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ESP: PubMed Auto Bibliography 09 Jul 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: 2026-07-07
Longitudinal vaginal microbiomes and quality-of-life patterns during tamoxifen therapy in breast cancer: a pilot study.
Scientific reports pii:10.1038/s41598-026-59886-w [Epub ahead of print].
Tamoxifen is widely used in breast cancer treatment, but its effects on vaginal microbiome remain poorly understood. This prospective longitudinal pilot study explored vaginal microbiota profiles and quality-of-life parameters in women receiving tamoxifen for breast cancer in Seoul, South Korea (2023-2024). Eleven women initiating tamoxifen therapy were enrolled. Vaginal swabs were collected at baseline (V0) and 6 months (V6). Microbiota was profiled using 16 S rRNA gene sequencing. Quality of life was assessed using the 11-item Menopause Rating Scale. Participants were stratified by baseline colonization patterns. Overall community composition did not show a significant shift between baseline and 6 months. In the full-cohort taxa-level paired analysis, Gardnerella vaginalis (G. vaginalis) showed a nominal, non-FDR-significant increase from baseline to 6 months, and no taxon remained significant after multiple-comparison correction. A negative correlation was observed between G. vaginalis and Lactobacillus iners (L. iners) (ρ = -0.6, raw P < 0.01, FDR q < 0.05). Among participants with baseline G. vaginalis detection, 4 of 5 showed increased relative abundance at 6 months, although the confidence interval was wide. G. vaginalis abundance was associated with worse sexual-function-related quality-of-life scores in exploratory analyses, but item-level MRS comparisons did not remain significant after correction for multiple testing. In this small hypothesis-generating pilot cohort, women receiving tamoxifen showed largely stable overall vaginal community composition over 6 months, with an exploratory signal of G. vaginalis expansion among participants colonized at baseline. These findings should be interpreted cautiously given the small sample size, absence of a control group, treatment heterogeneity, and post hoc subgroup analysis, and require validation in larger controlled cohorts.
Additional Links: PMID-42414431
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PubMed:
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@article {pmid42414431,
year = {2026},
author = {Jeong, HG and Ryu, KJ and Joo, M and Park, S and Park, HT},
title = {Longitudinal vaginal microbiomes and quality-of-life patterns during tamoxifen therapy in breast cancer: a pilot study.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-59886-w},
pmid = {42414431},
issn = {2045-2322},
support = {O2412321//Korea University Anam Hospital/ ; K2513591//Korea University Anam Hospital/ ; RS-2025-02243104//Korea Health Industry Development Institute/Republic of Korea ; },
abstract = {Tamoxifen is widely used in breast cancer treatment, but its effects on vaginal microbiome remain poorly understood. This prospective longitudinal pilot study explored vaginal microbiota profiles and quality-of-life parameters in women receiving tamoxifen for breast cancer in Seoul, South Korea (2023-2024). Eleven women initiating tamoxifen therapy were enrolled. Vaginal swabs were collected at baseline (V0) and 6 months (V6). Microbiota was profiled using 16 S rRNA gene sequencing. Quality of life was assessed using the 11-item Menopause Rating Scale. Participants were stratified by baseline colonization patterns. Overall community composition did not show a significant shift between baseline and 6 months. In the full-cohort taxa-level paired analysis, Gardnerella vaginalis (G. vaginalis) showed a nominal, non-FDR-significant increase from baseline to 6 months, and no taxon remained significant after multiple-comparison correction. A negative correlation was observed between G. vaginalis and Lactobacillus iners (L. iners) (ρ = -0.6, raw P < 0.01, FDR q < 0.05). Among participants with baseline G. vaginalis detection, 4 of 5 showed increased relative abundance at 6 months, although the confidence interval was wide. G. vaginalis abundance was associated with worse sexual-function-related quality-of-life scores in exploratory analyses, but item-level MRS comparisons did not remain significant after correction for multiple testing. In this small hypothesis-generating pilot cohort, women receiving tamoxifen showed largely stable overall vaginal community composition over 6 months, with an exploratory signal of G. vaginalis expansion among participants colonized at baseline. These findings should be interpreted cautiously given the small sample size, absence of a control group, treatment heterogeneity, and post hoc subgroup analysis, and require validation in larger controlled cohorts.},
}
RevDate: 2026-07-07
Oxytocin and RAGE signaling at the intersection of social neurodevelopment and inflammation.
Journal of translational medicine pii:10.1186/s12967-026-08395-5 [Epub ahead of print].
BACKGROUND: Autism spectrum disorder (ASD) prevalence continues to rise despite no recent changes to screening or diagnostic criteria. A complete understanding of the pathophysiology of ASD remains elusive. Gestational and postnatal inflammation correlate strongly with ASD prevalence, which is supported by maternal immune activation prevalence studies, maternal immunoglobulin found in fetal brains with ASD and altered T-cell populations in ASD children. Elevated TNF-α, interleukins, nuclear factors, and toll-like receptor levels reported in subgroups of ASD children provide evidence of a chronic inflammatory process posited to be a consequence of a cellular danger response impacting T-cells, neutrophils, macrophages, and microglia.
MAIN BODY: The RAGE system is a multi-ligand receptor within the immunoglobulin (Ig) superfamily that plays a role in inflammatory gene signaling and may help explain how early prenatal and ongoing inflammatory insults are linked to the autistic phenotype. ASD patients demonstrate differences in RAGE signaling; elevations in inflammatory gene expression ligands (AGEs, HMGB1, S100 family), decreases in esRAGE, regionally altered C1q, and impaired APP metabolism. Each of these ligands serves a role as either increasing inflammatory gene expression, modulating transport of biomolecules, or mediating immune cell migration and phagocytosis. Additionally, the RAGE system has been demonstrated to be involved in gut-blood and blood-brain oxytocin transport. In the mouse model, chronic inflammation is associated with impaired oxytocin transport across these barriers. Young children with ASD have lower serum oxytocin levels than age-matched controls, and serum OXT levels correlate with social communication testing across all groups of children. ASD patients have an increased prevalence of asthma, atopic dermatitis, allergic rhinitis, and irritable bowel syndrome, indicating an ongoing inflammatory hyperactivity in some ASD subgroups that may disturb oxytocin transport, predisposing ASD symptomology. Furthermore, the gut microbiome and its metabolites influence RAGE signaling and may partially explain the differences in microbiome composition in ASD patients.
CONCLUSION: Altered RAGE signaling is the proposed mechanistic link between ongoing inflammation and impaired oxytocinergic signaling contributing to ASD pathogenesis in certain subgroups. Further research into the biomarkers involved could identify subpopulations of ASD patients that would benefit from early modulation of the RAGE system.
Additional Links: PMID-42415063
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PubMed:
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@article {pmid42415063,
year = {2026},
author = {Shoup, J and Sadle, C and Buckley, A and Song, ZH and Nagarajan, N and Barnes, G},
title = {Oxytocin and RAGE signaling at the intersection of social neurodevelopment and inflammation.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08395-5},
pmid = {42415063},
issn = {1479-5876},
support = {P30ES030283/ES/NIEHS NIH HHS/United States ; AR230178P1//U.S. Department of Defense/ ; },
abstract = {BACKGROUND: Autism spectrum disorder (ASD) prevalence continues to rise despite no recent changes to screening or diagnostic criteria. A complete understanding of the pathophysiology of ASD remains elusive. Gestational and postnatal inflammation correlate strongly with ASD prevalence, which is supported by maternal immune activation prevalence studies, maternal immunoglobulin found in fetal brains with ASD and altered T-cell populations in ASD children. Elevated TNF-α, interleukins, nuclear factors, and toll-like receptor levels reported in subgroups of ASD children provide evidence of a chronic inflammatory process posited to be a consequence of a cellular danger response impacting T-cells, neutrophils, macrophages, and microglia.
MAIN BODY: The RAGE system is a multi-ligand receptor within the immunoglobulin (Ig) superfamily that plays a role in inflammatory gene signaling and may help explain how early prenatal and ongoing inflammatory insults are linked to the autistic phenotype. ASD patients demonstrate differences in RAGE signaling; elevations in inflammatory gene expression ligands (AGEs, HMGB1, S100 family), decreases in esRAGE, regionally altered C1q, and impaired APP metabolism. Each of these ligands serves a role as either increasing inflammatory gene expression, modulating transport of biomolecules, or mediating immune cell migration and phagocytosis. Additionally, the RAGE system has been demonstrated to be involved in gut-blood and blood-brain oxytocin transport. In the mouse model, chronic inflammation is associated with impaired oxytocin transport across these barriers. Young children with ASD have lower serum oxytocin levels than age-matched controls, and serum OXT levels correlate with social communication testing across all groups of children. ASD patients have an increased prevalence of asthma, atopic dermatitis, allergic rhinitis, and irritable bowel syndrome, indicating an ongoing inflammatory hyperactivity in some ASD subgroups that may disturb oxytocin transport, predisposing ASD symptomology. Furthermore, the gut microbiome and its metabolites influence RAGE signaling and may partially explain the differences in microbiome composition in ASD patients.
CONCLUSION: Altered RAGE signaling is the proposed mechanistic link between ongoing inflammation and impaired oxytocinergic signaling contributing to ASD pathogenesis in certain subgroups. Further research into the biomarkers involved could identify subpopulations of ASD patients that would benefit from early modulation of the RAGE system.},
}
RevDate: 2026-07-07
CmpDate: 2026-07-08
Defined bacterial consortium highlights the impact of intestinal bacteria on DNA methylation and tumorigenesis.
Genome biology, 27(1):.
BACKGROUND: Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in the United States. While the gut microbiota has been shown to influence CRC development, the specific contribution of bacteria to DNA methylation and carcinogenesis remains underexplored.
RESULTS: We colonize two groups of GF Apc[Min/+] mice with two consortia, one harboring a pks[+] E. coli strain with "low-pks" activity (DSMZ) and the second with a clinical isolate exhibiting "high-pks" activity (UM149). These colonized mice are exposed to DSS-induced colitis, and analyzed for tumor burden, DNA methylation, and transcriptional changes. We find that colonization with C13-UM149 leads to more tumors, increased cell proliferation, and higher DNA damage compared to C13-DSMZ (p < 0.05). Methylation analyses show that C13-DSMZ causes extensive promoter hypermethylation and altered gene expression. Differential DNA methylation in mice colonized with either C13-DSMZ or C13-UM149 is associated with changes in pathways controlling tumor suppression, cell proliferation, inflammation, and Wnt signaling. In C13-DSMZ mice, hypermethylation is associated with gene expression involved in tumor suppression in both tumors and normal tissue, whereas hypomethylation is linked to expression of genes promoting Wnt signaling. In C13-UM149 mice, methylation changes were connected to genes involved in epithelial proliferation, extracellular matrix remodeling, and inflammatory responses.
CONCLUSIONS: These findings demonstrate that intestinal bacteria with distinct pks activities differentially modulate DNA methylation thereby influencing gene expression and tumor development. This highlights bacterial modulation of epigenetic responses as a potential mechanism underlying CRC progression.
Additional Links: PMID-42415118
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@article {pmid42415118,
year = {2026},
author = {Mercado-Rodriguez, C and Chitre, S and Park, PH and Yang, Y and Pompetti, A and Gharaibeh, RZ and Brant, JO and Issa, JJ and Jobin, C},
title = {Defined bacterial consortium highlights the impact of intestinal bacteria on DNA methylation and tumorigenesis.},
journal = {Genome biology},
volume = {27},
number = {1},
pages = {},
pmid = {42415118},
issn = {1474-760X},
support = {NCI R01CA214005/NH/NIH HHS/United States ; },
mesh = {Animals ; *DNA Methylation ; Mice ; *Carcinogenesis/genetics ; Cell Proliferation ; *Colorectal Neoplasms/microbiology/genetics/pathology ; Colitis/microbiology/chemically induced/genetics ; *Gastrointestinal Microbiome ; Promoter Regions, Genetic ; Escherichia coli ; DNA Damage ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in the United States. While the gut microbiota has been shown to influence CRC development, the specific contribution of bacteria to DNA methylation and carcinogenesis remains underexplored.
RESULTS: We colonize two groups of GF Apc[Min/+] mice with two consortia, one harboring a pks[+] E. coli strain with "low-pks" activity (DSMZ) and the second with a clinical isolate exhibiting "high-pks" activity (UM149). These colonized mice are exposed to DSS-induced colitis, and analyzed for tumor burden, DNA methylation, and transcriptional changes. We find that colonization with C13-UM149 leads to more tumors, increased cell proliferation, and higher DNA damage compared to C13-DSMZ (p < 0.05). Methylation analyses show that C13-DSMZ causes extensive promoter hypermethylation and altered gene expression. Differential DNA methylation in mice colonized with either C13-DSMZ or C13-UM149 is associated with changes in pathways controlling tumor suppression, cell proliferation, inflammation, and Wnt signaling. In C13-DSMZ mice, hypermethylation is associated with gene expression involved in tumor suppression in both tumors and normal tissue, whereas hypomethylation is linked to expression of genes promoting Wnt signaling. In C13-UM149 mice, methylation changes were connected to genes involved in epithelial proliferation, extracellular matrix remodeling, and inflammatory responses.
CONCLUSIONS: These findings demonstrate that intestinal bacteria with distinct pks activities differentially modulate DNA methylation thereby influencing gene expression and tumor development. This highlights bacterial modulation of epigenetic responses as a potential mechanism underlying CRC progression.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*DNA Methylation
Mice
*Carcinogenesis/genetics
Cell Proliferation
*Colorectal Neoplasms/microbiology/genetics/pathology
Colitis/microbiology/chemically induced/genetics
*Gastrointestinal Microbiome
Promoter Regions, Genetic
Escherichia coli
DNA Damage
Mice, Inbred C57BL
RevDate: 2026-07-07
CmpDate: 2026-07-08
The role of the vaginal microbiome in pregnancy loss and preterm birth: a commentary.
Maternal health, neonatology and perinatology, 12(1):.
BACKGROUND: Eubiosis or dysbiosis of the vaginal microbiome may influence the rate of pregnancy loss and preterm birth, the major cause of neonatal and perinatal mortality worldwide.
METHODS: This was a comparison of two vaginal microbiome studies; one a cohort study and the other a multinational randomised controlled feasibility study. Both studies used cultivation-independent molecular microbiological techniques that together have implications on the risk of pregnancy loss and preterm birth in association with vaginal dysbiosis.
RESULTS: The cohort study identified a risk-associated vaginal microbiome signature in association with early pregnancy-loss that comprised an increase in the relative abundance of potentially dysbiotic organisms such as Lactobacillus iners, Sneathia and Prevotella spp and a concomitant decrease in the abundance of eubiotic microorganisms such as Lactobacillus crispatus. Convergent evidence across the two studies demonstrated that a synbiotic intervention was able to shift the vaginal microbiome from the signature demonstrated by Skafte-Holm et al., to a decrease in the abundance of Prevotella, Gardnerella and Atopobium spp, while simultaneously increasing the abundance of eubiotic vaginal Lactobacillus spp.
CONCLUSIONS: We concluded that there is convergent evidence across the two studies which might otherwise have gone unnoticed. While neither study was powered to demonstrate clinical endpoints and did not establish causal relationships between microbiome modulation and pregnancy outcomes, when administered regularly, vaginal commensal probiotics in ice-cream were effective in optimizing both the vaginal and intestinal microbiota in pregnant women at increased risk of pregnancy loss, particularly preterm birth. This emphasises the need for adequately powered trials to test whether early pregnancy vaginal microbiome modulation can improve clinical outcomes.
Additional Links: PMID-42415152
PubMed:
Citation:
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@article {pmid42415152,
year = {2026},
author = {Lamont, RF and Bartolomaeus, TUP and Borum, LS and Forslund-Startceva, SK and Jørgensen, JS},
title = {The role of the vaginal microbiome in pregnancy loss and preterm birth: a commentary.},
journal = {Maternal health, neonatology and perinatology},
volume = {12},
number = {1},
pages = {},
pmid = {42415152},
issn = {2054-958X},
abstract = {BACKGROUND: Eubiosis or dysbiosis of the vaginal microbiome may influence the rate of pregnancy loss and preterm birth, the major cause of neonatal and perinatal mortality worldwide.
METHODS: This was a comparison of two vaginal microbiome studies; one a cohort study and the other a multinational randomised controlled feasibility study. Both studies used cultivation-independent molecular microbiological techniques that together have implications on the risk of pregnancy loss and preterm birth in association with vaginal dysbiosis.
RESULTS: The cohort study identified a risk-associated vaginal microbiome signature in association with early pregnancy-loss that comprised an increase in the relative abundance of potentially dysbiotic organisms such as Lactobacillus iners, Sneathia and Prevotella spp and a concomitant decrease in the abundance of eubiotic microorganisms such as Lactobacillus crispatus. Convergent evidence across the two studies demonstrated that a synbiotic intervention was able to shift the vaginal microbiome from the signature demonstrated by Skafte-Holm et al., to a decrease in the abundance of Prevotella, Gardnerella and Atopobium spp, while simultaneously increasing the abundance of eubiotic vaginal Lactobacillus spp.
CONCLUSIONS: We concluded that there is convergent evidence across the two studies which might otherwise have gone unnoticed. While neither study was powered to demonstrate clinical endpoints and did not establish causal relationships between microbiome modulation and pregnancy outcomes, when administered regularly, vaginal commensal probiotics in ice-cream were effective in optimizing both the vaginal and intestinal microbiota in pregnant women at increased risk of pregnancy loss, particularly preterm birth. This emphasises the need for adequately powered trials to test whether early pregnancy vaginal microbiome modulation can improve clinical outcomes.},
}
RevDate: 2026-07-07
Dynamic, transition and variation of cervicovaginal microbiome and HPV infection and cervical dysplasia and cancer: a systematic review.
Infectious agents and cancer pii:10.1186/s13027-026-00777-0 [Epub ahead of print].
BACKGROUND: Cervical cancer is the fourth most common malignancy in women worldwide, with approximately 660,000 new cases and 350,000 deaths annually. The burden falls disproportionately on low- and middle-income countries. Although persistent infection with high-risk HPV (hrHPV) is the necessary cause, most infected women clear the virus spontaneously, implicating additional cofactors, including the cervicovaginal microbiome in determining oncogenic outcomes.
METHODS: PubMed was searched through September 10, 2024, to identify longitudinal studies assessing cervicovaginal microbiota in relation to HPV infection or cervical lesion outcomes at two or more time points. Methodological quality was evaluated using the Newcastle-Ottawa Scale (NOS). Given the substantial heterogeneity, a structured thematic synthesis was performed across three predefined domains: (a) baseline microbiome composition and clinical outcomes; (b) community state type (CST) dynamics and temporal stability; and (c) microbiome changes following treatment.
RESULTS: Twelve studies enrolling 1,663 women across 11 countries met inclusion criteria. NOS scores ranged from 4 to 9. Lactobacillus-dominated CSTs at baseline were consistently associated with HPV clearance and CIN regression, while Lactobacillus-depleted states showed higher transition rates and unfavourable outcomes. Prior L.iners (CST III) dominance was repeatedly linked to favourable outcomes, although evidence on this species remains conflicting. Cervicovaginal dysbiosis frequently preceded HPV persistence or lesion progression.
CONCLUSION: Sustained Lactobacillus-dominated CST stability, rather than dominance by any single species, is the most consistent microbiome factor associated with favourable HPV and cervical lesion outcomes. Standardized longitudinal designs incorporating metagenomic sequencing, frequent sampling intervals, and rigorous confounder adjustment are needed to advance mechanistic understanding.
Not applicable.
Additional Links: PMID-42415156
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PubMed:
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@article {pmid42415156,
year = {2026},
author = {Houvessou, GM and Antonieta Alfane, NW and Mahoche, M},
title = {Dynamic, transition and variation of cervicovaginal microbiome and HPV infection and cervical dysplasia and cancer: a systematic review.},
journal = {Infectious agents and cancer},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13027-026-00777-0},
pmid = {42415156},
issn = {1750-9378},
abstract = {BACKGROUND: Cervical cancer is the fourth most common malignancy in women worldwide, with approximately 660,000 new cases and 350,000 deaths annually. The burden falls disproportionately on low- and middle-income countries. Although persistent infection with high-risk HPV (hrHPV) is the necessary cause, most infected women clear the virus spontaneously, implicating additional cofactors, including the cervicovaginal microbiome in determining oncogenic outcomes.
