerobes should be considered when selecting antibiotic treatments, particularly for LTC individuals.},
}
RevDate: 2026-05-28
Structure of a Stand-Alone Homodimeric Nonribosomal Peptide Synthetase Condensation Domain Reveals Occlusion of the Canonical Carrier-Protein Interface.
The Journal of biological chemistry pii:S0021-9258(26)02080-6 [Epub ahead of print].
Fatty acid amides (FAAs) produced by gut-resident bacteria act as potent modulators of host G-protein coupled receptor signaling, yet the enzymatic mechanisms underlying their biosynthesis remain poorly understood. In many bacteria from the gut microbiome, including Coprococcus eutactus, FAA production is mediated by a nonribosomal peptide synthetase (NRPS)-like pathway that includes OaaC, a free-standing condensation domain that catalyzes amide bond formation between acyl carrier protein (ACP) tethered fatty acids and small-molecule amine acceptors. Here, we combine structural, biophysical, biochemical, and evolutionary analyses to interrogate the molecular basis of OaaC function. Solution scattering and X-ray crystallography reveal that OaaC adopts an atypical homodimeric architecture that occludes the canonical ACP-binding surface and donor access pathways. Mass photometry demonstrates that this homodimer is stable in the absence of substrates and is insensitive to free fatty acids, free amines, and apo-ACP. In contrast, holo or acyl-loaded OaaACP selectively destabilizes the homodimer forming the OaaC-OaaACP complex population. LC-MS reconstitution assays confirm that OaaC catalyzes fatty acid amide formation in vitro and can utilize acyl donors spanning multiple chain lengths and saturation states. Phylogenetic and sequence analyses place FAA-associated condensation domains in a distinct clade most closely related to starter condensation domains and reveal a conserved noncanonical active site motif that differentiates them from PCP-dependent NRPS condensation domains. Together, these findings support a model in which OaaC activity is regulated through substrate-dependent modulation of oligomeric state, providing a model framework for understanding FAA biosynthesis in gut microbes and expanding the known functional diversity of NRPS condensation domains.
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@article {pmid42208893,
year = {2026},
author = {Singh, J and Grant, TD and Gulick, AM},
title = {Structure of a Stand-Alone Homodimeric Nonribosomal Peptide Synthetase Condensation Domain Reveals Occlusion of the Canonical Carrier-Protein Interface.},
journal = {The Journal of biological chemistry},
volume = {},
number = {},
pages = {113208},
doi = {10.1016/j.jbc.2026.113208},
pmid = {42208893},
issn = {1083-351X},
abstract = {Fatty acid amides (FAAs) produced by gut-resident bacteria act as potent modulators of host G-protein coupled receptor signaling, yet the enzymatic mechanisms underlying their biosynthesis remain poorly understood. In many bacteria from the gut microbiome, including Coprococcus eutactus, FAA production is mediated by a nonribosomal peptide synthetase (NRPS)-like pathway that includes OaaC, a free-standing condensation domain that catalyzes amide bond formation between acyl carrier protein (ACP) tethered fatty acids and small-molecule amine acceptors. Here, we combine structural, biophysical, biochemical, and evolutionary analyses to interrogate the molecular basis of OaaC function. Solution scattering and X-ray crystallography reveal that OaaC adopts an atypical homodimeric architecture that occludes the canonical ACP-binding surface and donor access pathways. Mass photometry demonstrates that this homodimer is stable in the absence of substrates and is insensitive to free fatty acids, free amines, and apo-ACP. In contrast, holo or acyl-loaded OaaACP selectively destabilizes the homodimer forming the OaaC-OaaACP complex population. LC-MS reconstitution assays confirm that OaaC catalyzes fatty acid amide formation in vitro and can utilize acyl donors spanning multiple chain lengths and saturation states. Phylogenetic and sequence analyses place FAA-associated condensation domains in a distinct clade most closely related to starter condensation domains and reveal a conserved noncanonical active site motif that differentiates them from PCP-dependent NRPS condensation domains. Together, these findings support a model in which OaaC activity is regulated through substrate-dependent modulation of oligomeric state, providing a model framework for understanding FAA biosynthesis in gut microbes and expanding the known functional diversity of NRPS condensation domains.},
}
RevDate: 2026-05-28
From microbiomes to predictive ecosystems: challenges and opportunities in artificial intelligence-based approaches.