METHODS: PubMed was searched through September 10, 2024, to identify longitudinal studies assessing cervicovaginal microbiota in relation to HPV infection or cervical lesion outcomes at two or more time points. Methodological quality was evaluated using the Newcastle-Ottawa Scale (NOS). Given the substantial heterogeneity, a structured thematic synthesis was performed across three predefined domains: (a) baseline microbiome composition and clinical outcomes; (b) community state type (CST) dynamics and temporal stability; and (c) microbiome changes following treatment.
RESULTS: Twelve studies enrolling 1,663 women across 11 countries met inclusion criteria. NOS scores ranged from 4 to 9. Lactobacillus-dominated CSTs at baseline were consistently associated with HPV clearance and CIN regression, while Lactobacillus-depleted states showed higher transition rates and unfavourable outcomes. Prior L.iners (CST III) dominance was repeatedly linked to favourable outcomes, although evidence on this species remains conflicting. Cervicovaginal dysbiosis frequently preceded HPV persistence or lesion progression.
CONCLUSION: Sustained Lactobacillus-dominated CST stability, rather than dominance by any single species, is the most consistent microbiome factor associated with favourable HPV and cervical lesion outcomes. Standardized longitudinal designs incorporating metagenomic sequencing, frequent sampling intervals, and rigorous confounder adjustment are needed to advance mechanistic understanding.
Not applicable.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
A metabolite-dependent mechanism by which Bifidobacterium animalis subsp. lactis promotes Bacteroides colonization.
Gut microbes, 18(1):2696647.
Prokaryote-prokaryote symbiotic relationships influence interactions within microbial communities, affecting colonization, survival, and organization. Unlike competition, consortium species facilitate growth via metabolite cross-feeding. This study explored interactions between two early human gut colonizers: partially aerotolerant Bifidobacterium spp. and strict anaerobic Bacteroides spp., using omics techniques. Promotion of Bacteroides spp. growth by Bifidobacterium animalis subsp. lactis was demonstrated through co-culture experiments in anaerobic conditions. Metabolomic analysis revealed over 150 unique metabolites present in B. animalis subsp. lactis supernatants are absent in other Bifidobacterium species, including 3-hydroxycapric acid, D-alanyl-D-alanine, 2-isopropylmalic acid, and D-glucose 2-phosphate. These compounds served as nutritional substrates, including carbon and nitrogen sources, significantly enhancing Bacteroides spp. growth. In murine models, early colonization by B. animalis subsp. lactis consolidated Bacteroides fragilis colonization (1.7 × 10[4] to 9.7 × 10[6] copy number/g fecal sample) by providing these metabolites as a niche. These findings highlight B. animalis subsp. lactis plays a critical role in gut colonization of Bacteroides spp. via its exclusive metabolic profile, offering insights into partitioned metabolic activity within gut communities and emphasizing the importance of specific metabolites in early microbial establishment.
Additional Links: PMID-42415234
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PubMed:
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@article {pmid42415234,
year = {2026},
author = {Shahin, K and Wang, L and He, Z and Lv, B and Van Alin, A and Lo-Man, R and Wu, H and Sansonetti, P and Collard, JM},
title = {A metabolite-dependent mechanism by which Bifidobacterium animalis subsp. lactis promotes Bacteroides colonization.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2696647},
doi = {10.1080/19490976.2026.2696647},
pmid = {42415234},
issn = {1949-0984},
mesh = {Animals ; *Bacteroides/growth & development/metabolism ; Humans ; Mice ; Feces/microbiology ; *Bifidobacterium animalis/metabolism/growth & development ; *Gastrointestinal Microbiome ; Symbiosis ; Bifidobacterium/metabolism ; Metabolome ; Coculture Techniques ; Bacteroides fragilis/growth & development/metabolism ; },
abstract = {Prokaryote-prokaryote symbiotic relationships influence interactions within microbial communities, affecting colonization, survival, and organization. Unlike competition, consortium species facilitate growth via metabolite cross-feeding. This study explored interactions between two early human gut colonizers: partially aerotolerant Bifidobacterium spp. and strict anaerobic Bacteroides spp., using omics techniques. Promotion of Bacteroides spp. growth by Bifidobacterium animalis subsp. lactis was demonstrated through co-culture experiments in anaerobic conditions. Metabolomic analysis revealed over 150 unique metabolites present in B. animalis subsp. lactis supernatants are absent in other Bifidobacterium species, including 3-hydroxycapric acid, D-alanyl-D-alanine, 2-isopropylmalic acid, and D-glucose 2-phosphate. These compounds served as nutritional substrates, including carbon and nitrogen sources, significantly enhancing Bacteroides spp. growth. In murine models, early colonization by B. animalis subsp. lactis consolidated Bacteroides fragilis colonization (1.7 × 10[4] to 9.7 × 10[6] copy number/g fecal sample) by providing these metabolites as a niche. These findings highlight B. animalis subsp. lactis plays a critical role in gut colonization of Bacteroides spp. via its exclusive metabolic profile, offering insights into partitioned metabolic activity within gut communities and emphasizing the importance of specific metabolites in early microbial establishment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Bacteroides/growth & development/metabolism
Humans
Mice
Feces/microbiology
*Bifidobacterium animalis/metabolism/growth & development
*Gastrointestinal Microbiome
Symbiosis
Bifidobacterium/metabolism
Metabolome
Coculture Techniques
Bacteroides fragilis/growth & development/metabolism
RevDate: 2026-07-08
CmpDate: 2026-07-08
Targeting the Organ-Brain Axis: The Modulatory Role of Peripheral Organs in Depression.
Comprehensive Physiology, 16(4):e70216.
Major Depressive Disorder (MDD) is a highly prevalent mental illness whose pathophysiology remains incompletely understood. Although MDD has traditionally been conceptualized primarily as a disorder of central nervous system dysfunction, accumulating evidence supports a broader brain-body framework, particularly in biologically defined subgroups characterized by inflammatory, metabolic, endocrine, autonomic, or microbiome-related abnormalities. This review summarizes how selected peripheral organs, including the gut, liver, heart, spleen, skeletal muscle, adipose tissue, bone marrow, and endocrine glands, may communicate with the brain through neural, metabolic, immune, endocrine, and microbial pathways. Emerging preclinical and clinical evidence suggests that these peripheral signals may participate in neuroinflammation and physiological alterations associated with depressive phenotypes. However, their causal status in humans remains incompletely established, and peripheral alterations may represent contributors to, correlates of, or consequences of central pathological states. We further discuss how multi-organ communication networks may converge on shared central pathways and provide a conceptual framework for understanding selected MDD phenotypes. Finally, we evaluate therapeutic strategies targeting systemic inflammation, metabolic homeostasis, and endocrine regulation, while emphasizing current translational limitations.
Additional Links: PMID-42415406
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@article {pmid42415406,
year = {2026},
author = {Han, J and Zhang, W and Zhang, Y and Ding, J},
title = {Targeting the Organ-Brain Axis: The Modulatory Role of Peripheral Organs in Depression.},
journal = {Comprehensive Physiology},
volume = {16},
number = {4},
pages = {e70216},
doi = {10.1002/cph4.70216},
pmid = {42415406},
issn = {2040-4603},
support = {32300731//National Natural Science Foundation of China/ ; 82473431//National Natural Science Foundation of China/ ; 2023ZKZD44//Innovation Program of Shanghai Municipal Education Commission/ ; },
mesh = {Humans ; *Brain/physiopathology/metabolism ; Animals ; *Major Depressive Disorder/physiopathology ; *Depression/physiopathology ; },
abstract = {Major Depressive Disorder (MDD) is a highly prevalent mental illness whose pathophysiology remains incompletely understood. Although MDD has traditionally been conceptualized primarily as a disorder of central nervous system dysfunction, accumulating evidence supports a broader brain-body framework, particularly in biologically defined subgroups characterized by inflammatory, metabolic, endocrine, autonomic, or microbiome-related abnormalities. This review summarizes how selected peripheral organs, including the gut, liver, heart, spleen, skeletal muscle, adipose tissue, bone marrow, and endocrine glands, may communicate with the brain through neural, metabolic, immune, endocrine, and microbial pathways. Emerging preclinical and clinical evidence suggests that these peripheral signals may participate in neuroinflammation and physiological alterations associated with depressive phenotypes. However, their causal status in humans remains incompletely established, and peripheral alterations may represent contributors to, correlates of, or consequences of central pathological states. We further discuss how multi-organ communication networks may converge on shared central pathways and provide a conceptual framework for understanding selected MDD phenotypes. Finally, we evaluate therapeutic strategies targeting systemic inflammation, metabolic homeostasis, and endocrine regulation, while emphasizing current translational limitations.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Brain/physiopathology/metabolism
Animals
*Major Depressive Disorder/physiopathology
*Depression/physiopathology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Integrative profiling of oral fungal communities across Mycobacterium Tuberculosis burden groups in Xpert-positive patients.
Annals of medicine, 58(1):2698284.
BACKGROUND: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a major global health burden. A growing body of evidence suggests that mucosal microbial communities may reflect or modulate host responses during infection. However, the oral microbiome in TB patients with different bacterial loads remains poorly characterized. This study aimed to investigate alterations in oral fungal communities among Xpert-positive patients, stratified by Mtb burden based on Xpert MTB/RIF testing.
METHODS: In this prospective multicenter cohort study (May-August 2024), 278 Xpert-positive TB patients were enrolled across five hospitals in China. Participants were stratified into high, medium, low, and very low Mtb burden groups according to Xpert MTB/RIF cycle threshold values. Paired sputum and tongue swab samples were collected. Oral fungal profiles were characterized via ITS sequencing, followed by taxonomic assignment, diversity analysis, and multivariable association testing (MaAsLin 2) to identify robust biomarkers.
RESULTS: Oral fungal community structure varied significantly across Mtb burden strata. Beta-diversity analysis revealed distinct clustering between the very low burden group and higher burden groups (high, medium, low). High-burden patients were enriched with environmental taxa such as Blumeria and Toxicocladosporium, whereas low-burden groups exhibited higher abundances of Candida, Aspergillus, and Penicillium. Notably, MaAsLin 2 analysis confirmed that Penicillium and Podosphaera were independently associated with lower Mtb burden after adjusting for confounders. Neutral model analysis indicated that stochastic processes predominantly drive the assembly of these oral fungal communities. Functional prediction suggested enhanced aerobic respiration and metabolic enzyme activity in high-burden groups.
CONCLUSIONS: This study analyzed the oral fungal microbiome stratified by Mtb burden strata in Xpert-positive patients, revealing distinct shifts in fungal composition and functional potential. Fungal dysbiosis and altered microbial metabolic capacity may offer insight into host-microbe interactions in pulmonary TB (PTB). These findings underscore the potential value of fungal microbiome profiling for assessing Mtb burden, beyond its application in TB diagnosis alone.
Additional Links: PMID-42415599
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@article {pmid42415599,
year = {2026},
author = {Wang, Y and Li, R and Tang, Z and Ma, Z and Dong, X and Shu, W and Cui, J and Wei, M and Liu, Z and Shen, D and Li, L and Pang, Y},
title = {Integrative profiling of oral fungal communities across Mycobacterium Tuberculosis burden groups in Xpert-positive patients.},
journal = {Annals of medicine},
volume = {58},
number = {1},
pages = {2698284},
doi = {10.1080/07853890.2026.2698284},
pmid = {42415599},
issn = {1365-2060},
mesh = {Humans ; *Mycobacterium tuberculosis/isolation & purification ; Prospective Studies ; Female ; *Mouth/microbiology ; Male ; Sputum/microbiology ; Adult ; Middle Aged ; China/epidemiology ; *Fungi/isolation & purification/classification/genetics ; *Mycobiome ; *Microbiota ; *Tuberculosis, Pulmonary/microbiology/diagnosis ; Bacterial Load ; },
abstract = {BACKGROUND: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a major global health burden. A growing body of evidence suggests that mucosal microbial communities may reflect or modulate host responses during infection. However, the oral microbiome in TB patients with different bacterial loads remains poorly characterized. This study aimed to investigate alterations in oral fungal communities among Xpert-positive patients, stratified by Mtb burden based on Xpert MTB/RIF testing.
METHODS: In this prospective multicenter cohort study (May-August 2024), 278 Xpert-positive TB patients were enrolled across five hospitals in China. Participants were stratified into high, medium, low, and very low Mtb burden groups according to Xpert MTB/RIF cycle threshold values. Paired sputum and tongue swab samples were collected. Oral fungal profiles were characterized via ITS sequencing, followed by taxonomic assignment, diversity analysis, and multivariable association testing (MaAsLin 2) to identify robust biomarkers.
RESULTS: Oral fungal community structure varied significantly across Mtb burden strata. Beta-diversity analysis revealed distinct clustering between the very low burden group and higher burden groups (high, medium, low). High-burden patients were enriched with environmental taxa such as Blumeria and Toxicocladosporium, whereas low-burden groups exhibited higher abundances of Candida, Aspergillus, and Penicillium. Notably, MaAsLin 2 analysis confirmed that Penicillium and Podosphaera were independently associated with lower Mtb burden after adjusting for confounders. Neutral model analysis indicated that stochastic processes predominantly drive the assembly of these oral fungal communities. Functional prediction suggested enhanced aerobic respiration and metabolic enzyme activity in high-burden groups.
CONCLUSIONS: This study analyzed the oral fungal microbiome stratified by Mtb burden strata in Xpert-positive patients, revealing distinct shifts in fungal composition and functional potential. Fungal dysbiosis and altered microbial metabolic capacity may offer insight into host-microbe interactions in pulmonary TB (PTB). These findings underscore the potential value of fungal microbiome profiling for assessing Mtb burden, beyond its application in TB diagnosis alone.},
}
MeSH Terms:
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Humans
*Mycobacterium tuberculosis/isolation & purification
Prospective Studies
Female
*Mouth/microbiology
Male
Sputum/microbiology
Adult
Middle Aged
China/epidemiology
*Fungi/isolation & purification/classification/genetics
*Mycobiome
*Microbiota
*Tuberculosis, Pulmonary/microbiology/diagnosis
Bacterial Load
RevDate: 2026-07-08
CmpDate: 2026-07-08
[Series: Important medical-dental interactions. Oral manifestations in patients with intestinal diseases].
Nederlands tijdschrift voor tandheelkunde, 133(7-08):336-344.
The intestine, consisting of the small and large intestines, is a functional and immunologically active organ in which digestion, absorption, and defence are closely intertwined. Immediately following the stomach is the duodenum, where the food chyme comes into contact with pancreatic digestive juices and bile, enabling further nutrient breakdown. The primary function of the small intestine is the absorption of nutrients through the intestinal mucosa. The large intestine is responsible for the reabsorption of water and electrolytes and is home to a diverse microbiome, consisting of various microorganisms involved in the digestion of complex carbohydrates. This microbiome is constantly interacting with the intestinal immune system, maintaining a delicate balance between tolerance and immune activation. Disruption of this balance can lead to or contribute to various conditions, some of which are discussed in this overview.
Additional Links: PMID-42415676
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@article {pmid42415676,
year = {2026},
author = {Brand, HS and Boukema, IC and Oldenburg, L and Opperman, RCM and de Boer, NKH},
title = {[Series: Important medical-dental interactions. Oral manifestations in patients with intestinal diseases].},
journal = {Nederlands tijdschrift voor tandheelkunde},
volume = {133},
number = {7-08},
pages = {336-344},
doi = {10.5177/ntvt.07/08.26020},
pmid = {42415676},
issn = {0028-2200},
mesh = {Humans ; *Intestinal Diseases/complications/immunology ; *Intestinal Mucosa/microbiology ; },
abstract = {The intestine, consisting of the small and large intestines, is a functional and immunologically active organ in which digestion, absorption, and defence are closely intertwined. Immediately following the stomach is the duodenum, where the food chyme comes into contact with pancreatic digestive juices and bile, enabling further nutrient breakdown. The primary function of the small intestine is the absorption of nutrients through the intestinal mucosa. The large intestine is responsible for the reabsorption of water and electrolytes and is home to a diverse microbiome, consisting of various microorganisms involved in the digestion of complex carbohydrates. This microbiome is constantly interacting with the intestinal immune system, maintaining a delicate balance between tolerance and immune activation. Disruption of this balance can lead to or contribute to various conditions, some of which are discussed in this overview.},
}
MeSH Terms:
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Humans
*Intestinal Diseases/complications/immunology
*Intestinal Mucosa/microbiology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Effects of metabolic syndrome on pulmonary infection in pediatric bronchial asthma: a narrative review.
Frontiers in pediatrics, 14:1770376.
Bronchial asthma is a heterogeneous disease characterized by chronic airway inflammation and airway hyperresponsiveness. It is the most common chronic airway inflammatory disease in children and severely affects their physical and mental health. The exacerbation of asthma in children often involves interactions among environmental triggers, the airway microbiome, and the innate immune response. Studies have confirmed that asthma in children is closely associated with lung infections. On the one hand, asthma in children increases the likelihood of lung infections; on the other hand, lung infections can significantly increase the likelihood of acute asthma attacks in children. Metabolic syndrome in children and adolescents is considered a risk factor for chronic diseases such as diabetes and cardiovascular and cerebrovascular diseases. Recent studies have shown that metabolic abnormalities in children are significantly associated with pulmonary infections and asthma in children. This review aims to review and analyze the specific effects of metabolic abnormalities on pulmonary infections and asthma exacerbations in children with asthma. Metabolic abnormalities in children cause chronic inflammation and alterations in the intestinal flora, which affect lung function, promote lung infection, and aggravate bronchial asthma in children.
Additional Links: PMID-42416090
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@article {pmid42416090,
year = {2026},
author = {He, L and Ye, Y},
title = {Effects of metabolic syndrome on pulmonary infection in pediatric bronchial asthma: a narrative review.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1770376},
pmid = {42416090},
issn = {2296-2360},
abstract = {Bronchial asthma is a heterogeneous disease characterized by chronic airway inflammation and airway hyperresponsiveness. It is the most common chronic airway inflammatory disease in children and severely affects their physical and mental health. The exacerbation of asthma in children often involves interactions among environmental triggers, the airway microbiome, and the innate immune response. Studies have confirmed that asthma in children is closely associated with lung infections. On the one hand, asthma in children increases the likelihood of lung infections; on the other hand, lung infections can significantly increase the likelihood of acute asthma attacks in children. Metabolic syndrome in children and adolescents is considered a risk factor for chronic diseases such as diabetes and cardiovascular and cerebrovascular diseases. Recent studies have shown that metabolic abnormalities in children are significantly associated with pulmonary infections and asthma in children. This review aims to review and analyze the specific effects of metabolic abnormalities on pulmonary infections and asthma exacerbations in children with asthma. Metabolic abnormalities in children cause chronic inflammation and alterations in the intestinal flora, which affect lung function, promote lung infection, and aggravate bronchial asthma in children.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
The gut microbiome in early life predicts malaria susceptibility.
Frontiers in cellular and infection microbiology, 16:1769376.
BACKGROUND: Despite intensive international efforts and broad implementation of control and prevention efforts, malaria continues to take a devastating toll on the most vulnerable populations, especially infants and young children. Emerging data support an important role for gut microbiome disruption in exacerbating, and potentially contributing to, adverse outcomes in malaria in young children. Less well understood are the role of the gut microbiome in early infancy in determining malaria susceptibility and how malaria exposure may impact gut microbial communities during this highly dynamic and sensitive period of microbiome development.
METHODS: To address these gaps, we recruited mother-infant dyads at birth in malaria-endemic eastern Democratic Republic of Congo. Infant fecal samples collected at six weeks, and at three, six and 12 months of age, as well as at passive malaria sick and post-treatment visits, were subjected to full length 16S rRNA sequencing.
RESULTS: Significant differences in relative abundance of a number of bacterial species distinguished those infants who never had a malaria visit from those who did, and those malaria episodes resulted in gut dysbiosis. Classifier analysis with Boruta selection revealed preliminary predictive capacity of the six-week fecal microbiome for malaria susceptibility through the first year of life, with a modest signal partially intertwined with bednet use. Healthy gut-associated Bifidobacterium breve and its metabolic partner Cutibacterium avidum, along with Megasphaera micronuciformis were associated with malaria resistance, whereas bacteria previously associated with pathogenic processes, including Streptococcus salivarius, Klebsiella pneumoniae, and Rothia mucilaginosa, associated with malaria susceptibility.
CONCLUSIONS: These results provide the first evidence that gut microbial composition in early infancy is associated with subsequent malaria susceptibility. These associations, if confirmed in larger cohorts, may inform future investigation of microbiome-targeted strategies to support resistance to malaria in early life.
Additional Links: PMID-42416278
PubMed:
Citation:
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@article {pmid42416278,
year = {2026},
author = {Dutton, CL and Follis, M and Munaweera, J and Maisha, FM and Mulligan, CJ and Moore, JM},
title = {The gut microbiome in early life predicts malaria susceptibility.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1769376},
pmid = {42416278},
issn = {2235-2988},
mesh = {Humans ; Infant ; Female ; Feces/microbiology ; *Gastrointestinal Microbiome ; Democratic Republic of the Congo/epidemiology ; RNA, Ribosomal, 16S/genetics ; *Malaria/epidemiology ; Disease Susceptibility ; *Bacteria/classification/genetics/isolation & purification ; Male ; Infant, Newborn ; DNA, Ribosomal/genetics/chemistry ; Dysbiosis ; DNA, Bacterial/genetics/chemistry ; Sequence Analysis, DNA ; },
abstract = {BACKGROUND: Despite intensive international efforts and broad implementation of control and prevention efforts, malaria continues to take a devastating toll on the most vulnerable populations, especially infants and young children. Emerging data support an important role for gut microbiome disruption in exacerbating, and potentially contributing to, adverse outcomes in malaria in young children. Less well understood are the role of the gut microbiome in early infancy in determining malaria susceptibility and how malaria exposure may impact gut microbial communities during this highly dynamic and sensitive period of microbiome development.
METHODS: To address these gaps, we recruited mother-infant dyads at birth in malaria-endemic eastern Democratic Republic of Congo. Infant fecal samples collected at six weeks, and at three, six and 12 months of age, as well as at passive malaria sick and post-treatment visits, were subjected to full length 16S rRNA sequencing.
RESULTS: Significant differences in relative abundance of a number of bacterial species distinguished those infants who never had a malaria visit from those who did, and those malaria episodes resulted in gut dysbiosis. Classifier analysis with Boruta selection revealed preliminary predictive capacity of the six-week fecal microbiome for malaria susceptibility through the first year of life, with a modest signal partially intertwined with bednet use. Healthy gut-associated Bifidobacterium breve and its metabolic partner Cutibacterium avidum, along with Megasphaera micronuciformis were associated with malaria resistance, whereas bacteria previously associated with pathogenic processes, including Streptococcus salivarius, Klebsiella pneumoniae, and Rothia mucilaginosa, associated with malaria susceptibility.
CONCLUSIONS: These results provide the first evidence that gut microbial composition in early infancy is associated with subsequent malaria susceptibility. These associations, if confirmed in larger cohorts, may inform future investigation of microbiome-targeted strategies to support resistance to malaria in early life.},
}
MeSH Terms:
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Humans
Infant
Female
Feces/microbiology
*Gastrointestinal Microbiome
Democratic Republic of the Congo/epidemiology
RNA, Ribosomal, 16S/genetics
*Malaria/epidemiology
Disease Susceptibility
*Bacteria/classification/genetics/isolation & purification
Male
Infant, Newborn
DNA, Ribosomal/genetics/chemistry
Dysbiosis
DNA, Bacterial/genetics/chemistry
Sequence Analysis, DNA
RevDate: 2026-07-08
CmpDate: 2026-07-08
Mechanisms of caries induced by sugars: a narratives review from microbial metabolism to oral ecological imbalance and public health strategies for caries prevention.
Frontiers in cellular and infection microbiology, 16:1834886.
Dental caries is defined as a chronic, multifactorial disease characterized by the demineralization of dental hard tissues resulting from the acid production by oral microbial communities metabolizing dietary sugars. The ingestion of sugars is a pivotal ecological factor in the progression of caries, with mechanisms that extend beyond merely providing substrates for cariogenic bacteria. This review explores the influence of sugars on the metabolism, adhesion, biofilm formation, and interspecies interactions of oral microorganisms, with a particular focus on species such as Streptococcus mutans, Lactobacilli, Actinomyces, and Candida albicans. The disruption of the oral microbiome balance by these sugars initiates and promotes the process of caries. The review comprehensively summarizes contemporary public health strategies for caries prevention based on microbial ecological theories, including the limitations of sugar intake, fluoride application, probiotics, and ecological management, assessing their effectiveness and challenges. The objective of this study is to establish a theoretical framework and practical guidelines for the precise prevention of dental caries.
Additional Links: PMID-42416280
PubMed:
Citation:
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@article {pmid42416280,
year = {2026},
author = {Zhang, A and Yang, J and Wang, X and Xehesbek, B and Zhang, J and Hu, X and Zhang, B and Huang, R},
title = {Mechanisms of caries induced by sugars: a narratives review from microbial metabolism to oral ecological imbalance and public health strategies for caries prevention.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1834886},
pmid = {42416280},
issn = {2235-2988},
mesh = {*Dental Caries/prevention & control/microbiology/etiology ; Humans ; Microbiota ; Biofilms/growth & development ; Streptococcus mutans/metabolism ; Lactobacillus/metabolism ; *Mouth/microbiology ; *Sugars/metabolism/adverse effects ; Candida albicans/metabolism ; Microbial Interactions ; Actinomyces/metabolism ; *Dietary Sugars/adverse effects/metabolism ; Probiotics ; },
abstract = {Dental caries is defined as a chronic, multifactorial disease characterized by the demineralization of dental hard tissues resulting from the acid production by oral microbial communities metabolizing dietary sugars. The ingestion of sugars is a pivotal ecological factor in the progression of caries, with mechanisms that extend beyond merely providing substrates for cariogenic bacteria. This review explores the influence of sugars on the metabolism, adhesion, biofilm formation, and interspecies interactions of oral microorganisms, with a particular focus on species such as Streptococcus mutans, Lactobacilli, Actinomyces, and Candida albicans. The disruption of the oral microbiome balance by these sugars initiates and promotes the process of caries. The review comprehensively summarizes contemporary public health strategies for caries prevention based on microbial ecological theories, including the limitations of sugar intake, fluoride application, probiotics, and ecological management, assessing their effectiveness and challenges. The objective of this study is to establish a theoretical framework and practical guidelines for the precise prevention of dental caries.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Dental Caries/prevention & control/microbiology/etiology
Humans
Microbiota
Biofilms/growth & development
Streptococcus mutans/metabolism
Lactobacillus/metabolism
*Mouth/microbiology
*Sugars/metabolism/adverse effects
Candida albicans/metabolism
Microbial Interactions
Actinomyces/metabolism
*Dietary Sugars/adverse effects/metabolism
Probiotics
RevDate: 2026-07-08
CmpDate: 2026-07-08
Uterine leiomyoma, retained fetal cranial bones, and reproductive microbiome analysis in a fallow deer (Dama dama): a case report.
Frontiers in veterinary science, 13:1872878.
Pathological and microbiological surveillance of wildlife can reveal clinically silent but biologically important reproductive disorders. This case report describes a middle-aged (6-7 years) fallow deer hind (Dama dama) in good body condition, legally culled in Hungary, in which post-mortem examination identified a uterine leiomyoma in the left uterine horn and retained fetal cranial bones in the cranial vagina. To the best of our knowledge, this is the first published description of uterine leiomyoma in this species. Gross pathology, histopathology, and desmin immunohistochemistry supported the diagnosis of leiomyoma, and 16S rRNA amplicon sequencing was used to compare the microbiomes of the unaffected uterine horn, affected uterine tissue, and feces. The affected uterine sample showed a microbial profile more similar to that of feces than the unaffected uterine sample, with an increased relative abundance of genera, including Bacteroides, Escherichia-Shigella, and Turicibacter. As this was a single post-mortem case, no treatment was administered. These findings suggest a possible association between chronic mechanical obstruction, retained fetal material, and marked local microbial alteration, while also illustrating the limitations of causal inference from single-animal microbiome data. This case expands the differential diagnosis of reproductive tract lesions in wild ruminants and highlights the value of integrating pathology with careful microbiome interpretation in wildlife case reports.
Additional Links: PMID-42416294
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Citation:
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@article {pmid42416294,
year = {2026},
author = {Szőke, Z and Fehér, P and Ferenczi, S and Lakatos, I and Stéger, V and Sükösd, Á and Sükösd, F and Sára, L},
title = {Uterine leiomyoma, retained fetal cranial bones, and reproductive microbiome analysis in a fallow deer (Dama dama): a case report.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1872878},
pmid = {42416294},
issn = {2297-1769},
abstract = {Pathological and microbiological surveillance of wildlife can reveal clinically silent but biologically important reproductive disorders. This case report describes a middle-aged (6-7 years) fallow deer hind (Dama dama) in good body condition, legally culled in Hungary, in which post-mortem examination identified a uterine leiomyoma in the left uterine horn and retained fetal cranial bones in the cranial vagina. To the best of our knowledge, this is the first published description of uterine leiomyoma in this species. Gross pathology, histopathology, and desmin immunohistochemistry supported the diagnosis of leiomyoma, and 16S rRNA amplicon sequencing was used to compare the microbiomes of the unaffected uterine horn, affected uterine tissue, and feces. The affected uterine sample showed a microbial profile more similar to that of feces than the unaffected uterine sample, with an increased relative abundance of genera, including Bacteroides, Escherichia-Shigella, and Turicibacter. As this was a single post-mortem case, no treatment was administered. These findings suggest a possible association between chronic mechanical obstruction, retained fetal material, and marked local microbial alteration, while also illustrating the limitations of causal inference from single-animal microbiome data. This case expands the differential diagnosis of reproductive tract lesions in wild ruminants and highlights the value of integrating pathology with careful microbiome interpretation in wildlife case reports.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
DepMicroDiff: Diffusion-Based Dependency-Aware Multimodal Imputation for Microbiome Data.
Computational and structural biotechnology journal, 35(1):0150.
Microbiome data analysis is essential for understanding host health and disease, yet its inherent sparsity and noise pose major challenges for accurate imputation, hindering downstream tasks such as biomarker discovery. Existing imputation methods, including recent diffusion-based models, often fail to capture the complex interdependencies between microbial taxa and overlook contextual metadata that can inform imputation. We introduce DepMicroDiff, a novel framework that combines diffusion-based generative modeling with a Dependency-Aware Transformer (DAT) to explicitly capture both mutual pairwise dependencies and autoregressive relationships. DepMicroDiff is further enhanced by variational autoencoder-based pretraining across diverse cancer datasets and conditioning on patient metadata encoded via a pretrained Transformer-based encoder (Bidirectional Encoder Representations from Transformers). Experiments on The Cancer Genome Atlas microbiome datasets show that DepMicroDiff substantially outperforms state-of-the-art baselines, achieving higher Pearson correlation coefficient (up to 0.788), cosine similarity (up to 0.812), and lower root mean square error and mean absolute error across multiple cancer types, demonstrating its robustness and generalizability for microbiome imputation.
Additional Links: PMID-42416328
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@article {pmid42416328,
year = {2026},
author = {Sadia, RT and Cheng, Q},
title = {DepMicroDiff: Diffusion-Based Dependency-Aware Multimodal Imputation for Microbiome Data.},
journal = {Computational and structural biotechnology journal},
volume = {35},
number = {1},
pages = {0150},
pmid = {42416328},
issn = {2001-0370},
abstract = {Microbiome data analysis is essential for understanding host health and disease, yet its inherent sparsity and noise pose major challenges for accurate imputation, hindering downstream tasks such as biomarker discovery. Existing imputation methods, including recent diffusion-based models, often fail to capture the complex interdependencies between microbial taxa and overlook contextual metadata that can inform imputation. We introduce DepMicroDiff, a novel framework that combines diffusion-based generative modeling with a Dependency-Aware Transformer (DAT) to explicitly capture both mutual pairwise dependencies and autoregressive relationships. DepMicroDiff is further enhanced by variational autoencoder-based pretraining across diverse cancer datasets and conditioning on patient metadata encoded via a pretrained Transformer-based encoder (Bidirectional Encoder Representations from Transformers). Experiments on The Cancer Genome Atlas microbiome datasets show that DepMicroDiff substantially outperforms state-of-the-art baselines, achieving higher Pearson correlation coefficient (up to 0.788), cosine similarity (up to 0.812), and lower root mean square error and mean absolute error across multiple cancer types, demonstrating its robustness and generalizability for microbiome imputation.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Plant-specific microbial diversity facilitates functional redundancy at the soil-root interface.
Plant and soil, 523(2):811-825.
AIMS: Plant-specific microbial diversity reflecting host-microbe coevolution was frequently shown at the structural level but less on the functional scale. We studied the microbiome of three compartments at the soil root interface (root endosphere, rhizosphere, bulk soil) of medicinal plants cultivated under organic management in Egypt. The study aimed to examine the impact of the rhizosphere on microbial community composition and diversity in desert agricultural soil, as well as to identify specific functions associated with the rhizosphere.
METHODS: The microbiome community structure, diversity, and microbial functioning were evaluated through the utilization of 16S rRNA gene amplicon and shotgun metagenome sequencing.
RESULTS: We found the typical rhizosphere effect and plant-species-specific enrichment of bacterial diversity. The annual plants Calendula officinalis and Matricaria chamomilla (Asteraceae) were more similar than the perennial Solanum distichum (Solanaceae). Altogether, plant species explained 50.5% of the variation in bacterial community structures in the rhizosphere. Our results indicate a stronger effect of the plant species in terms of modulating bacterial community structures in the rhizosphere than in root endosphere samples. The plant-driven rhizosphere effect could be linked to redundant plant beneficial functions in the microbiome, while enrichment of specific genes related to amino acid ion transport and metabolism, carbohydrate transport and metabolism, defense mechanisms, and secondary metabolites biosynthesis were more specific.
CONCLUSIONS: The study explores the microbiome continuum at the soil-root interface of medicinal plant species, revealing significant bacterial community structure shifts and plant specificity. The study provides insights into the essential microbiome components contributing to rhizosphere functionality.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11104-024-07097-5.
Additional Links: PMID-42416386
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Citation:
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@article {pmid42416386,
year = {2026},
author = {Wicaksono, WA and Köberl, M and White, RA and Jansson, JK and Jansson, C and Cernava, T and Berg, G},
title = {Plant-specific microbial diversity facilitates functional redundancy at the soil-root interface.},
journal = {Plant and soil},
volume = {523},
number = {2},
pages = {811-825},
pmid = {42416386},
issn = {0032-079X},
abstract = {AIMS: Plant-specific microbial diversity reflecting host-microbe coevolution was frequently shown at the structural level but less on the functional scale. We studied the microbiome of three compartments at the soil root interface (root endosphere, rhizosphere, bulk soil) of medicinal plants cultivated under organic management in Egypt. The study aimed to examine the impact of the rhizosphere on microbial community composition and diversity in desert agricultural soil, as well as to identify specific functions associated with the rhizosphere.
METHODS: The microbiome community structure, diversity, and microbial functioning were evaluated through the utilization of 16S rRNA gene amplicon and shotgun metagenome sequencing.
RESULTS: We found the typical rhizosphere effect and plant-species-specific enrichment of bacterial diversity. The annual plants Calendula officinalis and Matricaria chamomilla (Asteraceae) were more similar than the perennial Solanum distichum (Solanaceae). Altogether, plant species explained 50.5% of the variation in bacterial community structures in the rhizosphere. Our results indicate a stronger effect of the plant species in terms of modulating bacterial community structures in the rhizosphere than in root endosphere samples. The plant-driven rhizosphere effect could be linked to redundant plant beneficial functions in the microbiome, while enrichment of specific genes related to amino acid ion transport and metabolism, carbohydrate transport and metabolism, defense mechanisms, and secondary metabolites biosynthesis were more specific.
CONCLUSIONS: The study explores the microbiome continuum at the soil-root interface of medicinal plant species, revealing significant bacterial community structure shifts and plant specificity. The study provides insights into the essential microbiome components contributing to rhizosphere functionality.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11104-024-07097-5.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Nasal cavity microbial makeup and the influence on psychiatric symptoms following fire exposure in firefighters.
Frontiers in microbiomes, 5:1832151.
BACKGROUND: Firefighters experience high levels of occupational stress and trauma, increasing their risk of depression, anxiety, and post-traumatic stress disorder (PTSD). Although microbial communities may influence brain function and behavior through neural pathways, the nasal microbiome remains understudied. This study examined associations between nasal microbiome characteristics and psychiatric symptoms among firefighters.
METHODS: We conducted a cross-sectional study of 34 firefighters recruited from Texas fire stations. Participants completed validated questionnaires assessing depression, anxiety, and PTSD. Nasal swabs were collected before and after fire suppression and 16S rRNA sequencing was used to characterize microbial communities. Alpha and beta diversity, relative abundance, and differential microbial associations with psychiatric outcomes were assessed using logistic, linear, and linear mixed regression methods.
RESULTS: Sixteen participants (47%) met criteria for depression, six (18%) for anxiety, and four (12%) for PTSD. Alpha diversity was significantly lower in individuals with anxiety (adjusted p = 0.04) while there were no differences in beta diversity or differences in either diversity for PTSD or depression. Increased abundance of the genus Ruminococcus was associated with increased odds of anxiety, while Hydrotalea was associated with PTSD. Depression scores were positively associated with several genera including Aerococcus (1.22; 95%CI: 0.43-2.02) and Dermabacter (1.50; 95% CI: 0.37-2.63). Fire suppression was associated with increased Enhydrobacter (2.08; 95% CI: 0.80 to 3.46) and decreased Hymenobacter (-1.25; 95% CI: -2.22 to -0.27) abundance.
CONCLUSIONS: This study identifies preliminary links between nasal microbiome composition and psychiatric symptoms in firefighters and suggests that fire suppression may alter nasal microbial communities.
Additional Links: PMID-42416499
PubMed:
Citation:
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@article {pmid42416499,
year = {2026},
author = {Grunsted, P and Xu, C and Janitz, A and Reese, J and Campbell, J and Santiago-Rodriguez, TM and Cregeen, SJJ and Petrosino, JF and Hwang, J},
title = {Nasal cavity microbial makeup and the influence on psychiatric symptoms following fire exposure in firefighters.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1832151},
pmid = {42416499},
issn = {2813-4338},
abstract = {BACKGROUND: Firefighters experience high levels of occupational stress and trauma, increasing their risk of depression, anxiety, and post-traumatic stress disorder (PTSD). Although microbial communities may influence brain function and behavior through neural pathways, the nasal microbiome remains understudied. This study examined associations between nasal microbiome characteristics and psychiatric symptoms among firefighters.
METHODS: We conducted a cross-sectional study of 34 firefighters recruited from Texas fire stations. Participants completed validated questionnaires assessing depression, anxiety, and PTSD. Nasal swabs were collected before and after fire suppression and 16S rRNA sequencing was used to characterize microbial communities. Alpha and beta diversity, relative abundance, and differential microbial associations with psychiatric outcomes were assessed using logistic, linear, and linear mixed regression methods.
RESULTS: Sixteen participants (47%) met criteria for depression, six (18%) for anxiety, and four (12%) for PTSD. Alpha diversity was significantly lower in individuals with anxiety (adjusted p = 0.04) while there were no differences in beta diversity or differences in either diversity for PTSD or depression. Increased abundance of the genus Ruminococcus was associated with increased odds of anxiety, while Hydrotalea was associated with PTSD. Depression scores were positively associated with several genera including Aerococcus (1.22; 95%CI: 0.43-2.02) and Dermabacter (1.50; 95% CI: 0.37-2.63). Fire suppression was associated with increased Enhydrobacter (2.08; 95% CI: 0.80 to 3.46) and decreased Hymenobacter (-1.25; 95% CI: -2.22 to -0.27) abundance.