The Lancet. Microbe pii:S2666-5247(26)00083-2 [Epub ahead of print].
Microbiome systems encompass diverse ecological niches and host associations, with their scale and complexity challenging traditional analytical frameworks. Advances in artificial intelligence are transforming microbiome research by enabling improved integrative analyses of microbial genomes, community structure, and functional potential. In this Review, we outline how these developments create opportunities for microbiome research to move beyond descriptive analyses towards predictive modelling and hypothesis generation, including emerging insights into microbial function, host-microbe interactions, and ecosystem-level organisation. As the field grapples with challenges in model interpretability, generalisability, and causal inference, emerging strategies, such as multiomics and multicohort integration, provide promising avenues to deepen biological understanding. Addressing ethical considerations, including data privacy, algorithmic bias, and equitable access, will be crucial for translating artificial intelligence-driven microbiome discoveries into robust and inclusive clinical applications.
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@article {pmid42208955,
year = {2026},
author = {Yu, W and Qu, H and Wang, S and Shi, M and Lu, Y and Xia, S and Stanton, C and Zhang, C and Wang, Y and Zhu, T and Zhu, D and Zhou, X and Ross, RP and Zhou, Z and Huang, Y},
title = {From microbiomes to predictive ecosystems: challenges and opportunities in artificial intelligence-based approaches.},
journal = {The Lancet. Microbe},
volume = {},
number = {},
pages = {101428},
doi = {10.1016/j.lanmic.2026.101428},
pmid = {42208955},
issn = {2666-5247},
abstract = {Microbiome systems encompass diverse ecological niches and host associations, with their scale and complexity challenging traditional analytical frameworks. Advances in artificial intelligence are transforming microbiome research by enabling improved integrative analyses of microbial genomes, community structure, and functional potential. In this Review, we outline how these developments create opportunities for microbiome research to move beyond descriptive analyses towards predictive modelling and hypothesis generation, including emerging insights into microbial function, host-microbe interactions, and ecosystem-level organisation. As the field grapples with challenges in model interpretability, generalisability, and causal inference, emerging strategies, such as multiomics and multicohort integration, provide promising avenues to deepen biological understanding. Addressing ethical considerations, including data privacy, algorithmic bias, and equitable access, will be crucial for translating artificial intelligence-driven microbiome discoveries into robust and inclusive clinical applications.},
}
RevDate: 2026-05-28
The endogenous peptide GPR15L shapes the intestinal microbiota to counteract colitis.
Gut pii:gutjnl-2025-337619 [Epub ahead of print].
BACKGROUND: The peptide GPR15L is produced by colonic epithelial cells and has been implicated in T cell recruitment to the large intestine. However, its role in chronic colitis has been unclear so far.
OBJECTIVE: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD.
DESIGN: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alters the course of acute dextran sodium sulfate colitis and T cell transfer colitis. The impact of GPR15L on microbiota was explored with co-housing, littermate and faecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival.
RESULTS: GPR15L clearly mitigated experimental colitis, but this was independent of T cell recruitment and GPR15. Instead, we observed that the effects of GPR15L were mediated by altered microbiomes in the large intestine and, consistently, showed that GPR15L acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of GPR15L counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival.
CONCLUSIONS: GPR15L is a host-defence peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
Additional Links: PMID-42209192
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@article {pmid42209192,
year = {2026},
author = {Leggio, M and Schramm, S and Dietz, L and Ocón, B and Wirtz, S and Puertolas Balint, F and Yilmaz, B and Petzold, J and Liu, LJ and Dedden, M and Ekici, A and , and Meng, X and Bingham, D and Ullrich, KA and Heltmann-Meyer, S and Günther, C and Hildner, K and Atreya, R and Atreya, I and Müller, TM and Gerlach, RG and Schroeder, BO and Macpherson, A and Butcher, EC and Neurath, MF and Zundler, S and , },
title = {The endogenous peptide GPR15L shapes the intestinal microbiota to counteract colitis.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-337619},
pmid = {42209192},
issn = {1468-3288},
abstract = {BACKGROUND: The peptide GPR15L is produced by colonic epithelial cells and has been implicated in T cell recruitment to the large intestine. However, its role in chronic colitis has been unclear so far.
OBJECTIVE: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD.