CONCLUSIONS: This study identifies preliminary links between nasal microbiome composition and psychiatric symptoms in firefighters and suggests that fire suppression may alter nasal microbial communities.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Contact sensitization to hair care allergens in scalp seborrheic dermatitis: associations with disease severity and microbiota profiles.
Frontiers in allergy, 7:1862176.
BACKGROUND: Scalp seborrheic dermatitis (SSD) is a chronic inflammatory skin disorder characterized by impaired barrier function and intolerance to topical products. However, the relationship between contact sensitization and scalp microbiota in SSD remains unclear.
METHODS: A total of 63 participants underwent patch testing with 62 allergens and were grouped according to the presence or absence of scalp involvement. Clinical assessments included symptom severity, transepidermal water loss, and stratum corneum hydration. Bacterial 16S rRNA V3-V4 sequencing and fungal ITS1 sequencing were performed in a subset of 36 patients with SSD to evaluate associations between allergen sensitization and scalp microbiota.
RESULTS: The most frequent sensitizers in patients with SSD were cobalt chloride, cetrimonium bromide, p-methylaminophenol, nickel sulfate, decyl glucoside, and minoxidil, although overall sensitization rates did not differ significantly between SSD and control groups. Specific allergens were associated with age, sex, disease duration, and disease severity. Increased transepidermal water loss was correlated with fragrance and preservative allergens. Minoxidil sensitization was negatively associated with Malassezia, whereas several fragrance and preservative allergens were correlated with Candida, Staphylococcus, and Corynebacterium.
CONCLUSION: Patients with SSD showed distinct sensitization patterns associated with clinical characteristics, barrier dysfunction, and scalp microbiota alterations. These findings suggest that patch test reactivity in SSD should be interpreted in the broader context of allergen exposure, skin barrier status, and microbial imbalance.
Additional Links: PMID-42416500
PubMed:
Citation:
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@article {pmid42416500,
year = {2026},
author = {Cui, C and Xie, Y and Yuan, J and Ni, J and Wang, Y and Wei, A and Tao, R},
title = {Contact sensitization to hair care allergens in scalp seborrheic dermatitis: associations with disease severity and microbiota profiles.},
journal = {Frontiers in allergy},
volume = {7},
number = {},
pages = {1862176},
pmid = {42416500},
issn = {2673-6101},
abstract = {BACKGROUND: Scalp seborrheic dermatitis (SSD) is a chronic inflammatory skin disorder characterized by impaired barrier function and intolerance to topical products. However, the relationship between contact sensitization and scalp microbiota in SSD remains unclear.
METHODS: A total of 63 participants underwent patch testing with 62 allergens and were grouped according to the presence or absence of scalp involvement. Clinical assessments included symptom severity, transepidermal water loss, and stratum corneum hydration. Bacterial 16S rRNA V3-V4 sequencing and fungal ITS1 sequencing were performed in a subset of 36 patients with SSD to evaluate associations between allergen sensitization and scalp microbiota.
RESULTS: The most frequent sensitizers in patients with SSD were cobalt chloride, cetrimonium bromide, p-methylaminophenol, nickel sulfate, decyl glucoside, and minoxidil, although overall sensitization rates did not differ significantly between SSD and control groups. Specific allergens were associated with age, sex, disease duration, and disease severity. Increased transepidermal water loss was correlated with fragrance and preservative allergens. Minoxidil sensitization was negatively associated with Malassezia, whereas several fragrance and preservative allergens were correlated with Candida, Staphylococcus, and Corynebacterium.
CONCLUSION: Patients with SSD showed distinct sensitization patterns associated with clinical characteristics, barrier dysfunction, and scalp microbiota alterations. These findings suggest that patch test reactivity in SSD should be interpreted in the broader context of allergen exposure, skin barrier status, and microbial imbalance.},
}
RevDate: 2026-07-08
Enterohepatic Circulation of Polystyrene Nanoplastics Promotes Intestinal Inflammation by Impairing Enteric Neurons.
ACS nano [Epub ahead of print].
Microplastics (MPs) are emerging contaminants of increasing concern, yet their in vivo fate and mechanisms of intestinal toxicity remain poorly defined. Here, we demonstrate that polystyrene nanoplastics (PS-NPs) undergo a previously overlooked enterohepatic recirculation pathway that markedly enhances their intestinal retention. Using oral exposure and a Zombie mouse model with intravenous PS-NPs delivery, we show that systemically absorbed PS-NPs are efficiently captured by the liver, concentrated in the gallbladder, and subsequently reintroduced into the intestine via bile. Chronic PS-NPs exposure caused pronounced epithelial injury, including goblet cell loss, tight-junction disruption, and robust cytokine-mediated inflammation. Multiomics analyses revealed gut microbial dysbiosis, extensive shifts in metabolite profiles, and enrichment of neuroactive signaling pathways, suggesting microbiome-metabolite contributions to toxicity. We further identified significant enteric neurotoxicity characterized by reduced expression of vasoactive intestinal peptide, increased expression of tyrosine hydroxylase, and downregulation of the mechanosensitive PIEZO1 channel. Together, these findings establish hepatobiliary recycling as a key driver of intestinal PS-NPs accumulation and demonstrate that epithelial damage, microbiome-metabolite imbalance, and enteric nervous system dysfunction collectively mediate PS-NPs-induced gut pathology. This work provides mechanistic insights essential for evaluating the health risks of environmental PS-NPs exposure.
Additional Links: PMID-42417008
Publisher:
PubMed:
Citation:
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@article {pmid42417008,
year = {2026},
author = {Wang, X and Wang, Q and Jiang, W and Wang, B and Zhang, X and Wang, T},
title = {Enterohepatic Circulation of Polystyrene Nanoplastics Promotes Intestinal Inflammation by Impairing Enteric Neurons.},
journal = {ACS nano},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsnano.6c00685},
pmid = {42417008},
issn = {1936-086X},
abstract = {Microplastics (MPs) are emerging contaminants of increasing concern, yet their in vivo fate and mechanisms of intestinal toxicity remain poorly defined. Here, we demonstrate that polystyrene nanoplastics (PS-NPs) undergo a previously overlooked enterohepatic recirculation pathway that markedly enhances their intestinal retention. Using oral exposure and a Zombie mouse model with intravenous PS-NPs delivery, we show that systemically absorbed PS-NPs are efficiently captured by the liver, concentrated in the gallbladder, and subsequently reintroduced into the intestine via bile. Chronic PS-NPs exposure caused pronounced epithelial injury, including goblet cell loss, tight-junction disruption, and robust cytokine-mediated inflammation. Multiomics analyses revealed gut microbial dysbiosis, extensive shifts in metabolite profiles, and enrichment of neuroactive signaling pathways, suggesting microbiome-metabolite contributions to toxicity. We further identified significant enteric neurotoxicity characterized by reduced expression of vasoactive intestinal peptide, increased expression of tyrosine hydroxylase, and downregulation of the mechanosensitive PIEZO1 channel. Together, these findings establish hepatobiliary recycling as a key driver of intestinal PS-NPs accumulation and demonstrate that epithelial damage, microbiome-metabolite imbalance, and enteric nervous system dysfunction collectively mediate PS-NPs-induced gut pathology. This work provides mechanistic insights essential for evaluating the health risks of environmental PS-NPs exposure.},
}
RevDate: 2026-07-08
Management of Type 2 Diabetes Mellitus: Targeting Gut Microbiome Therapy.
The American journal of Chinese medicine [Epub ahead of print].
Marked by high blood glucose and systemic metabolic dysfunction, type 2 diabetes mellitus (T2DM) is a significant health issue with a rapidly increasing worldwide prevalence. Recent studies have highlighted the gut microbiota as a key determinant of host metabolism, and identified that the composition and metabolic activity are closely linked to the development and progression of T2DM. This review comprehensively explores the intricate connection between T2DM and the gut microbiota, with a particular focus on how traditional Chinese medicine (TCM) can influence intestinal microbiota composition to manage disease. It also discusses the therapeutic potential of TCM, which includes natural medicinal extracts like baicalin, berberine, tetrahydrocurcumin, ginsenoside Rb1, ophiopogonin D, and resveratrol, compound formulations, and acupuncture, in regulating the intestinal microbiota ecosystem to manage T2DM. Although the current evidence suggests that these interventions may slow T2DM progression, most studies have been confined to animal models and early clinical trials which lack adequate clinical evidence to confirm their efficacy. This discrepancy has created an imbalance between theoretical and validated clinical applications. Building on existing research, future research should focus on large-scale clinical trials and advanced multi-omics studies to uncover the potential of TCM in managing T2DM through the gut microbiota.
Additional Links: PMID-42417102
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PubMed:
Citation:
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@article {pmid42417102,
year = {2026},
author = {Bibi, A and Zhou, L and You, M and Niu, H and Tasleem, MW and Wu, H and Zhang, H},
title = {Management of Type 2 Diabetes Mellitus: Targeting Gut Microbiome Therapy.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-26},
doi = {10.1142/S0192415X26500497},
pmid = {42417102},
issn = {1793-6853},
abstract = {Marked by high blood glucose and systemic metabolic dysfunction, type 2 diabetes mellitus (T2DM) is a significant health issue with a rapidly increasing worldwide prevalence. Recent studies have highlighted the gut microbiota as a key determinant of host metabolism, and identified that the composition and metabolic activity are closely linked to the development and progression of T2DM. This review comprehensively explores the intricate connection between T2DM and the gut microbiota, with a particular focus on how traditional Chinese medicine (TCM) can influence intestinal microbiota composition to manage disease. It also discusses the therapeutic potential of TCM, which includes natural medicinal extracts like baicalin, berberine, tetrahydrocurcumin, ginsenoside Rb1, ophiopogonin D, and resveratrol, compound formulations, and acupuncture, in regulating the intestinal microbiota ecosystem to manage T2DM. Although the current evidence suggests that these interventions may slow T2DM progression, most studies have been confined to animal models and early clinical trials which lack adequate clinical evidence to confirm their efficacy. This discrepancy has created an imbalance between theoretical and validated clinical applications. Building on existing research, future research should focus on large-scale clinical trials and advanced multi-omics studies to uncover the potential of TCM in managing T2DM through the gut microbiota.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
[Updated international guidelines for the diagnosis and management of patients with urinary tract infection: an analytical review].
Urologiia (Moscow, Russia : 1999).
The latest 2025 guidelines of the European Association of Urology (EAU), the American Urological Association, the Canadian Urological Association, and the Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction (AUA/CUA/SUFU) introduce a new classification system for urinary tract infections (UTIs) and update sections on cystitis and asymptomatic bacteriuria (ABU). Current approaches to the management of patients with UTIs, ABU, and even symptomatic bacteriuria are being reconsidered. In the era of increasing antimicrobial resistance among uropathogens, advances in researching of human microbiome and urobiome have changed the long-standing assumption that any bacteriuria necessarily requires antimicrobial treatment. At present, even in patients with a confirmed diagnosis of acute bacterial cystitis, international recommendations consider symptomatic treatment and a watchful waiting strategy as acceptable options for selected patient groups. The new UTI classification, diagnostic features and symptoms of UTIs and ABU, non-antibiotic treatment options for cystitis, and age-related characteristics of UTI presentation are discussed in this review. Key aspects of the pathogenesis of recurrent UTIs are briefly addressed. Various urine sampling approaches are discussed, along with a differentiated strategy for prescribing antimicrobial therapy to women with acute and recurrent cystitis and non-antibiotic measures for recurrence prevention. The diagnostic value of urinalysis has also expanded to include new indicators of microbial load and assessment of urine contamination. The role of modern molecular diagnostic methods, beyond standard urine culture, in the diagnosis and treatment of UTIs is analyzed. The need to adhere to principles of rational antibiotic use to avoid collateral damage associated with antimicrobial therapy for UTIs is emphasized.
Additional Links: PMID-42417340
PubMed:
Citation:
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@article {pmid42417340,
year = {2025},
author = {Perepanova T, S and Kozlov R, S and Pushkar D, Y and Apolikhin O, I and Kaprin A, D},
title = {[Updated international guidelines for the diagnosis and management of patients with urinary tract infection: an analytical review].},
journal = {Urologiia (Moscow, Russia : 1999)},
volume = {},
number = {6},
pages = {164-172},
pmid = {42417340},
issn = {1728-2985},
mesh = {Humans ; *Urinary Tract Infections/diagnosis/therapy/drug therapy ; Female ; *Practice Guidelines as Topic ; Cystitis/diagnosis ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {The latest 2025 guidelines of the European Association of Urology (EAU), the American Urological Association, the Canadian Urological Association, and the Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction (AUA/CUA/SUFU) introduce a new classification system for urinary tract infections (UTIs) and update sections on cystitis and asymptomatic bacteriuria (ABU). Current approaches to the management of patients with UTIs, ABU, and even symptomatic bacteriuria are being reconsidered. In the era of increasing antimicrobial resistance among uropathogens, advances in researching of human microbiome and urobiome have changed the long-standing assumption that any bacteriuria necessarily requires antimicrobial treatment. At present, even in patients with a confirmed diagnosis of acute bacterial cystitis, international recommendations consider symptomatic treatment and a watchful waiting strategy as acceptable options for selected patient groups. The new UTI classification, diagnostic features and symptoms of UTIs and ABU, non-antibiotic treatment options for cystitis, and age-related characteristics of UTI presentation are discussed in this review. Key aspects of the pathogenesis of recurrent UTIs are briefly addressed. Various urine sampling approaches are discussed, along with a differentiated strategy for prescribing antimicrobial therapy to women with acute and recurrent cystitis and non-antibiotic measures for recurrence prevention. The diagnostic value of urinalysis has also expanded to include new indicators of microbial load and assessment of urine contamination. The role of modern molecular diagnostic methods, beyond standard urine culture, in the diagnosis and treatment of UTIs is analyzed. The need to adhere to principles of rational antibiotic use to avoid collateral damage associated with antimicrobial therapy for UTIs is emphasized.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Urinary Tract Infections/diagnosis/therapy/drug therapy
Female
*Practice Guidelines as Topic
Cystitis/diagnosis
Anti-Bacterial Agents/therapeutic use
RevDate: 2026-07-08
Interleukin-17A mediates cardiorenal injury in oxalate nephropathy.
Cardiovascular research pii:8728291 [Epub ahead of print].
AIMS: Cardiovascular disease (CVD) is the leading cause of mortality in chronic kidney disease (CKD). While CKD is known to give rise to systemic inflammation, its inciting factors remain poorly defined. Oxalate, long implicated in rare genetic kidney disorders, accumulates with decreased kidney function and has emerged as a driver of inflammation and independent risk factor for CVD. Here, we investigate the immunological mechanisms linking oxalate nephropathy to systemic inflammation, cardiac damage and kidney injury.
METHODS AND RESULTS: Oxalate nephropathy was induced in C57Bl6/N mice through an oxalate-enriched diet. Oxalate induced systemic immune activation, renal fibrosis, and adverse cardiac remodeling, including pulmonary congestion with systolic and diastolic dysfunction. Flow cytometry analysis identified interleukin (IL)-17A as a dominant inflammatory effector, with expansion of Th17 and Th17-like Treg in the kidney, intestine, and spleen. Bulk mRNA sequencing confirmed these findings in kidney and heart. In line, plasma IL-17A was increased in oxalate-fed mice. Confirming the oxalate-IL-17A relationship, plasma IL-17A was elevated in patients with primary hyperoxaluria. Gut microbiome analysis by 16S amplicon sequencing showed only mild oxalate-induced alterations in mice. However, soluble oxalate directly enhanced Th17 polarization and disrupted mitochondrial respiration in vitro. In vivo, antibody-mediated IL-17A blockade improved kidney function, cardiac fibrosis, reduced neutrophil infiltration, and partially restored cardiac function in oxalate-fed mice.
CONCLUSIONS: Our study identifies oxalate as a systemic immunometabolic stressor and IL-17A as a central mediator of oxalate-induced cardiorenal injury. These findings establish the oxalate-IL-17A axis as a mechanistic link between CKD and CVD and suggest IL-17A inhibition as a potential therapeutic strategy to reduce cardiovascular damage in CKD.
Additional Links: PMID-42417540
Publisher:
PubMed:
Citation:
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@article {pmid42417540,
year = {2026},
author = {Wimmer, MI and Reichel, M and Thiele, A and Yarritu, A and Matz-Rauch, A and Anandakumar, H and Hernandez Götz, L and Lesker, TR and Potapenko, O and Gebremedhin, N and Anders, W and Liévano Contreras, SV and Wang, R and Behrens, F and Hoppe, B and Nonn, O and Schiattarella, GG and Schaefer, F and Holle, J and Strowig, T and Zernecke, A and Eckardt, KU and Knauf, F and Wilck, N and Bartolomaeus, H},
title = {Interleukin-17A mediates cardiorenal injury in oxalate nephropathy.},
journal = {Cardiovascular research},
volume = {},
number = {},
pages = {},
doi = {10.1093/cvr/cvag158},
pmid = {42417540},
issn = {1755-3245},
abstract = {AIMS: Cardiovascular disease (CVD) is the leading cause of mortality in chronic kidney disease (CKD). While CKD is known to give rise to systemic inflammation, its inciting factors remain poorly defined. Oxalate, long implicated in rare genetic kidney disorders, accumulates with decreased kidney function and has emerged as a driver of inflammation and independent risk factor for CVD. Here, we investigate the immunological mechanisms linking oxalate nephropathy to systemic inflammation, cardiac damage and kidney injury.
METHODS AND RESULTS: Oxalate nephropathy was induced in C57Bl6/N mice through an oxalate-enriched diet. Oxalate induced systemic immune activation, renal fibrosis, and adverse cardiac remodeling, including pulmonary congestion with systolic and diastolic dysfunction. Flow cytometry analysis identified interleukin (IL)-17A as a dominant inflammatory effector, with expansion of Th17 and Th17-like Treg in the kidney, intestine, and spleen. Bulk mRNA sequencing confirmed these findings in kidney and heart. In line, plasma IL-17A was increased in oxalate-fed mice. Confirming the oxalate-IL-17A relationship, plasma IL-17A was elevated in patients with primary hyperoxaluria. Gut microbiome analysis by 16S amplicon sequencing showed only mild oxalate-induced alterations in mice. However, soluble oxalate directly enhanced Th17 polarization and disrupted mitochondrial respiration in vitro. In vivo, antibody-mediated IL-17A blockade improved kidney function, cardiac fibrosis, reduced neutrophil infiltration, and partially restored cardiac function in oxalate-fed mice.
CONCLUSIONS: Our study identifies oxalate as a systemic immunometabolic stressor and IL-17A as a central mediator of oxalate-induced cardiorenal injury. These findings establish the oxalate-IL-17A axis as a mechanistic link between CKD and CVD and suggest IL-17A inhibition as a potential therapeutic strategy to reduce cardiovascular damage in CKD.},
}
RevDate: 2026-07-08
Germination and Polishing Reshape Microbial Communities in Japonica and Indica Rice.
Journal of agricultural and food chemistry [Epub ahead of print].
Germination is a process used to improve the nutritional quality of rice. However, its impact on rice microbiomes remains poorly understood. This study evaluated the microbiota of two rice ecotypes, low-amylose (Mochi) and high-amylose (BRS Formoso), after germination and polishing using 16S rRNA and ITS amplicon sequencing. Bacterial alpha diversity was highest in commercial brown rice (Shannon index 3.21) and lowest in commercial polished rice (1.50). Beta diversity indicated that germination exerted a similar effect on bacterial community composition in both ecotypes. Principal Coordinate Analysis suggested that polishing did not markedly influence microbiome composition relative to germination. The microbial profiles of Mochi and BRS Formoso were dominated by Pantoea, Pseudomonas, Rhizopus, and Moesziomyces. Overall, germination strongly influenced bacterial and fungal communities, emerging as the main factor shaping microbial structure and dynamics. These findings provide new insights into how processing affects the rice microbiome, with implications for food quality and safety.
Additional Links: PMID-42417706
Publisher:
PubMed:
Citation:
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@article {pmid42417706,
year = {2026},
author = {Oliveira, MEAS and Lucino, D and Garcia, GJY and Bertozzi, BG and Bassinello, PZ and Colombari Filho, JM and Piler de Carvalho, CW and Góes-Neto, A and Rocha, LO and Kabuki, DY and Freitas Silva, O and Takeiti, CY},
title = {Germination and Polishing Reshape Microbial Communities in Japonica and Indica Rice.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c02819},
pmid = {42417706},
issn = {1520-5118},
abstract = {Germination is a process used to improve the nutritional quality of rice. However, its impact on rice microbiomes remains poorly understood. This study evaluated the microbiota of two rice ecotypes, low-amylose (Mochi) and high-amylose (BRS Formoso), after germination and polishing using 16S rRNA and ITS amplicon sequencing. Bacterial alpha diversity was highest in commercial brown rice (Shannon index 3.21) and lowest in commercial polished rice (1.50). Beta diversity indicated that germination exerted a similar effect on bacterial community composition in both ecotypes. Principal Coordinate Analysis suggested that polishing did not markedly influence microbiome composition relative to germination. The microbial profiles of Mochi and BRS Formoso were dominated by Pantoea, Pseudomonas, Rhizopus, and Moesziomyces. Overall, germination strongly influenced bacterial and fungal communities, emerging as the main factor shaping microbial structure and dynamics. These findings provide new insights into how processing affects the rice microbiome, with implications for food quality and safety.},
}
RevDate: 2026-07-08
Investigating short-term dynamics of gut microbiome composition in the Western deer mouse.
Integrative and comparative biology pii:8728359 [Epub ahead of print].
The gut microbiome plays an important role in mammalian host health and ability to adapt to environmental conditions. While the gut microbiome is often considered fairly stable over short periods of time in the absence of a dramatic stressor, relatively little is known about the actual time scale of microbiome shifts, particularly in wildlife species. Most existing temporal studies utilize captive subjects, while here we employ the Western deer mouse, Peromyscus sonoriensis, in a field-based study to assess short-term microbiome dynamics (less than two days) in the wild. Mice were live-trapped at several urban and rural parks over a two-night trapping period in and around Spokane, Washington, USA in May of 2024. We collected fecal samples from 43 different individuals, capturing two to four time points per individual, and bacterial community composition was determined via 16S profiling with Nanopore sequencing. Genus-level profiles were compared across time points for each individual, showing relative consistency in types of taxa present for most mice, but some marked shifts in Ligilactobacillus in some mice. Calculation of intraclass correlation coefficients, however, showed low stability in alpha diversity (Shannon index) over time, suggesting greater variability than initially anticipated. Analysis with respect to site urbanization, sex, and age showed a significant effect of age when accounting for homogeneity of variance, with additional exploration of urbanization and sex needed in future work. These results provide important insight into the understudied area of host microbiome dynamics and highlight the complex relationships between microbiome, health, and environment.
Additional Links: PMID-42417710
Publisher:
PubMed:
Citation:
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@article {pmid42417710,
year = {2026},
author = {LePage, J and Wetherelt, H and Addis, E and Dizney, L and Beck, AE},
title = {Investigating short-term dynamics of gut microbiome composition in the Western deer mouse.},
journal = {Integrative and comparative biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/icb/icag094},
pmid = {42417710},
issn = {1557-7023},
abstract = {The gut microbiome plays an important role in mammalian host health and ability to adapt to environmental conditions. While the gut microbiome is often considered fairly stable over short periods of time in the absence of a dramatic stressor, relatively little is known about the actual time scale of microbiome shifts, particularly in wildlife species. Most existing temporal studies utilize captive subjects, while here we employ the Western deer mouse, Peromyscus sonoriensis, in a field-based study to assess short-term microbiome dynamics (less than two days) in the wild. Mice were live-trapped at several urban and rural parks over a two-night trapping period in and around Spokane, Washington, USA in May of 2024. We collected fecal samples from 43 different individuals, capturing two to four time points per individual, and bacterial community composition was determined via 16S profiling with Nanopore sequencing. Genus-level profiles were compared across time points for each individual, showing relative consistency in types of taxa present for most mice, but some marked shifts in Ligilactobacillus in some mice. Calculation of intraclass correlation coefficients, however, showed low stability in alpha diversity (Shannon index) over time, suggesting greater variability than initially anticipated. Analysis with respect to site urbanization, sex, and age showed a significant effect of age when accounting for homogeneity of variance, with additional exploration of urbanization and sex needed in future work. These results provide important insight into the understudied area of host microbiome dynamics and highlight the complex relationships between microbiome, health, and environment.},
}
RevDate: 2026-07-08
Environmental variation structures northern peatland soil microbiome composition and function in a reindeer herding area exclosure experiment.
FEMS microbiology ecology pii:8728361 [Epub ahead of print].
Northern peatlands store large carbon stocks but are sensitive to disturbance. Hydrology, vegetation, herbivory and snow conditions may affect soil microorganisms involved in methane (CH4) cycling and nitrous oxide (N2O) production/reduction. We investigated how reindeer exclusion and snow depth (increased and reduced relative to ambient) manipulations (ongoing for three seasons) influenced archaeal and bacterial communities in a boreal rich fen. Metagenomic (MG) and metatranscriptomic (MT) sequencing were combined with pore-water chemistry and CH4 flux measurements to link the microbiome to ecosystem processes. Microbial communities differed between outside and inside the exclosure. However, these patterns primarily reflected underlying hydrological variation. Slightly wetter inside plots showed higher expression of denitrification genes (norB, nosZ) and lower (nirS+nirK)/nosZ ratios, indicating greater potential for complete denitrification to N2 instead of N2O. Methane dynamics were mainly associated with vegetation: plots associated with Carex rostrata exhibited lower pmoA/mcrA ratios and elevated CH4 fluxes. Snow manipulations had subtle effects: reduced snow depth decreased the expression of taxa dependent on microbial interactions, while effect to the investigated metabolic marker genes was small. Overall hydrology, leading to variations in redox conditions and nutrient availability, together with vegetation appeared as the primary drivers on microbial greenhouse gas processes in this peatland.
Additional Links: PMID-42417728
Publisher:
PubMed:
Citation:
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@article {pmid42417728,
year = {2026},
author = {Välikangas, T and Fritze, H and Pitkänen, JM and Peltoniemi, K and Järvi-Laturi, E and Christensen, TR and Väisänen, M and Lämsä, J and Paavola, R and Hultman, J},
title = {Environmental variation structures northern peatland soil microbiome composition and function in a reindeer herding area exclosure experiment.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag072},
pmid = {42417728},
issn = {1574-6941},
abstract = {Northern peatlands store large carbon stocks but are sensitive to disturbance. Hydrology, vegetation, herbivory and snow conditions may affect soil microorganisms involved in methane (CH4) cycling and nitrous oxide (N2O) production/reduction. We investigated how reindeer exclusion and snow depth (increased and reduced relative to ambient) manipulations (ongoing for three seasons) influenced archaeal and bacterial communities in a boreal rich fen. Metagenomic (MG) and metatranscriptomic (MT) sequencing were combined with pore-water chemistry and CH4 flux measurements to link the microbiome to ecosystem processes. Microbial communities differed between outside and inside the exclosure. However, these patterns primarily reflected underlying hydrological variation. Slightly wetter inside plots showed higher expression of denitrification genes (norB, nosZ) and lower (nirS+nirK)/nosZ ratios, indicating greater potential for complete denitrification to N2 instead of N2O. Methane dynamics were mainly associated with vegetation: plots associated with Carex rostrata exhibited lower pmoA/mcrA ratios and elevated CH4 fluxes. Snow manipulations had subtle effects: reduced snow depth decreased the expression of taxa dependent on microbial interactions, while effect to the investigated metabolic marker genes was small. Overall hydrology, leading to variations in redox conditions and nutrient availability, together with vegetation appeared as the primary drivers on microbial greenhouse gas processes in this peatland.},
}
RevDate: 2026-07-08
Metagenomics comparison identifies shared pathogenic microbiome in humans, pigs and chickens.
Applied microbiology and biotechnology pii:10.1007/s00253-026-13948-1 [Epub ahead of print].
Integrating human, animal, and environmental health is crucial for combating infectious diseases, as an estimated 60 to 75% of emerging infectious diseases originate from zoonotic sources globally. In this study, we analysed 1274 shotgun metagenomic faecal samples of humans, pigs, and chickens collected across multiple countries to estimate levels of microbial sharing at the species-level genome bins (SGBs) resolution. We confirm that host species, rather than geography, significantly structures the gut microbial community, as shown by alpha and beta diversity analyses. Despite this high host specificity, we identified substantial cross-host sharing of SGBs, including taxa recognised as pathogens such as Escherichia coli, Clostridium perfringens, Clostridium innocuum, Clostridium disporicum, Enterococcus species, and Streptococcus alactolyticus. Core taxa were predominantly host-specific, while non-core taxa were more frequently shared across humans, pigs, and chickens. LEfSe analysis identified distinctive microbial signatures for each host, further supporting differences in community composition. These findings demonstrate that unrelated and geographically distant humans and livestock can harbour highly similar microbial populations with pathogenic potential. This work provides molecular evidence supporting the need for integrated One Health surveillance to better detect, manage, and prevent zoonotic and reverse zoonotic transmission events across interconnected human, animal, and environmental systems. KEY POINTS: • There is substantial cross-host sharing of species-level genome bins, including potential pathogens • Core taxa are predominantly host-specific • Non-core taxa are more likely to be shared across humans, pigs, and chickens.
Additional Links: PMID-42417977
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PubMed:
Citation:
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@article {pmid42417977,
year = {2026},
author = {Yu, SJ and Stanley, D and Van, TTH and Steel, JC and Bajagai, YS},
title = {Metagenomics comparison identifies shared pathogenic microbiome in humans, pigs and chickens.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13948-1},
pmid = {42417977},
issn = {1432-0614},
support = {PRO-017656//AgriFutures Australia/ ; PRO-017656//AgriFutures Australia/ ; },
abstract = {Integrating human, animal, and environmental health is crucial for combating infectious diseases, as an estimated 60 to 75% of emerging infectious diseases originate from zoonotic sources globally. In this study, we analysed 1274 shotgun metagenomic faecal samples of humans, pigs, and chickens collected across multiple countries to estimate levels of microbial sharing at the species-level genome bins (SGBs) resolution. We confirm that host species, rather than geography, significantly structures the gut microbial community, as shown by alpha and beta diversity analyses. Despite this high host specificity, we identified substantial cross-host sharing of SGBs, including taxa recognised as pathogens such as Escherichia coli, Clostridium perfringens, Clostridium innocuum, Clostridium disporicum, Enterococcus species, and Streptococcus alactolyticus. Core taxa were predominantly host-specific, while non-core taxa were more frequently shared across humans, pigs, and chickens. LEfSe analysis identified distinctive microbial signatures for each host, further supporting differences in community composition. These findings demonstrate that unrelated and geographically distant humans and livestock can harbour highly similar microbial populations with pathogenic potential. This work provides molecular evidence supporting the need for integrated One Health surveillance to better detect, manage, and prevent zoonotic and reverse zoonotic transmission events across interconnected human, animal, and environmental systems. KEY POINTS: • There is substantial cross-host sharing of species-level genome bins, including potential pathogens • Core taxa are predominantly host-specific • Non-core taxa are more likely to be shared across humans, pigs, and chickens.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Rhizome differentiation is associated with metabolic specialization and rhizosphere microbial assembly in Rheum officinale Baill.
Plant cell reports, 45(8):.
Distinct rhizome architectures are associated with differences in metabolic profiles and rhizosphere microbial composition within a single plant. Rhizome differentiation is a common developmental feature in perennial medicinal plants, yet its association with secondary metabolism and rhizosphere microbial assembly remains poorly understood. Here, we investigated the functional divergence between main rhizome (DH) and lateral rhizome (DC) of Rheum officinale Baill. using integrated metabolomic and transcriptomic analyses, quantitative real-time PCR (qRT-PCR) validation, and rhizosphere microbiome analyses. Metabolomic profiling revealed distinct patterns in anthraquinone allocation among rhizome types. DC exhibited a higher relative abundance of total detected anthraquinones and was enriched in both free anthraquinones (e.g., rhein) and selected glycosylated anthraquinones (e.g., chrysophanol 1-tetraglucoside), whereas DH preferentially accumulated other glycosylated metabolites such as cassiaside B2. Transcriptomic analysis identified 484 differentially expressed genes (DEGs) associated with these metabolic differences. Genes involved in anthraquinone biosynthesis and modification, including polyketide synthase (PKS), cytochrome P450 (CYP450), O-methyltransferase (OMT), and UDP-glycosyltransferase (UGT) family members, exhibited differential expression patterns associated with rhizome type, which were further validated by qRT-PCR. Although overall rhizosphere microbial diversity showed no significant differences between rhizome types, specific taxonomic shifts were observed, with Stenotrophomonas enriched in DC and Bacilli enriched in DH. Integrated analysis indicated correlation patterns among rhizome architecture, anthraquinone metabolism, transcriptional variation, and rhizosphere microbial composition. However, the directionality and underlying mechanisms of these relationships remain unresolved and warrant further mechanistic investigation. This study provides new insights into the biological basis of rhizome differentiation in Rheum officinale Baill.
Additional Links: PMID-42418003
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@article {pmid42418003,
year = {2026},
author = {Yin, L and Wu, J and Wang, X and Mou, Z and Gan, J and Xiao, Q},
title = {Rhizome differentiation is associated with metabolic specialization and rhizosphere microbial assembly in Rheum officinale Baill.},
journal = {Plant cell reports},
volume = {45},
number = {8},
pages = {},
pmid = {42418003},
issn = {1432-203X},
support = {MYK2026013//Hubei Minzu University/ ; 31260057//National Natural Science Foundation of China/ ; 2023BCB066//Key Research and Development Program of Hubei Province/ ; 2024BSB013//Central Government Guided Local Science and Technology Development Fund of Hubei Province/ ; E [2025] TG31//Central Financial Forestry Science and Technology Promotion Demonstration Project/ ; 2019ACA120//Major Technical Innovation Special Project of the Hubei Provincial Department of Science and Technology/ ; },
mesh = {*Rhizome/metabolism/microbiology/genetics ; *Rhizosphere ; *Rheum/metabolism/microbiology/genetics ; Metabolomics ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Anthraquinones/metabolism ; Microbiota ; Metabolome ; Transcriptome ; },
abstract = {Distinct rhizome architectures are associated with differences in metabolic profiles and rhizosphere microbial composition within a single plant. Rhizome differentiation is a common developmental feature in perennial medicinal plants, yet its association with secondary metabolism and rhizosphere microbial assembly remains poorly understood. Here, we investigated the functional divergence between main rhizome (DH) and lateral rhizome (DC) of Rheum officinale Baill. using integrated metabolomic and transcriptomic analyses, quantitative real-time PCR (qRT-PCR) validation, and rhizosphere microbiome analyses. Metabolomic profiling revealed distinct patterns in anthraquinone allocation among rhizome types. DC exhibited a higher relative abundance of total detected anthraquinones and was enriched in both free anthraquinones (e.g., rhein) and selected glycosylated anthraquinones (e.g., chrysophanol 1-tetraglucoside), whereas DH preferentially accumulated other glycosylated metabolites such as cassiaside B2. Transcriptomic analysis identified 484 differentially expressed genes (DEGs) associated with these metabolic differences. Genes involved in anthraquinone biosynthesis and modification, including polyketide synthase (PKS), cytochrome P450 (CYP450), O-methyltransferase (OMT), and UDP-glycosyltransferase (UGT) family members, exhibited differential expression patterns associated with rhizome type, which were further validated by qRT-PCR. Although overall rhizosphere microbial diversity showed no significant differences between rhizome types, specific taxonomic shifts were observed, with Stenotrophomonas enriched in DC and Bacilli enriched in DH. Integrated analysis indicated correlation patterns among rhizome architecture, anthraquinone metabolism, transcriptional variation, and rhizosphere microbial composition. However, the directionality and underlying mechanisms of these relationships remain unresolved and warrant further mechanistic investigation. This study provides new insights into the biological basis of rhizome differentiation in Rheum officinale Baill.},
}
MeSH Terms:
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*Rhizome/metabolism/microbiology/genetics
*Rhizosphere
*Rheum/metabolism/microbiology/genetics
Metabolomics
Gene Expression Profiling
Gene Expression Regulation, Plant
Anthraquinones/metabolism
Microbiota
Metabolome
Transcriptome
RevDate: 2026-07-08
CmpDate: 2026-07-08
Endophytic microorganisms from 'Bordô' grapes as biological control agents against Colletotrichum and Botrytis.
Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 57(1):.
Colletotrichum spp. and Botrytis cinerea are the main causal agents of grape bunch rot in Brazil. Although chemical control is widely used, it has limitations, such as the selection of resistant pathogen populations and environmental concerns. Biological control emerges as a promising alternative; however, commercial products for viticulture remain limited. We hypothesized that by prospecting endophytic microorganisms from berries of Vitis hosts more resistant to rots, it would be possible to identify isolates with greater biocontrol potential. In this study, 52 endophytic isolates from berries of V. labrusca cv. 'Bordô' were evaluated. In vitro assays showed mycelial growth inhibition of C. nymphaeae and B. cinerea of up to 33% and 60%, respectively. Three isolates antagonistic to both pathogens were molecularly identified as AvCaPR20-VA4L (Clavispora asparagi), AvZmPR20-VB5B (Zygoascus meyerae), and AvTmPR20-PA1N (Tatumella sp.). In postharvest assays, the isolates achieved 31.5-73.5% control of grape ripe rot (C. nymphaeae) and 39.1-59.4% control of gray mold (B. cinerea), with AvTmPR20-PA1N showing the highest efficacy, comparable to chlorothalonil. In untreated berries, disease incidence reached 53.1% for grape ripe rot and 100% for gray mold. Next-generation sequencing of the natural berry microbiota revealed the recurrent presence of Clavispora and Tatumella in non-inoculated 'Bordô' vines, confirming their natural association with grape berry tissues. These findings highlight the potential of exploring microbial diversity from naturally resistant plants as a sustainable strategy for biological disease management in viticulture.
Additional Links: PMID-42418044
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@article {pmid42418044,
year = {2026},
author = {Zela, CI and Castellar, C and de Oliveira Franco, D and Graf, AL and Calegario, RF and De Mio, LLM},
title = {Endophytic microorganisms from 'Bordô' grapes as biological control agents against Colletotrichum and Botrytis.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42418044},
issn = {1678-4405},
mesh = {*Vitis/microbiology ; *Botrytis/growth & development/physiology ; *Colletotrichum/growth & development/physiology ; *Biological Control Agents ; *Plant Diseases/microbiology/prevention & control ; *Endophytes/isolation & purification/genetics/physiology/classification ; Antibiosis ; Phylogeny ; Brazil ; },
abstract = {Colletotrichum spp. and Botrytis cinerea are the main causal agents of grape bunch rot in Brazil. Although chemical control is widely used, it has limitations, such as the selection of resistant pathogen populations and environmental concerns. Biological control emerges as a promising alternative; however, commercial products for viticulture remain limited. We hypothesized that by prospecting endophytic microorganisms from berries of Vitis hosts more resistant to rots, it would be possible to identify isolates with greater biocontrol potential. In this study, 52 endophytic isolates from berries of V. labrusca cv. 'Bordô' were evaluated. In vitro assays showed mycelial growth inhibition of C. nymphaeae and B. cinerea of up to 33% and 60%, respectively. Three isolates antagonistic to both pathogens were molecularly identified as AvCaPR20-VA4L (Clavispora asparagi), AvZmPR20-VB5B (Zygoascus meyerae), and AvTmPR20-PA1N (Tatumella sp.). In postharvest assays, the isolates achieved 31.5-73.5% control of grape ripe rot (C. nymphaeae) and 39.1-59.4% control of gray mold (B. cinerea), with AvTmPR20-PA1N showing the highest efficacy, comparable to chlorothalonil. In untreated berries, disease incidence reached 53.1% for grape ripe rot and 100% for gray mold. Next-generation sequencing of the natural berry microbiota revealed the recurrent presence of Clavispora and Tatumella in non-inoculated 'Bordô' vines, confirming their natural association with grape berry tissues. These findings highlight the potential of exploring microbial diversity from naturally resistant plants as a sustainable strategy for biological disease management in viticulture.},
}
MeSH Terms:
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*Vitis/microbiology
*Botrytis/growth & development/physiology
*Colletotrichum/growth & development/physiology
*Biological Control Agents
*Plant Diseases/microbiology/prevention & control
*Endophytes/isolation & purification/genetics/physiology/classification
Antibiosis
Phylogeny
Brazil
RevDate: 2026-07-08
CmpDate: 2026-07-08
The functionality of the cysteinyl leukotriene receptor 1 (CysLTR1) in the lung by metabolomics analysis of bronchoalveolar lavage fluid.