DESIGN: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alters the course of acute dextran sodium sulfate colitis and T cell transfer colitis. The impact of GPR15L on microbiota was explored with co-housing, littermate and faecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival.
RESULTS: GPR15L clearly mitigated experimental colitis, but this was independent of T cell recruitment and GPR15. Instead, we observed that the effects of GPR15L were mediated by altered microbiomes in the large intestine and, consistently, showed that GPR15L acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of GPR15L counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival.
CONCLUSIONS: GPR15L is a host-defence peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.},
}
RevDate: 2026-05-28
Single nucleotide variants drive evolutionary phage-host arms race in anaerobic carbon dioxide-converting microbiome.
Nature communications pii:10.1038/s41467-026-73084-2 [Epub ahead of print].
Microbial bioconversions are shaped by environmental perturbations and the adaptation of resident microbiomes. Prokaryotes coexist with bacteriophages, yet their coevolutionary trajectories remain underexplored. Here, we investigate the effects of a cultivation vessel leak on an anaerobic consortium performing carbon dioxide reduction. Using time-series shotgun metagenomic sequencing, we reconstruct microbial and viral genomes to track community shifts. We further apply single-nucleotide variant profiling and CRISPR array analysis to monitor viral microdiversity and host defense mechanisms. After bioaugmentation restores bioconversion efficiency, the consortium undergoes pronounced restructuring, with new dominant taxa emerging from the rare biosphere. We identify patterns consistent with phage predation selectively removing certain species, while others exhibit resilience to infection. This shift aligns with a widespread viral outbreak and a transient increased frequency of single nucleotide variants in bacterial CRISPR-Cas defense genes. Expansion of CRISPR spacers further supports that CRISPR-mediated processes influence microbial resilience. Concurrently, phages infecting resilient hosts exhibited adaptive evolution, marked by high genetic heterogeneity. Selective pressure varies across their genomes, targeting infectivity genes and protospacer-adjacent motifs. These findings highlight a dynamic evolutionary arms race driven by the selection of beneficial genetic variants, providing a mechanistic framework for multi-omics investigations, and informing biotechnological applications, including phage-based microbiome manipulation.
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@article {pmid42209465,
year = {2026},
author = {Ghiotto, G and Zampieri, G and Orellana, E and Chatzis, A and Kougias, PG and Camargo, A and Roux, S and Campanaro, S and Kyrpides, NC and Treu, L},
title = {Single nucleotide variants drive evolutionary phage-host arms race in anaerobic carbon dioxide-converting microbiome.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-73084-2},
pmid = {42209465},
issn = {2041-1723},
abstract = {Microbial bioconversions are shaped by environmental perturbations and the adaptation of resident microbiomes. Prokaryotes coexist with bacteriophages, yet their coevolutionary trajectories remain underexplored. Here, we investigate the effects of a cultivation vessel leak on an anaerobic consortium performing carbon dioxide reduction. Using time-series shotgun metagenomic sequencing, we reconstruct microbial and viral genomes to track community shifts. We further apply single-nucleotide variant profiling and CRISPR array analysis to monitor viral microdiversity and host defense mechanisms. After bioaugmentation restores bioconversion efficiency, the consortium undergoes pronounced restructuring, with new dominant taxa emerging from the rare biosphere. We identify patterns consistent with phage predation selectively removing certain species, while others exhibit resilience to infection. This shift aligns with a widespread viral outbreak and a transient increased frequency of single nucleotide variants in bacterial CRISPR-Cas defense genes. Expansion of CRISPR spacers further supports that CRISPR-mediated processes influence microbial resilience. Concurrently, phages infecting resilient hosts exhibited adaptive evolution, marked by high genetic heterogeneity. Selective pressure varies across their genomes, targeting infectivity genes and protospacer-adjacent motifs. These findings highlight a dynamic evolutionary arms race driven by the selection of beneficial genetic variants, providing a mechanistic framework for multi-omics investigations, and informing biotechnological applications, including phage-based microbiome manipulation.},
}
RevDate: 2026-05-28
Combined high-quality metagenomics reveals off-target effects of albendazole, ivermectin-albendazole and moxidectin-albendazole on the human gut bacteria.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-01018-3 [Epub ahead of print].