Metabolomics : Official journal of the Metabolomic Society, 22(4):.
INTRODUCTION: The cysteinyl leukotriene receptor 1 (CysLTR1) is known as a potent lipid mediator with a well-established role in inflammatory regulation and lung disease. While its involvement in immune cell recruitment has been previously reported, its broader impact on pulmonary metabolism remains poorly understood.
OBJECTIVES: The study aims to investigate the metabolic consequences of a CysLTR1 deletion in mice to elucidate its role in pulmonary metabolic homeostasis.
METHODS: Bronchoalveolar lavage fluid (BALF) was collected from CysLTR1 knockout (KO) and wild-type (WT) mice (n = 4 per group), and analysed using standardized untargeted gas chromatography-time-of-flight mass spectrometry (GC-TOFMS) metabolomics.
RESULTS: Metabolomics analyses of the BALF collected from the CysLTR1 KO mice presented significantly reduced levels of glucose, glucosamine, and glyceric acid, indicating the role of the CysLTR in lung glucose uptake and consequently lung glycolysis and gluconeogenesis. This is further supported by reductions in myo-inositol and D-chiro-inositol, also supporting previous findings that this occurs due to insulin resistance. Consequential disruption of various glucose-dependent pathways, including the pentose phosphate pathway (reduced gluconic acid, sedoheptulose and xylose) and purine metabolism (reduced 1-methylinosine) indicates a consequential altered nucleotide turnover, and the significantly reduced concentrations of butanoic acid, decan-2-ol, and 1-hexadecanol, indicate changes to fatty acid metabolism in the lung, as a compensatory response to the initial glucose deficiency induced by the CysLTR1 KO. Lastly, the changes to mandelic acid, glutaric acid, tricarballylic acid, and decan-2-ol, furthermore, indicate the role of CysLTR1 in the composition/metabolism of the microbiome.
CONCLUSION: This study expands our knowledge on the role of CysLTR1 beyond its role in immune regulation, which may contribute to a better understanding of CysLTR1 associated lung diseases and in the development of improved therapeutic strategies.
Additional Links: PMID-42418110
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Citation:
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@article {pmid42418110,
year = {2026},
author = {Adeosun, WB and Poswayo, SKL and Parihar, SP and Loots, DT},
title = {The functionality of the cysteinyl leukotriene receptor 1 (CysLTR1) in the lung by metabolomics analysis of bronchoalveolar lavage fluid.},
journal = {Metabolomics : Official journal of the Metabolomic Society},
volume = {22},
number = {4},
pages = {},
pmid = {42418110},
issn = {1573-3890},
mesh = {Animals ; *Receptors, Leukotriene/metabolism/genetics ; *Bronchoalveolar Lavage Fluid/chemistry ; *Metabolomics/methods ; Mice ; *Lung/metabolism ; Mice, Knockout ; Gas Chromatography-Mass Spectrometry ; Male ; Mice, Inbred C57BL ; },
abstract = {INTRODUCTION: The cysteinyl leukotriene receptor 1 (CysLTR1) is known as a potent lipid mediator with a well-established role in inflammatory regulation and lung disease. While its involvement in immune cell recruitment has been previously reported, its broader impact on pulmonary metabolism remains poorly understood.
OBJECTIVES: The study aims to investigate the metabolic consequences of a CysLTR1 deletion in mice to elucidate its role in pulmonary metabolic homeostasis.
METHODS: Bronchoalveolar lavage fluid (BALF) was collected from CysLTR1 knockout (KO) and wild-type (WT) mice (n = 4 per group), and analysed using standardized untargeted gas chromatography-time-of-flight mass spectrometry (GC-TOFMS) metabolomics.
RESULTS: Metabolomics analyses of the BALF collected from the CysLTR1 KO mice presented significantly reduced levels of glucose, glucosamine, and glyceric acid, indicating the role of the CysLTR in lung glucose uptake and consequently lung glycolysis and gluconeogenesis. This is further supported by reductions in myo-inositol and D-chiro-inositol, also supporting previous findings that this occurs due to insulin resistance. Consequential disruption of various glucose-dependent pathways, including the pentose phosphate pathway (reduced gluconic acid, sedoheptulose and xylose) and purine metabolism (reduced 1-methylinosine) indicates a consequential altered nucleotide turnover, and the significantly reduced concentrations of butanoic acid, decan-2-ol, and 1-hexadecanol, indicate changes to fatty acid metabolism in the lung, as a compensatory response to the initial glucose deficiency induced by the CysLTR1 KO. Lastly, the changes to mandelic acid, glutaric acid, tricarballylic acid, and decan-2-ol, furthermore, indicate the role of CysLTR1 in the composition/metabolism of the microbiome.
CONCLUSION: This study expands our knowledge on the role of CysLTR1 beyond its role in immune regulation, which may contribute to a better understanding of CysLTR1 associated lung diseases and in the development of improved therapeutic strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Receptors, Leukotriene/metabolism/genetics
*Bronchoalveolar Lavage Fluid/chemistry
*Metabolomics/methods
Mice
*Lung/metabolism
Mice, Knockout
Gas Chromatography-Mass Spectrometry
Male
Mice, Inbred C57BL
RevDate: 2026-07-08
CmpDate: 2026-07-08
A microbial mirage: when microbiome metrics may obscure ecological meaning.
Microbial genomics, 12(7):.
Metrics such as alpha diversity, inferred functional potential and network complexity have become standard metrics in microbiome research. While they offer convenient ways to summarize complex data, these metrics may sometimes obscure more than they reveal. Alpha diversity, for example, measures richness and evenness. However, two samples may exhibit identical diversity scores, yet one could be dominated by beneficial taxa and the other by pathogens. Similarly, the presence of genes associated with particular functions does not guarantee that those functions are expressed or ecologically relevant under given conditions. Functional inference is also limited by database bias and often lacks empirical validation. Likewise, correlation-based network analyses can produce spurious associations driven by shared environmental covariates, sequencing depth or batch effects. These issues are routinely encountered in genomic workflows - from 16S/ITS amplicon surveys to shotgun metagenomics, genome-resolved metagenomics and gene-centric network analyses - where apparently 'clean' summary metrics can mask very different ecological realities. Here, we use simple, domain-relevant examples to illustrate how over-reliance on these metrics can lead to misinterpretation. Rather than rejecting these approaches, we outline when they are most informative, when they require caution and what complementary analyses can strengthen ecological inference. We propose a practical framework based on four questions: what exactly is being summarized, at what biological level, under which ecological conditions and with what form of validation? While acknowledging their value, we argue for greater critical scrutiny in their application and interpretation, and advocate for approaches that prioritize functional validation, temporal resolution and systems thinking to support more meaningful ecological insight.
Additional Links: PMID-42418242
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PubMed:
Citation:
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@article {pmid42418242,
year = {2026},
author = {Robinson, JM and Guentas, L and Breed, MF},
title = {A microbial mirage: when microbiome metrics may obscure ecological meaning.},
journal = {Microbial genomics},
volume = {12},
number = {7},
pages = {},
doi = {10.1099/mgen.0.001777},
pmid = {42418242},
issn = {2057-5858},
mesh = {*Microbiota/genetics ; *Metagenomics/methods ; *Bacteria/genetics/classification ; RNA, Ribosomal, 16S/genetics ; Ecology ; },
abstract = {Metrics such as alpha diversity, inferred functional potential and network complexity have become standard metrics in microbiome research. While they offer convenient ways to summarize complex data, these metrics may sometimes obscure more than they reveal. Alpha diversity, for example, measures richness and evenness. However, two samples may exhibit identical diversity scores, yet one could be dominated by beneficial taxa and the other by pathogens. Similarly, the presence of genes associated with particular functions does not guarantee that those functions are expressed or ecologically relevant under given conditions. Functional inference is also limited by database bias and often lacks empirical validation. Likewise, correlation-based network analyses can produce spurious associations driven by shared environmental covariates, sequencing depth or batch effects. These issues are routinely encountered in genomic workflows - from 16S/ITS amplicon surveys to shotgun metagenomics, genome-resolved metagenomics and gene-centric network analyses - where apparently 'clean' summary metrics can mask very different ecological realities. Here, we use simple, domain-relevant examples to illustrate how over-reliance on these metrics can lead to misinterpretation. Rather than rejecting these approaches, we outline when they are most informative, when they require caution and what complementary analyses can strengthen ecological inference. We propose a practical framework based on four questions: what exactly is being summarized, at what biological level, under which ecological conditions and with what form of validation? While acknowledging their value, we argue for greater critical scrutiny in their application and interpretation, and advocate for approaches that prioritize functional validation, temporal resolution and systems thinking to support more meaningful ecological insight.},
}
MeSH Terms:
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*Microbiota/genetics
*Metagenomics/methods
*Bacteria/genetics/classification
RNA, Ribosomal, 16S/genetics
Ecology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Mapping potential pathogen profiling in cetacean blow: comparative insights from sequencing technologies.
Microbial genomics, 12(7):.
Cetaceans play a critical role in marine ecosystems and function as sentinel species for detecting environmental perturbations, underscoring the importance of assessing their health for effective marine conservation. This study employed 16S rRNA gene sequencing to characterize the prokaryotic communities present in exhaled breath condensate (EBC) samples from cetaceans, utilizing both short-read (Illumina) and long-read (PacBio) sequencing platforms. Putative pathogenic taxa were identified using the Multiple Bacterial Pathogen Detection (MBPD) database. Substantial differences in microbial community composition were observed between sequencing approaches. The PacBio platform yielded 2,373 amplicon sequence variants (ASVs) spanning 30 bacterial phyla, with 614 ASVs identified as potential pathogens. In contrast, the Illumina dataset generated 350 ASVs across 17 phyla, of which 46 were flagged as potentially pathogenic. Discrepancies were also evident in diversity metrics: PacBio-derived profiles exhibited higher alpha diversity and produced beta diversity clustering patterns that corresponded with sample metadata, while Illumina-based profiles did not reveal meaningful clustering. Distinct EBC microbial signatures were identified for Globicephala macrorhynchus and Delphinus delphis, with clear differences from the surrounding seawater microbiota. These findings support the use of EBC as a non-invasive and informative tool for respiratory microbiome analysis in marine mammals. Notably, this study provides the first characterization of the respiratory microbiota in D. delphis, offering a valuable methodological baseline for future research into host-microbiome interactions, health assessment and putative pathogen monitoring in free-ranging cetacean populations, using non-invasive approaches.
Additional Links: PMID-42418267
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PubMed:
Citation:
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@article {pmid42418267,
year = {2026},
author = {Jaitner, JF and Gambardella, N and Afonso, L and Valente, R and Tomasino, MP and Correia, AM and Rosso, M and Alves, F and Magalhães, C},
title = {Mapping potential pathogen profiling in cetacean blow: comparative insights from sequencing technologies.},
journal = {Microbial genomics},
volume = {12},
number = {7},
pages = {},
doi = {10.1099/mgen.0.001773},
pmid = {42418267},
issn = {2057-5858},
mesh = {Animals ; RNA, Ribosomal, 16S/genetics ; *Bacteria/genetics/classification/isolation & purification/pathogenicity ; *Microbiota/genetics ; *Cetacea/microbiology ; High-Throughput Nucleotide Sequencing/methods ; Phylogeny ; Sequence Analysis, DNA/methods ; },
abstract = {Cetaceans play a critical role in marine ecosystems and function as sentinel species for detecting environmental perturbations, underscoring the importance of assessing their health for effective marine conservation. This study employed 16S rRNA gene sequencing to characterize the prokaryotic communities present in exhaled breath condensate (EBC) samples from cetaceans, utilizing both short-read (Illumina) and long-read (PacBio) sequencing platforms. Putative pathogenic taxa were identified using the Multiple Bacterial Pathogen Detection (MBPD) database. Substantial differences in microbial community composition were observed between sequencing approaches. The PacBio platform yielded 2,373 amplicon sequence variants (ASVs) spanning 30 bacterial phyla, with 614 ASVs identified as potential pathogens. In contrast, the Illumina dataset generated 350 ASVs across 17 phyla, of which 46 were flagged as potentially pathogenic. Discrepancies were also evident in diversity metrics: PacBio-derived profiles exhibited higher alpha diversity and produced beta diversity clustering patterns that corresponded with sample metadata, while Illumina-based profiles did not reveal meaningful clustering. Distinct EBC microbial signatures were identified for Globicephala macrorhynchus and Delphinus delphis, with clear differences from the surrounding seawater microbiota. These findings support the use of EBC as a non-invasive and informative tool for respiratory microbiome analysis in marine mammals. Notably, this study provides the first characterization of the respiratory microbiota in D. delphis, offering a valuable methodological baseline for future research into host-microbiome interactions, health assessment and putative pathogen monitoring in free-ranging cetacean populations, using non-invasive approaches.},
}
MeSH Terms:
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Animals
RNA, Ribosomal, 16S/genetics
*Bacteria/genetics/classification/isolation & purification/pathogenicity
*Microbiota/genetics
*Cetacea/microbiology
High-Throughput Nucleotide Sequencing/methods
Phylogeny
Sequence Analysis, DNA/methods
RevDate: 2026-07-08
CmpDate: 2026-07-08
Geographic and Orientia infection status influence on the bacterial microbiome of free-living chiggers in North Carolina, USA.
PloS one, 21(7):e0353174 pii:PONE-D-25-67871.
Chiggers (larval Trombiculid mites) serve as vectors for Orientia species that cause scrub typhus, a potentially serious illness in humans with a broadening global distribution. To date, there is limited research on the chigger microbiome in the United States (US) compared to some other parts of the world. Investigating chigger bacterial communities is essential for understanding the potential role they play in pathogen transmission dynamics within these arthropods. This study investigated the bacterial communities of free-living chiggers collected from sites across the three ecoregions in North Carolina using 16S rDNA gene targeted next-generation sequencing. Molecular identification of the chigger revealed three species: Eutrombicula splendens, Eutrombicula tinami, and Pseudoschoengastia sp. All three trombiculid mite species occurred at least once in the Mountains and Piedmont, except for E. tinami, which was absent from the Coastal Plain ecoregion. Microbiome analysis revealed significant differences in alpha and beta diversity among the collection sites for E. splendens. No significant differences in overall microbiome diversity were observed between E. splendens and Pseudoschoengastia sp., the two dominant chigger species. However, the microbiome of E. splendens alone exhibited significant differences in both Shannon diversity and beta diversity between Orientia-infected and uninfected individuals. Within E. splendens, genera like Brevibacillus and Telluria were more abundant in Orientia-positive chiggers, while Methylobacterium was more abundant in Orientia-negative chiggers. We also found potentially pathogenic bacterial genera, including Rickettsia, Listeria, Legionella, Staphylococcus, and Streptococcus sequences. These findings suggest that geography and Orientia infection influence chigger-associated bacterial communities, potentially affecting their vector competence.
Additional Links: PMID-42418460
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PubMed:
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@article {pmid42418460,
year = {2026},
author = {Chen, K and Travanty, NV and Garshong, RA and Wasserberg, G and Apperson, CS and Roe, RM and Ponnusamy, L},
title = {Geographic and Orientia infection status influence on the bacterial microbiome of free-living chiggers in North Carolina, USA.},
journal = {PloS one},
volume = {21},
number = {7},
pages = {e0353174},
doi = {10.1371/journal.pone.0353174},
pmid = {42418460},
issn = {1932-6203},
mesh = {Animals ; North Carolina/epidemiology ; *Microbiota ; *Trombiculidae/microbiology ; RNA, Ribosomal, 16S/genetics ; *Scrub Typhus/microbiology/transmission/epidemiology ; *Orientia tsutsugamushi ; Phylogeny ; Geography ; },
abstract = {Chiggers (larval Trombiculid mites) serve as vectors for Orientia species that cause scrub typhus, a potentially serious illness in humans with a broadening global distribution. To date, there is limited research on the chigger microbiome in the United States (US) compared to some other parts of the world. Investigating chigger bacterial communities is essential for understanding the potential role they play in pathogen transmission dynamics within these arthropods. This study investigated the bacterial communities of free-living chiggers collected from sites across the three ecoregions in North Carolina using 16S rDNA gene targeted next-generation sequencing. Molecular identification of the chigger revealed three species: Eutrombicula splendens, Eutrombicula tinami, and Pseudoschoengastia sp. All three trombiculid mite species occurred at least once in the Mountains and Piedmont, except for E. tinami, which was absent from the Coastal Plain ecoregion. Microbiome analysis revealed significant differences in alpha and beta diversity among the collection sites for E. splendens. No significant differences in overall microbiome diversity were observed between E. splendens and Pseudoschoengastia sp., the two dominant chigger species. However, the microbiome of E. splendens alone exhibited significant differences in both Shannon diversity and beta diversity between Orientia-infected and uninfected individuals. Within E. splendens, genera like Brevibacillus and Telluria were more abundant in Orientia-positive chiggers, while Methylobacterium was more abundant in Orientia-negative chiggers. We also found potentially pathogenic bacterial genera, including Rickettsia, Listeria, Legionella, Staphylococcus, and Streptococcus sequences. These findings suggest that geography and Orientia infection influence chigger-associated bacterial communities, potentially affecting their vector competence.},
}
MeSH Terms:
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Animals
North Carolina/epidemiology
*Microbiota
*Trombiculidae/microbiology
RNA, Ribosomal, 16S/genetics
*Scrub Typhus/microbiology/transmission/epidemiology
*Orientia tsutsugamushi
Phylogeny
Geography
RevDate: 2026-07-08
CmpDate: 2026-07-08
Phage intervention improves colitis and response to corticosteroids by attenuating virulence of Crohn's disease-associated bacteria.
Science translational medicine, 18(857):eadz4589.
Adherent-invasive Escherichia coli (AIEC) exhibits proinflammatory properties and has been implicated in the pathogenesis of Crohn's disease (CD), a form of inflammatory bowel disease (IBD). Antibiotic use in CD lacks specificity and may worsen microbiome disruption, prompting interest in bacteriophages (phages) for targeted microbiome editing. Here, we identified HER259, a phage active against clinical AIEC isolates. HER259 ameliorated colitis in gnotobiotic models and attenuated the virulence of AIEC strain NRG857c, including suppression of the FimH adhesin through inversion of the fimS promoter to its "off" orientation. The effects were confirmed in CD-microbiota colitis models. Withdrawal of HER259 treatment led to reversion of the fimS promoter and reactivated colitis. The HER259 phage also enhanced the therapeutic effect of subtherapeutic budesonide independent of microbial drug metabolism. These findings support targeted phage therapy as an adjunct treatment approach in IBD, demonstrating modulation of bacterial virulence and improved response to conventional treatments that may reduce drug-related side effects.