Human whipworm infections caused by Trichuris trichiura and Trichuris incognita remain a major public health problem, affecting over 400 million people globally and responding poorly to standard benzimidazole chemotherapy. Ivermectin-albendazole and moxidectin-albendazole have emerged as promising combination therapies, but recent in vitro evidence suggests that ivermectin and moxidectin may also affect gut bacteria. We therefore characterized their off-target effects on the gut microbiome in a randomized controlled trial including 204 Trichuris spp.-infected individuals in Côte d'Ivoire treated with albendazole (400 mg), ivermectin-albendazole (200 µg/kg/400 mg), or moxidectin-albendazole (8 mg/400 mg). By combining Illumina short reads and Nanopore long reads, we recovered over 800 high-quality metagenome-assembled genomes. Albendazole and moxidectin-albendazole induced taxonomic shifts with only mild functional consequences. In contrast, individuals receiving higher absolute ivermectin doses based on their bodyweight (≥ 15 mg) showed pronounced changes in taxonomic composition and microbial function, whereas the resistome remained largely stable. These findings confirm that ivermectin can exert antibacterial off-target effects in the human gut beyond those previously observed in vitro. Given its central role in parasite control, its broader microbiome effects warrant careful evaluation in future treatment strategies.
Additional Links: PMID-42209510
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@article {pmid42209510,
year = {2026},
author = {Dommann, J and Sprecher, VP and Beisel, C and Ballmer, D and Hürlimann, E and Coulibaly, JT and Keiser, J and Schneeberger, PHH},
title = {Combined high-quality metagenomics reveals off-target effects of albendazole, ivermectin-albendazole and moxidectin-albendazole on the human gut bacteria.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01018-3},
pmid = {42209510},
issn = {2055-5008},
support = {101019223/ERC_/European Research Council/International ; 101019223/ERC_/European Research Council/International ; },
abstract = {Human whipworm infections caused by Trichuris trichiura and Trichuris incognita remain a major public health problem, affecting over 400 million people globally and responding poorly to standard benzimidazole chemotherapy. Ivermectin-albendazole and moxidectin-albendazole have emerged as promising combination therapies, but recent in vitro evidence suggests that ivermectin and moxidectin may also affect gut bacteria. We therefore characterized their off-target effects on the gut microbiome in a randomized controlled trial including 204 Trichuris spp.-infected individuals in Côte d'Ivoire treated with albendazole (400 mg), ivermectin-albendazole (200 µg/kg/400 mg), or moxidectin-albendazole (8 mg/400 mg). By combining Illumina short reads and Nanopore long reads, we recovered over 800 high-quality metagenome-assembled genomes. Albendazole and moxidectin-albendazole induced taxonomic shifts with only mild functional consequences. In contrast, individuals receiving higher absolute ivermectin doses based on their bodyweight (≥ 15 mg) showed pronounced changes in taxonomic composition and microbial function, whereas the resistome remained largely stable. These findings confirm that ivermectin can exert antibacterial off-target effects in the human gut beyond those previously observed in vitro. Given its central role in parasite control, its broader microbiome effects warrant careful evaluation in future treatment strategies.},
}
RevDate: 2026-05-28
The gut commensal Bacteroides thetaiotaomicron harbors prevalent class A and D β-lactamases with cross-taxa dissemination potential.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-01024-5 [Epub ahead of print].
The abundant gut commensal Bacteroides thetaiotaomicron is repeatedly challenged by β-lactam exposure in the human intestine, yet its β-lactamase repertoire and dissemination potential remain incompletely characterized. Here, we screened 626 publicly available B. thetaiotaomicron genomes and identified 1059 putative β-lactamase homologs, all belonging to class A or class D families. Four highly prevalent representatives-BTA-1 and CfxA-3 (class A) and OXA-347 and OXA-1327 (class D)-were prioritized for experimental validation. Heterologous expression in Escherichia coli revealed heterogeneous resistance phenotypes, with ones conferring only modest MIC increases (e.g., OXA-347, ~2-fold for amoxicillin) and others producing strong resistance to penicillins (e.g., BTA-1caused a 256-fold increase in amoxicillin MIC). Purified BTA-1 and OXA-347 were active under gut-relevant conditions, with pH optima at 7 and 8 and temperature optima at 40 °C and 30 °C, respectively. Notably, OXA-347 hydrolyzed representatives of penicillins, cephalosporins, carbapenems, and monobactams, and mass spectrometry confirmed β-lactam ring opening. Beyond B. thetaiotaomicron, these β-lactamase alleles were detected across multiple gut commensal genera as well as taxa annotated as opportunistic pathogens. Genomic context analyses showed similar gene-cluster patterns in B. thetaiotaomicron, across gut commensal genera, and in opportunistic-pathogen-associated taxa. Collectively, our findings clarify the diversity, activity, and distribution of B. thetaiotaomicron-associated β-lactamases across the gut microbiome and clinically relevant taxa.
Additional Links: PMID-42209531
Publisher:
PubMed:
Citation:
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hide bibtex listing
@article {pmid42209531,
year = {2026},
author = {Song, T and Hou, Z and Zhang, C and Luo, T and Wen, P and Mei, L and Yuan, D and Shen, X and Dong, H and Zhao, K and Chu, Y and Wang, X and Chen, F and Sun, W and Lin, J and Jiang, W},
title = {The gut commensal Bacteroides thetaiotaomicron harbors prevalent class A and D β-lactamases with cross-taxa dissemination potential.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01024-5},
pmid = {42209531},
issn = {2055-5008},
support = {No. HZ(2025)108//Zunyi Municipal Bureau of Industry and Science and Technology/ ; No. MTXYJCY(2025)008//Special Project of the Liquor Industry Research Center of Moutai Institute/ ; },
abstract = {The abundant gut commensal Bacteroides thetaiotaomicron is repeatedly challenged by β-lactam exposure in the human intestine, yet its β-lactamase repertoire and dissemination potential remain incompletely characterized. Here, we screened 626 publicly available B. thetaiotaomicron genomes and identified 1059 putative β-lactamase homologs, all belonging to class A or class D families. Four highly prevalent representatives-BTA-1 and CfxA-3 (class A) and OXA-347 and OXA-1327 (class D)-were prioritized for experimental validation. Heterologous expression in Escherichia coli revealed heterogeneous resistance phenotypes, with ones conferring only modest MIC increases (e.g., OXA-347, ~2-fold for amoxicillin) and others producing strong resistance to penicillins (e.g., BTA-1caused a 256-fold increase in amoxicillin MIC). Purified BTA-1 and OXA-347 were active under gut-relevant conditions, with pH optima at 7 and 8 and temperature optima at 40 °C and 30 °C, respectively. Notably, OXA-347 hydrolyzed representatives of penicillins, cephalosporins, carbapenems, and monobactams, and mass spectrometry confirmed β-lactam ring opening. Beyond B. thetaiotaomicron, these β-lactamase alleles were detected across multiple gut commensal genera as well as taxa annotated as opportunistic pathogens. Genomic context analyses showed similar gene-cluster patterns in B. thetaiotaomicron, across gut commensal genera, and in opportunistic-pathogen-associated taxa. Collectively, our findings clarify the diversity, activity, and distribution of B. thetaiotaomicron-associated β-lactamases across the gut microbiome and clinically relevant taxa.},
}
RevDate: 2026-05-28
Development of an Oxford nanopore sequencing technology-based whole genome sequencing method for Plasmodium falciparum to support malaria molecular surveillance.
Scientific reports pii:10.1038/s41598-026-46451-8 [Epub ahead of print].
Whole genome sequencing (WGS) is critical for malaria molecular surveillance (MMS). While short-read platforms have been widely used for Plasmodium falciparum genomics; they have limitations in resolving repetitive regions and structural variation in this highly complex genome. Long-read technologies, such as those developed by Oxford nanopore technologies (ONT), offer complementary capabilities and may be particularly suitable for low-resource settings. We optimized an ONT-based WGS protocol for P. falciparum from DBS and whole blood samples. Laboratory strains (3D7, HB3, and Dd2) were mixed with whole blood to create mock infections and dried blood spots (DBS). DNA was extracted using Qiagen or Tween-Chelex 100, and parasite DNA was enriched using McrBC/MspJI digestion, NEBNext microbiome DNA enrichment Kit (NMDEK), and selective whole genome amplification (sWGA). Parasite and human DNA levels were quantified by multiplex qPCR. Sequencing was performed on ONT (R10.4.1 flow cell). The protocol was validated with? clinical samples from a therapeutic efficacy study. Tween-Chelex 100 had a higher DNA yield compared to Qiagen kit (2-4 Ct value difference), though Qiagen extractions gave longer reads (median 2791 vs. 2252 bp). NMDEK effectively depleted human DNA by increasing the Ct value of β-tubulin human gene by ~ 10 cycles, while sWGA increased parasite DNA. Combined enrichment yielded > 75% parasite DNA at 100 p/µl and > 90% genome coverage. WGS of mock and clinical samples achieved median read lengths > 2 kb, > 30× depth, and 99.8% accuracy. Whole blood outperformed DBS in depth and coverage. ONT WGS showed high concordance with Sanger sequencing and detected additional mutations and structural variants, including pfmdr1 and pfgch1 copy number variations. The optimized ONT-WGS protocol enabled accurate, high-coverage sequencing from whole blood and DBS. It provides a practical option for generating long-read data with relatively rapid turnaround and modest infrastructure requirements, supporting its application for MMS in malaria-endemic settings.