Additional Links: PMID-42418560
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PubMed:
Citation:
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@article {pmid42418560,
year = {2026},
author = {Jackson, K and Galipeau, HJ and Hann, A and Constante, M and Zangara, MT and Bording-Jorgensen, M and Fuentes, A and Ho, H and Wang, J and Shimbori, C and Moayyedi, P and Surette, M and Bercik, P and Coombes, BK and Hosseinidoust, Z and Verdu, EF},
title = {Phage intervention improves colitis and response to corticosteroids by attenuating virulence of Crohn's disease-associated bacteria.},
journal = {Science translational medicine},
volume = {18},
number = {857},
pages = {eadz4589},
doi = {10.1126/scitranslmed.adz4589},
pmid = {42418560},
issn = {1946-6242},
mesh = {*Crohn Disease/microbiology/drug therapy ; Animals ; *Colitis/microbiology/drug therapy/complications/therapy ; Virulence/drug effects ; Escherichia coli/pathogenicity/drug effects ; *Bacteriophages/physiology ; *Adrenal Cortex Hormones/therapeutic use/pharmacology ; Humans ; *Phage Therapy ; Budesonide/therapeutic use/pharmacology ; Female ; Promoter Regions, Genetic/genetics ; },
abstract = {Adherent-invasive Escherichia coli (AIEC) exhibits proinflammatory properties and has been implicated in the pathogenesis of Crohn's disease (CD), a form of inflammatory bowel disease (IBD). Antibiotic use in CD lacks specificity and may worsen microbiome disruption, prompting interest in bacteriophages (phages) for targeted microbiome editing. Here, we identified HER259, a phage active against clinical AIEC isolates. HER259 ameliorated colitis in gnotobiotic models and attenuated the virulence of AIEC strain NRG857c, including suppression of the FimH adhesin through inversion of the fimS promoter to its "off" orientation. The effects were confirmed in CD-microbiota colitis models. Withdrawal of HER259 treatment led to reversion of the fimS promoter and reactivated colitis. The HER259 phage also enhanced the therapeutic effect of subtherapeutic budesonide independent of microbial drug metabolism. These findings support targeted phage therapy as an adjunct treatment approach in IBD, demonstrating modulation of bacterial virulence and improved response to conventional treatments that may reduce drug-related side effects.},
}
MeSH Terms:
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hide MeSH Terms
*Crohn Disease/microbiology/drug therapy
Animals
*Colitis/microbiology/drug therapy/complications/therapy
Virulence/drug effects
Escherichia coli/pathogenicity/drug effects
*Bacteriophages/physiology
*Adrenal Cortex Hormones/therapeutic use/pharmacology
Humans
*Phage Therapy
Budesonide/therapeutic use/pharmacology
Female
Promoter Regions, Genetic/genetics
RevDate: 2026-07-08
CmpDate: 2026-07-08
Nutrition Therapy in Critically Ill Adults.
The New England journal of medicine, 395(2):162-174.
In the acute phase of critical illness, adults have severe catabolism, inflammation, muscle loss, and gut dysfunction, all of which shape nutritional requirements. Early enteral nutrition supports gut integrity and microbiome health, but trials have shown that early short-term parenteral nutrition is a safe alternative when enteral feeding is not possible. Large trials have shown that early full-dose energy delivery offers no benefit over restrictive dosing and may increase gastrointestinal and metabolic complications, findings that support a restrictive nutrition strategy, especially in patients who have circulatory shock or are at risk for refeeding syndrome. Similarly, large trials have shown no advantage of high-dose over standard-dose protein and suggest harm in patients with acute kidney injury. Because adverse events are common with enteral nutrition, safe nutrition delivery requires gradual advancement, strategies for prevention of refeeding syndrome, glycemic control, and avoidance of routine gastric residual volume monitoring. Patient heterogeneity underscores the need for precise, biomarker-guided, phase-specific nutrition to preserve lean muscle mass and improve recovery.
Additional Links: PMID-42418776
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PubMed:
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@article {pmid42418776,
year = {2026},
author = {Patel, JJ and McClave, SA},
title = {Nutrition Therapy in Critically Ill Adults.},
journal = {The New England journal of medicine},
volume = {395},
number = {2},
pages = {162-174},
doi = {10.1056/NEJMra2506111},
pmid = {42418776},
issn = {1533-4406},
mesh = {Humans ; *Critical Illness/therapy ; *Enteral Nutrition/adverse effects ; *Parenteral Nutrition/adverse effects ; Refeeding Syndrome/prevention & control ; Nutritional Requirements ; Energy Intake ; },
abstract = {In the acute phase of critical illness, adults have severe catabolism, inflammation, muscle loss, and gut dysfunction, all of which shape nutritional requirements. Early enteral nutrition supports gut integrity and microbiome health, but trials have shown that early short-term parenteral nutrition is a safe alternative when enteral feeding is not possible. Large trials have shown that early full-dose energy delivery offers no benefit over restrictive dosing and may increase gastrointestinal and metabolic complications, findings that support a restrictive nutrition strategy, especially in patients who have circulatory shock or are at risk for refeeding syndrome. Similarly, large trials have shown no advantage of high-dose over standard-dose protein and suggest harm in patients with acute kidney injury. Because adverse events are common with enteral nutrition, safe nutrition delivery requires gradual advancement, strategies for prevention of refeeding syndrome, glycemic control, and avoidance of routine gastric residual volume monitoring. Patient heterogeneity underscores the need for precise, biomarker-guided, phase-specific nutrition to preserve lean muscle mass and improve recovery.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Critical Illness/therapy
*Enteral Nutrition/adverse effects
*Parenteral Nutrition/adverse effects
Refeeding Syndrome/prevention & control
Nutritional Requirements
Energy Intake
RevDate: 2026-07-08
Rhizoplane microbiome: niche-specific recruitment and plant defense priming against bacterial wilt disease.
Plant physiology pii:8728598 [Epub ahead of print].
The plant microbiome plays a pivotal role in host adaptation and disease suppression, yet niche-specific microbial responses to biotic stress, particularly within distinct plant compartments, remain poorly understood. Here, we revealed that bacterial wilt disease (BWD) induced pronounced niche-specific microbiome alterations in tobacco, with the rhizoplane emerging as a critical hub for beneficial microbial recruitment and defense coordination. Utilizing 16S and ITS amplicon sequencing across six distinct plant niches, we observed significantly enhanced bacterial diversity and a striking enrichment of potentially beneficial microbes in the rhizoplane under BWD stress. Eight potent antagonistic bacterial strains were isolated from this key niche, with Stenotrophomonas sp. ASV61 and Chryseobacterium sp. ASV172 demonstrating robust in vitro biocontrol potential and confirming in vivo plant resistance and growth promotion. We further elucidated the superior biocontrol mechanisms of Chryseobacterium sp. ASV172, attributing its superior efficacy to enhanced colonization and flexirubin-mediated antagonism. Crucially, plant transcriptomic profiling unveiled that these beneficial microbes engaged in a signaling dialogue with host plants, dynamically modulating defense hormone pathways. While Ralstonia alone manipulated host defenses by sustaining salicylic acid (SA) responses, antagonistic strains re-directed the plant towards robust jasmonic acid (JA) signaling, thereby restoring a more effective defense posture. Collectively, our findings underscore the disproportionate importance of the rhizoplane over the rhizosphere in assembling a resilient microbiome against soil-borne diseases, paving the way for targeted rhizoplane microbiome engineering strategies for sustainable disease management.
Additional Links: PMID-42418792
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PubMed:
Citation:
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@article {pmid42418792,
year = {2026},
author = {Tao, J and Yu, S and Lu, P and Gu, M and Kong, M and Guo, J and Zhao, Z and Su, H and Li, H and Zhang, J and Jin, J and Cao, P},
title = {Rhizoplane microbiome: niche-specific recruitment and plant defense priming against bacterial wilt disease.},
journal = {Plant physiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/plphys/kiag483},
pmid = {42418792},
issn = {1532-2548},
abstract = {The plant microbiome plays a pivotal role in host adaptation and disease suppression, yet niche-specific microbial responses to biotic stress, particularly within distinct plant compartments, remain poorly understood. Here, we revealed that bacterial wilt disease (BWD) induced pronounced niche-specific microbiome alterations in tobacco, with the rhizoplane emerging as a critical hub for beneficial microbial recruitment and defense coordination. Utilizing 16S and ITS amplicon sequencing across six distinct plant niches, we observed significantly enhanced bacterial diversity and a striking enrichment of potentially beneficial microbes in the rhizoplane under BWD stress. Eight potent antagonistic bacterial strains were isolated from this key niche, with Stenotrophomonas sp. ASV61 and Chryseobacterium sp. ASV172 demonstrating robust in vitro biocontrol potential and confirming in vivo plant resistance and growth promotion. We further elucidated the superior biocontrol mechanisms of Chryseobacterium sp. ASV172, attributing its superior efficacy to enhanced colonization and flexirubin-mediated antagonism. Crucially, plant transcriptomic profiling unveiled that these beneficial microbes engaged in a signaling dialogue with host plants, dynamically modulating defense hormone pathways. While Ralstonia alone manipulated host defenses by sustaining salicylic acid (SA) responses, antagonistic strains re-directed the plant towards robust jasmonic acid (JA) signaling, thereby restoring a more effective defense posture. Collectively, our findings underscore the disproportionate importance of the rhizoplane over the rhizosphere in assembling a resilient microbiome against soil-borne diseases, paving the way for targeted rhizoplane microbiome engineering strategies for sustainable disease management.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
The Dual Role of the Gut Microbiota in Cancer Chemoresistance.
MicrobiologyOpen, 15(4):e70357.
Chemoresistance is one of the primary reasons that cancer chemotherapy fails to deliver successful treatment outcomes and contributes to poor overall survival rates for patients with cancer. New research has begun to shed light on the effects of the gut microbiome (GM). This new research will examine how certain microorganisms (referred to as "bad bacteria") can contribute to cancer treatment failure, as well as how others (such as Bifidobacterium, Akkermansia, and Lactobacillus) can enhance treatment success. This review will focus on the molecular mechanisms underlying these effects, including drug metabolism by microorganisms, modulation of the immune system by microorganisms, regulation of cellular apoptosis by microorganisms, and metabolic crosstalk between tumor tissue and the microbiome. Finally, we will look at new therapies under development that leverage knowledge of the microbiome to combat chemoresistance, including fecal microbiota transplantation, targeted probiotic and prebiotic supplementation, and dietary modifications. By studying the complex interactions among the host, the microbiome, and chemotherapeutic agents, we hope to demonstrate how microbiome-centered approaches can tailor and enhance an individual's cancer treatment while transforming the GM from a passive participant to an active target in cancer therapy.
Additional Links: PMID-42418807
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PubMed:
Citation:
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@article {pmid42418807,
year = {2026},
author = {Tahmasebi, H and Bahar, A and Khazaei, M and Arabestani, MR},
title = {The Dual Role of the Gut Microbiota in Cancer Chemoresistance.},
journal = {MicrobiologyOpen},
volume = {15},
number = {4},
pages = {e70357},
doi = {10.1002/mbo3.70357},
pmid = {42418807},
issn = {2045-8827},
mesh = {Humans ; *Drug Resistance, Neoplasm ; *Neoplasms/drug therapy/microbiology ; *Gastrointestinal Microbiome ; *Antineoplastic Agents/therapeutic use/metabolism/pharmacology ; Probiotics ; Fecal Microbiota Transplantation ; Animals ; },
abstract = {Chemoresistance is one of the primary reasons that cancer chemotherapy fails to deliver successful treatment outcomes and contributes to poor overall survival rates for patients with cancer. New research has begun to shed light on the effects of the gut microbiome (GM). This new research will examine how certain microorganisms (referred to as "bad bacteria") can contribute to cancer treatment failure, as well as how others (such as Bifidobacterium, Akkermansia, and Lactobacillus) can enhance treatment success. This review will focus on the molecular mechanisms underlying these effects, including drug metabolism by microorganisms, modulation of the immune system by microorganisms, regulation of cellular apoptosis by microorganisms, and metabolic crosstalk between tumor tissue and the microbiome. Finally, we will look at new therapies under development that leverage knowledge of the microbiome to combat chemoresistance, including fecal microbiota transplantation, targeted probiotic and prebiotic supplementation, and dietary modifications. By studying the complex interactions among the host, the microbiome, and chemotherapeutic agents, we hope to demonstrate how microbiome-centered approaches can tailor and enhance an individual's cancer treatment while transforming the GM from a passive participant to an active target in cancer therapy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Drug Resistance, Neoplasm
*Neoplasms/drug therapy/microbiology
*Gastrointestinal Microbiome
*Antineoplastic Agents/therapeutic use/metabolism/pharmacology
Probiotics
Fecal Microbiota Transplantation
Animals
RevDate: 2026-07-08
Deciphering underground decarboxylase activity towards Nε-modified lysine derivatives in enterobacteria.
Food chemistry, 524:150234 pii:S0308-8146(26)02394-0 [Epub ahead of print].
Thermal food processing generates diverse compounds interacting with the gut microbiota. Despite their abundance, the microbial turnover of diet-borne Nε-modified lysine derivatives remains largely unexplored. We demonstrate that the enterobacterial ornithine decarboxylase SpeC degrades the prevalent advanced glycation end product Nε-carboxymethyllysine (CML) to carboxymethylcadaverine via an underground activity (∼4 molecules/enzyme/min). This promiscuity extends to additional Nε-modified lysine derivatives - namely formylated (FmL), monomethylated (MML) and dimethylated (DML) lysine - yielding previously unknown biogenic amines (mono- and dimethylcadaverine, formylcadaverine). Functionally, SpeC enables Escherichia coli to utilize CML as a sole nitrogen source. In specific strains, this metabolism reinforces pH-stress responses, supporting survival under mild acidic conditions typical for the colon. Furthermore, SpeC orthologs are widespread across human gut genomes, correlating with geography, diet, and disease. Together, these findings suggest a potential diet-microbiome communication axis, linking the intake of modified dietary chemicals to microbial physiology and hypothesized host impacts.
Additional Links: PMID-42418876
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PubMed:
Citation:
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@article {pmid42418876,
year = {2026},
author = {Aveta, EF and Vougioukas, P and Qi, F and Mehler, J and Behringer, KI and Gericke, N and Walczak, M and Vallejo-Janeta, AP and Blank, T and Hellwig, M and Lassak, J},
title = {Deciphering underground decarboxylase activity towards Nε-modified lysine derivatives in enterobacteria.},
journal = {Food chemistry},
volume = {524},
number = {},
pages = {150234},
doi = {10.1016/j.foodchem.2026.150234},
pmid = {42418876},
issn = {1873-7072},
abstract = {Thermal food processing generates diverse compounds interacting with the gut microbiota. Despite their abundance, the microbial turnover of diet-borne Nε-modified lysine derivatives remains largely unexplored. We demonstrate that the enterobacterial ornithine decarboxylase SpeC degrades the prevalent advanced glycation end product Nε-carboxymethyllysine (CML) to carboxymethylcadaverine via an underground activity (∼4 molecules/enzyme/min). This promiscuity extends to additional Nε-modified lysine derivatives - namely formylated (FmL), monomethylated (MML) and dimethylated (DML) lysine - yielding previously unknown biogenic amines (mono- and dimethylcadaverine, formylcadaverine). Functionally, SpeC enables Escherichia coli to utilize CML as a sole nitrogen source. In specific strains, this metabolism reinforces pH-stress responses, supporting survival under mild acidic conditions typical for the colon. Furthermore, SpeC orthologs are widespread across human gut genomes, correlating with geography, diet, and disease. Together, these findings suggest a potential diet-microbiome communication axis, linking the intake of modified dietary chemicals to microbial physiology and hypothesized host impacts.},
}
RevDate: 2026-07-08
The composite detoxification agent alleviates the toxicity induced by mycotoxins in Hy-Line Brown laying hens by regulating antioxidant capacity and gut bacterial communities.
Poultry science, 105(10):107347 pii:S0032-5791(26)00978-8 [Epub ahead of print].
This study evaluated the efficacy of a composite detoxification agent in mitigating the adverse effects of naturally mold-contaminated feed in laying hens. A total of 800 Hy-Line Brown hens (156 days old) were randomly allocated to five dietary treatments (8 replicates with 20 birds per replicate), following a 7-d adaptation and a 113-d experimental period. The basal diet served as the control (CON group). Experimental treatments were structured as follows: ZH group (5% of normal corn in the feed replaced with moldy corn); ZJ group (5% of normal corn replaced with moldy corn + 0.1 g/kg composite detoxification agent); DH group (5% of normal soybean meal replaced with moldy cottonseed meal); DJ group (5% of normal soybean meal replaced with moldy cottonseed meal + 0.1 g/kg composite detoxification agent). Compared with CON, hens fed the ZH diet exhibited decreased (P < 0.05) egg production, average daily feed intake, egg weight, egg mass, and albumen quality, deteriorated feed conversion ratio. Serum biochemistry in ZH hens revealed lower total protein and alkaline phosphatase levels but higher blood urea nitrogen. Additionally, hens fed ZH diet displayed oxidative stress, characterized by elevated malondialdehyde (MDA) and reduced activities of total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and nitric oxide (NO) (P < 0.05). Although less pronounced, similar alterations were observed in DH hens. Supplementation with the composite detoxifier restored laying performance and improved antioxidant status in both ZJ and DJ groups. Notably, the detoxifier enhanced gut microbiota diversity, enriched beneficial taxa including Lactobacillus and Limosilactobacillus, and correlated with alterations in the microbiota-host axis. These results indicate that the composite detoxifier alleviates mycotoxin-induced impairments and supports its application for managing feed mycotoxicosis in commercial layer production.
Additional Links: PMID-42419211
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PubMed:
Citation:
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@article {pmid42419211,
year = {2026},
author = {Ma, Y and Gao, Q and Lu, J and Liu, X},
title = {The composite detoxification agent alleviates the toxicity induced by mycotoxins in Hy-Line Brown laying hens by regulating antioxidant capacity and gut bacterial communities.},
journal = {Poultry science},
volume = {105},
number = {10},
pages = {107347},
doi = {10.1016/j.psj.2026.107347},
pmid = {42419211},
issn = {1525-3171},
abstract = {This study evaluated the efficacy of a composite detoxification agent in mitigating the adverse effects of naturally mold-contaminated feed in laying hens. A total of 800 Hy-Line Brown hens (156 days old) were randomly allocated to five dietary treatments (8 replicates with 20 birds per replicate), following a 7-d adaptation and a 113-d experimental period. The basal diet served as the control (CON group). Experimental treatments were structured as follows: ZH group (5% of normal corn in the feed replaced with moldy corn); ZJ group (5% of normal corn replaced with moldy corn + 0.1 g/kg composite detoxification agent); DH group (5% of normal soybean meal replaced with moldy cottonseed meal); DJ group (5% of normal soybean meal replaced with moldy cottonseed meal + 0.1 g/kg composite detoxification agent). Compared with CON, hens fed the ZH diet exhibited decreased (P < 0.05) egg production, average daily feed intake, egg weight, egg mass, and albumen quality, deteriorated feed conversion ratio. Serum biochemistry in ZH hens revealed lower total protein and alkaline phosphatase levels but higher blood urea nitrogen. Additionally, hens fed ZH diet displayed oxidative stress, characterized by elevated malondialdehyde (MDA) and reduced activities of total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and nitric oxide (NO) (P < 0.05). Although less pronounced, similar alterations were observed in DH hens. Supplementation with the composite detoxifier restored laying performance and improved antioxidant status in both ZJ and DJ groups. Notably, the detoxifier enhanced gut microbiota diversity, enriched beneficial taxa including Lactobacillus and Limosilactobacillus, and correlated with alterations in the microbiota-host axis. These results indicate that the composite detoxifier alleviates mycotoxin-induced impairments and supports its application for managing feed mycotoxicosis in commercial layer production.},
}
RevDate: 2026-07-08
Biodegradable microplastics disrupt root exudate driven plant-microbe interactions, compromising plant growth and rhizosphere microenvironment health.
Journal of hazardous materials, 514:142930 pii:S0304-3894(26)01910-2 [Epub ahead of print].