Additional Links: PMID-42209548
Publisher:
PubMed:
Citation:
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@article {pmid42209548,
year = {2026},
author = {Bakari, C and Holzschuh, A and Seth, MD and Madebe, RA and Pereus, D and Mandara, CI and Schneeberger, P and Juliano, JJ and Bailey, JA and Ishengoma, DS and Nsanzabana, C},
title = {Development of an Oxford nanopore sequencing technology-based whole genome sequencing method for Plasmodium falciparum to support malaria molecular surveillance.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-46451-8},
pmid = {42209548},
issn = {2045-2322},
support = {INV. 002202 & INV. 067322//Gates Foundation, United States/ ; INV. 002202 & INV. 067322//Gates Foundation, United States/ ; INV. 002202 & INV. 067322//Gates Foundation, United States/ ; INV. 002202 & INV. 067322//Gates Foundation, United States/ ; INV. 002202 & INV. 067322//Gates Foundation, United States/ ; INV. 002202 & INV. 067322//Gates Foundation, United States/ ; },
abstract = {Whole genome sequencing (WGS) is critical for malaria molecular surveillance (MMS). While short-read platforms have been widely used for Plasmodium falciparum genomics; they have limitations in resolving repetitive regions and structural variation in this highly complex genome. Long-read technologies, such as those developed by Oxford nanopore technologies (ONT), offer complementary capabilities and may be particularly suitable for low-resource settings. We optimized an ONT-based WGS protocol for P. falciparum from DBS and whole blood samples. Laboratory strains (3D7, HB3, and Dd2) were mixed with whole blood to create mock infections and dried blood spots (DBS). DNA was extracted using Qiagen or Tween-Chelex 100, and parasite DNA was enriched using McrBC/MspJI digestion, NEBNext microbiome DNA enrichment Kit (NMDEK), and selective whole genome amplification (sWGA). Parasite and human DNA levels were quantified by multiplex qPCR. Sequencing was performed on ONT (R10.4.1 flow cell). The protocol was validated with? clinical samples from a therapeutic efficacy study. Tween-Chelex 100 had a higher DNA yield compared to Qiagen kit (2-4 Ct value difference), though Qiagen extractions gave longer reads (median 2791 vs. 2252 bp). NMDEK effectively depleted human DNA by increasing the Ct value of β-tubulin human gene by ~ 10 cycles, while sWGA increased parasite DNA. Combined enrichment yielded > 75% parasite DNA at 100 p/µl and > 90% genome coverage. WGS of mock and clinical samples achieved median read lengths > 2 kb, > 30× depth, and 99.8% accuracy. Whole blood outperformed DBS in depth and coverage. ONT WGS showed high concordance with Sanger sequencing and detected additional mutations and structural variants, including pfmdr1 and pfgch1 copy number variations. The optimized ONT-WGS protocol enabled accurate, high-coverage sequencing from whole blood and DBS. It provides a practical option for generating long-read data with relatively rapid turnaround and modest infrastructure requirements, supporting its application for MMS in malaria-endemic settings.},
}
RevDate: 2026-05-28
Gut microbiome screens could identify risk of Parkinson's disease years before symptoms appear.
Nature medicine [Epub ahead of print].
Additional Links: PMID-42209780
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42209780,
year = {2026},
author = {},
title = {Gut microbiome screens could identify risk of Parkinson's disease years before symptoms appear.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42209780},
issn = {1546-170X},
}
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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.