Microplastics (MPs) pollution already posed a serious threat to human health. Biodegradable (bio) plastics serve as alternatives to traditional plastics. However, the ecological impact of bio-MPs has not been adequately assessed. This study evaluates the effects of two types of bio-MPs (poly (butylene adipate-co-terephthalate) (PBAT) and polylactic acid (PLA)) on plant growth and the rhizosphere soil microenvironment. Exposure to bio-MPs significantly decreased tomato growth, soil enzyme activities, and rhizosphere microbial diversity. In addition, bio-MPs significantly reduced the abundance of beneficial microorganisms (growth-promoting, nutrient cycling, stress resistance) in the rhizosphere soil. The secretion levels of several root exudates decreased significantly, including citric acid, quinic acid, indole, p‑coumaric acid, and flavone. This decrease led to alterations in multiple metabolic pathways: the TCA cycle, the biosynthesis of phenylalanine, tyrosine, and tryptophan, and the phenylpropanoid biosynthesis pathway. Meanwhile, these specific metabolites showed a significant positive correlation with beneficial rhizosphere microorganisms. Compared with traditional MPs, these findings suggests that the presence of bio‑MPs may interfere with normal plant-microbe interactions, which is further associated with an imbalance in the rhizosphere ecological microenvironment and may ultimately contribute to impaired plant growth. In the meantime, the beneficial effects of root exudates on plant resistance against bio‑MP toxicity have also received preliminary confirmation. This finding provides valuable evidence for evaluating the impact of bio-plastics on plant rhizosphere soil health.
Additional Links: PMID-42419242
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PubMed:
Citation:
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@article {pmid42419242,
year = {2026},
author = {Liu, H and Yan, Y and Guo, Z and Gao, Y and An, Y and Zhou, J and Li, X and Wang, S and Feng, G and Gao, Q and Gou, Z},
title = {Biodegradable microplastics disrupt root exudate driven plant-microbe interactions, compromising plant growth and rhizosphere microenvironment health.},
journal = {Journal of hazardous materials},
volume = {514},
number = {},
pages = {142930},
doi = {10.1016/j.jhazmat.2026.142930},
pmid = {42419242},
issn = {1873-3336},
abstract = {Microplastics (MPs) pollution already posed a serious threat to human health. Biodegradable (bio) plastics serve as alternatives to traditional plastics. However, the ecological impact of bio-MPs has not been adequately assessed. This study evaluates the effects of two types of bio-MPs (poly (butylene adipate-co-terephthalate) (PBAT) and polylactic acid (PLA)) on plant growth and the rhizosphere soil microenvironment. Exposure to bio-MPs significantly decreased tomato growth, soil enzyme activities, and rhizosphere microbial diversity. In addition, bio-MPs significantly reduced the abundance of beneficial microorganisms (growth-promoting, nutrient cycling, stress resistance) in the rhizosphere soil. The secretion levels of several root exudates decreased significantly, including citric acid, quinic acid, indole, p‑coumaric acid, and flavone. This decrease led to alterations in multiple metabolic pathways: the TCA cycle, the biosynthesis of phenylalanine, tyrosine, and tryptophan, and the phenylpropanoid biosynthesis pathway. Meanwhile, these specific metabolites showed a significant positive correlation with beneficial rhizosphere microorganisms. Compared with traditional MPs, these findings suggests that the presence of bio‑MPs may interfere with normal plant-microbe interactions, which is further associated with an imbalance in the rhizosphere ecological microenvironment and may ultimately contribute to impaired plant growth. In the meantime, the beneficial effects of root exudates on plant resistance against bio‑MP toxicity have also received preliminary confirmation. This finding provides valuable evidence for evaluating the impact of bio-plastics on plant rhizosphere soil health.},
}
RevDate: 2026-07-08
Clinically prevalent transposons contribute to erm gene dissemination in the field soil under pseudo-persistent erythromycin contamination.
Journal of hazardous materials, 514:142927 pii:S0304-3894(26)01907-2 [Epub ahead of print].
Clinically relevant antibiotic resistance genes (ARGs) or their ancestral genes are widespread in natural soil microbiome at ultralow abundance. Whether and how long-term antibiotic pressure in soil accelerate dissemination of these ARGs remain unclear. Here, annual cycle of erythromycin exposure at levels around 5-20 μg∙kg[-1] was conducted in previously undisturbed field soil for consecutive five years, to simulate the pseudo-persistent characteristic of antibiotic contamination in soil environment. The primary clinically relevant macrolide resistance genes, rRNA methyltransferase genes (erm genes), were initially rare but gradually enriched, exhibiting a 37.8-fold increase after five years, which was greatly higher than macrolide efflux pump genes and inactivation genes (less than 2.3-fold). Among diverse mobile genetic elements, transposase gene tnpA exhibited potential association with the horizontal transfer of erm genes during long-term erythromycin exposure. From genetic and statistical evidence, enriched erm genes were presumed to locate on Bacilli with mobile transposable elements Tn554 and Tn551, which were clinically prevalent gene clusters in pathogens-Enterococcus and Staphylococcus. Thus, there may be a historical contribution of long-term erythromycin contamination to erm-carrying clinical transposable elements in soil microbiome. Our findings also demonstrated soil erythromycin exposure at levels much lower than laboratory-determined minimal selective concentrations (MSCs) still exhibits long-term effects on erm genes. Taking pseudo-persistent characteristic of antibiotic contamination, we further proposed long-term in-situ assessment with endpoint of clinically relevant ARGs to obtain a real-world MSC in the future studies.
Additional Links: PMID-42419245
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PubMed:
Citation:
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@article {pmid42419245,
year = {2026},
author = {Han, Z and Zhang, Y and Luan, X and Feng, H and Wang, Y and Deng, Y and Hu, C and Yang, M},
title = {Clinically prevalent transposons contribute to erm gene dissemination in the field soil under pseudo-persistent erythromycin contamination.},
journal = {Journal of hazardous materials},
volume = {514},
number = {},
pages = {142927},
doi = {10.1016/j.jhazmat.2026.142927},
pmid = {42419245},
issn = {1873-3336},
abstract = {Clinically relevant antibiotic resistance genes (ARGs) or their ancestral genes are widespread in natural soil microbiome at ultralow abundance. Whether and how long-term antibiotic pressure in soil accelerate dissemination of these ARGs remain unclear. Here, annual cycle of erythromycin exposure at levels around 5-20 μg∙kg[-1] was conducted in previously undisturbed field soil for consecutive five years, to simulate the pseudo-persistent characteristic of antibiotic contamination in soil environment. The primary clinically relevant macrolide resistance genes, rRNA methyltransferase genes (erm genes), were initially rare but gradually enriched, exhibiting a 37.8-fold increase after five years, which was greatly higher than macrolide efflux pump genes and inactivation genes (less than 2.3-fold). Among diverse mobile genetic elements, transposase gene tnpA exhibited potential association with the horizontal transfer of erm genes during long-term erythromycin exposure. From genetic and statistical evidence, enriched erm genes were presumed to locate on Bacilli with mobile transposable elements Tn554 and Tn551, which were clinically prevalent gene clusters in pathogens-Enterococcus and Staphylococcus. Thus, there may be a historical contribution of long-term erythromycin contamination to erm-carrying clinical transposable elements in soil microbiome. Our findings also demonstrated soil erythromycin exposure at levels much lower than laboratory-determined minimal selective concentrations (MSCs) still exhibits long-term effects on erm genes. Taking pseudo-persistent characteristic of antibiotic contamination, we further proposed long-term in-situ assessment with endpoint of clinically relevant ARGs to obtain a real-world MSC in the future studies.},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Decoding the microbiome: Insights into FMT for depression.
Cell host & microbe, 34(7):1154-1156.
While fecal microbiota transplantation (FMT) emerges as a promising microbiome-targeted treatment approach, its application in major depressive disorder (MDD) remains investigational. In this issue of Cell Host & Microbe, Wang et al. provide insights into the potential underpinnings of FMT in MDD and offer a step toward decoding the molecular pathways accompanying clinical response.
Additional Links: PMID-42419261
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PubMed:
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@article {pmid42419261,
year = {2026},
author = {Valles-Colomer, M and Foster, JA},
title = {Decoding the microbiome: Insights into FMT for depression.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1154-1156},
doi = {10.1016/j.chom.2026.06.004},
pmid = {42419261},
issn = {1934-6069},
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Major Depressive Disorder/therapy/microbiology ; *Microbiota ; Animals ; },
abstract = {While fecal microbiota transplantation (FMT) emerges as a promising microbiome-targeted treatment approach, its application in major depressive disorder (MDD) remains investigational. In this issue of Cell Host & Microbe, Wang et al. provide insights into the potential underpinnings of FMT in MDD and offer a step toward decoding the molecular pathways accompanying clinical response.},
}
MeSH Terms:
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*Fecal Microbiota Transplantation
Humans
*Major Depressive Disorder/therapy/microbiology
*Microbiota
Animals
RevDate: 2026-07-08
CmpDate: 2026-07-08
Toward precision microbiome therapeutics: From black box to blueprint.
Cell host & microbe, 34(7):1157-1161.
The gut microbiome influences human health, yet microbiome-mediated therapies have lagged as metagenomics identifies gut-colonizing microbes without clarifying functional networks. Prior microbiome "reset" approaches improved clinical outcomes despite limited mechanistic understanding. We argue a critical field inflection point: in situ genome editing of native bacteria enables mechanism-driven, programmable, species-specific therapeutics.
Additional Links: PMID-42419262
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PubMed:
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@article {pmid42419262,
year = {2026},
author = {Gelsinger, DR and Wang, HH},
title = {Toward precision microbiome therapeutics: From black box to blueprint.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1157-1161},
doi = {10.1016/j.chom.2026.06.014},
pmid = {42419262},
issn = {1934-6069},
mesh = {Humans ; Metagenomics ; *Gastrointestinal Microbiome/physiology/genetics ; Bacteria/genetics ; Animals ; Gene Editing ; *Precision Medicine/methods ; Microbiota ; },
abstract = {The gut microbiome influences human health, yet microbiome-mediated therapies have lagged as metagenomics identifies gut-colonizing microbes without clarifying functional networks. Prior microbiome "reset" approaches improved clinical outcomes despite limited mechanistic understanding. We argue a critical field inflection point: in situ genome editing of native bacteria enables mechanism-driven, programmable, species-specific therapeutics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Metagenomics
*Gastrointestinal Microbiome/physiology/genetics
Bacteria/genetics
Animals
Gene Editing
*Precision Medicine/methods
Microbiota
RevDate: 2026-07-08
CmpDate: 2026-07-08
Understanding ripple effects in the gut microbiome.
Cell host & microbe, 34(7):1162-1166.
Targeted perturbations of individual microbial taxa can propagate through complex ecological networks and generate ripple effects that reshape gut microbiota structure and function. Here, we discuss the need for predictive ecological and data-driven frameworks that enable precise and controllable microbiome engineering to minimize or leverage ripple effects.
Additional Links: PMID-42419263
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PubMed:
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@article {pmid42419263,
year = {2026},
author = {Zuo, W and Liu, YY and Shen, J and Dai, L},
title = {Understanding ripple effects in the gut microbiome.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1162-1166},
doi = {10.1016/j.chom.2026.06.002},
pmid = {42419263},
issn = {1934-6069},
mesh = {*Gastrointestinal Microbiome/physiology ; Humans ; Animals ; },
abstract = {Targeted perturbations of individual microbial taxa can propagate through complex ecological networks and generate ripple effects that reshape gut microbiota structure and function. Here, we discuss the need for predictive ecological and data-driven frameworks that enable precise and controllable microbiome engineering to minimize or leverage ripple effects.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Gastrointestinal Microbiome/physiology
Humans
Animals
RevDate: 2026-07-08
CmpDate: 2026-07-08
Operationalizing microbiome ecology in cancer care.
Cell host & microbe, 34(7):1167-1169.
Cancer treatment can disrupt the microbiome, worsening outcomes for cancer patients. Ecology frames these changes as transitions between measurable states, enabling the prediction of microbiome trajectories to support clinical decision making. Longitudinal monitoring and microbial restoration can translate microbiome ecology into strategies that improve cancer care.
Additional Links: PMID-42419264
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PubMed:
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@article {pmid42419264,
year = {2026},
author = {Xavier, JB},
title = {Operationalizing microbiome ecology in cancer care.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1167-1169},
doi = {10.1016/j.chom.2026.05.022},
pmid = {42419264},
issn = {1934-6069},
mesh = {Humans ; *Neoplasms/therapy/microbiology ; *Microbiota/drug effects ; *Dysbiosis/therapy ; Ecology ; },
abstract = {Cancer treatment can disrupt the microbiome, worsening outcomes for cancer patients. Ecology frames these changes as transitions between measurable states, enabling the prediction of microbiome trajectories to support clinical decision making. Longitudinal monitoring and microbial restoration can translate microbiome ecology into strategies that improve cancer care.},
}
MeSH Terms:
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Humans
*Neoplasms/therapy/microbiology
*Microbiota/drug effects
*Dysbiosis/therapy
Ecology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Improving the vaccine efficacy gap with microbial-derived therapies.
Cell host & microbe, 34(7):1170-1174.
Oral polio and rotavirus vaccines underperform in low-resource settings, a failing linked to distinct microbiome compositions. This Forum examines why empiric probiotics and broad taxonomic approaches are largely ineffective in boosting mucosal vaccine immunity and proposes mechanism-driven microbial therapies that modulate epithelial barriers, utilize immune-modulating metabolites, or mitigate viral interference.
Additional Links: PMID-42419265
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PubMed:
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@article {pmid42419265,
year = {2026},
author = {Kim, J and de Bree, G and Harris, V},
title = {Improving the vaccine efficacy gap with microbial-derived therapies.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1170-1174},
doi = {10.1016/j.chom.2026.06.009},
pmid = {42419265},
issn = {1934-6069},
mesh = {Humans ; *Vaccine Efficacy ; *Rotavirus Vaccines/immunology/administration & dosage ; *Probiotics/administration & dosage/therapeutic use ; Microbiota/immunology ; Immunity, Mucosal ; Animals ; Rotavirus Infections/prevention & control/immunology ; },
abstract = {Oral polio and rotavirus vaccines underperform in low-resource settings, a failing linked to distinct microbiome compositions. This Forum examines why empiric probiotics and broad taxonomic approaches are largely ineffective in boosting mucosal vaccine immunity and proposes mechanism-driven microbial therapies that modulate epithelial barriers, utilize immune-modulating metabolites, or mitigate viral interference.},
}
MeSH Terms:
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Humans
*Vaccine Efficacy
*Rotavirus Vaccines/immunology/administration & dosage
*Probiotics/administration & dosage/therapeutic use
Microbiota/immunology
Immunity, Mucosal
Animals
Rotavirus Infections/prevention & control/immunology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Engineering plant-associated microbiome for agriculture.
Cell host & microbe, 34(7):1175-1180.
Engineered plant-associated microbiomes provide a transformative approach for sustainable agriculture. In this Forum, we explore five strategies encompassing synthetic community design, native bacterial strain engineering, host-microbe co-adaptation, AI-driven design, and microbe-derived compounds. We assess the causes of repeated laboratory-to-field translation failures and argue for ecology-centric design principles.
Additional Links: PMID-42419266
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PubMed:
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@article {pmid42419266,
year = {2026},
author = {Zhang, J and Zhai, Q and Bai, Y},
title = {Engineering plant-associated microbiome for agriculture.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1175-1180},
doi = {10.1016/j.chom.2026.05.027},
pmid = {42419266},
issn = {1934-6069},
mesh = {*Microbiota ; *Agriculture/methods ; *Plants/microbiology ; Host Microbial Interactions ; Bacteria/genetics ; },
abstract = {Engineered plant-associated microbiomes provide a transformative approach for sustainable agriculture. In this Forum, we explore five strategies encompassing synthetic community design, native bacterial strain engineering, host-microbe co-adaptation, AI-driven design, and microbe-derived compounds. We assess the causes of repeated laboratory-to-field translation failures and argue for ecology-centric design principles.},
}
MeSH Terms:
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*Microbiota
*Agriculture/methods
*Plants/microbiology
Host Microbial Interactions
Bacteria/genetics
RevDate: 2026-07-08
CmpDate: 2026-07-08
Advances and challenges in microbiome transplantation.
Cell host & microbe, 34(7):1202-1219.
Over the past two decades, the microbiome has emerged as a central modifier of host health, whose manipulation may prevent or treat disease. Fecal microbiome transplantation (FMT) transfers stool from healthy donors to recipients to restore microbial structure and function. It is universally accepted as therapy for recurrent Clostridioides difficile infection (rCDI) and is studied across metabolic, neurological, oncological, and autoimmune disorders. However, challenges remain, including donor selection, possible transmission of infectious or non-communicable risks, and limited understanding of mechanisms driving benefits. This review summarizes FMT designs, mechanisms, indications, and obstacles. It discusses emerging strategies such as the use of microbial consortia and extra-intestinal microbiome transplantation and suggests that a better understanding of FMT functions, limitations, and off-target effects may enable safer, more generalizable modulation of microbiome-regulated diseases. Such a mechanistic understanding may manifest as refined donor screening, standardized protocols, tracked outcomes, and identified microbes and metabolites inducing durable clinical benefits.
Additional Links: PMID-42419268
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PubMed:
Citation:
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@article {pmid42419268,
year = {2026},
author = {Sen, P and Kaulmann, D and Youngster, I and Abdeen, SK and Elinav, E},
title = {Advances and challenges in microbiome transplantation.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1202-1219},
doi = {10.1016/j.chom.2026.06.006},
pmid = {42419268},
issn = {1934-6069},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects/trends ; *Clostridium Infections/therapy/microbiology ; *Microbiota ; Animals ; Clostridioides difficile ; Gastrointestinal Microbiome ; },
abstract = {Over the past two decades, the microbiome has emerged as a central modifier of host health, whose manipulation may prevent or treat disease. Fecal microbiome transplantation (FMT) transfers stool from healthy donors to recipients to restore microbial structure and function. It is universally accepted as therapy for recurrent Clostridioides difficile infection (rCDI) and is studied across metabolic, neurological, oncological, and autoimmune disorders. However, challenges remain, including donor selection, possible transmission of infectious or non-communicable risks, and limited understanding of mechanisms driving benefits. This review summarizes FMT designs, mechanisms, indications, and obstacles. It discusses emerging strategies such as the use of microbial consortia and extra-intestinal microbiome transplantation and suggests that a better understanding of FMT functions, limitations, and off-target effects may enable safer, more generalizable modulation of microbiome-regulated diseases. Such a mechanistic understanding may manifest as refined donor screening, standardized protocols, tracked outcomes, and identified microbes and metabolites inducing durable clinical benefits.},
}
MeSH Terms:
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Humans
*Fecal Microbiota Transplantation/methods/adverse effects/trends
*Clostridium Infections/therapy/microbiology
*Microbiota
Animals
Clostridioides difficile
Gastrointestinal Microbiome
RevDate: 2026-07-08
CmpDate: 2026-07-08
Ecological and dietary strategies to constrain Clostridioides difficile.
Cell host & microbe, 34(7):1220-1240.
Clostridioides difficile exemplifies a pathogen that leverages its metabolic plasticity to exploit nutrients that become available during community disruption, including host and microbiota-derived metabolites and substrates enriched in modern diets. These ecological dynamics underpin the high and growing burden of C. difficile infection (CDI), including recurrent disease and the rising prevalence of community-associated CDI. Fecal microbiota transplantation and standardized stool-derived products consistently re-establish colonization resistance through convergent functions that include secondary bile acid restoration, nutrient niche exclusion, and suppression of opportunistic pathogens. These principles have provided a valuable roadmap for rational consortia design. In this review, we synthesize current ecological mechanisms governing C. difficile colonization, persistence, and recurrence, highlight missing dimensions in diet intervention studies and mucosal colonization by C. difficile, and propose an ecology-informed, artificial intelligence-enabled precision framework that integrates host susceptibility, exposures, diet, community function, and pathogen features to guide personalized prevention and treatment.
Additional Links: PMID-42419269
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PubMed:
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@article {pmid42419269,
year = {2026},
author = {Engevik, MA and Hecht, AL and Allegretti, JR and Kashyap, PC},
title = {Ecological and dietary strategies to constrain Clostridioides difficile.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1220-1240},
doi = {10.1016/j.chom.2026.05.023},
pmid = {42419269},
issn = {1934-6069},
mesh = {Humans ; *Clostridioides difficile/physiology/pathogenicity/growth & development ; *Clostridium Infections/microbiology/prevention & control ; Fecal Microbiota Transplantation ; *Diet ; Animals ; Gastrointestinal Microbiome ; Microbiota ; Feces/microbiology ; Biofilms/growth & development ; },
abstract = {Clostridioides difficile exemplifies a pathogen that leverages its metabolic plasticity to exploit nutrients that become available during community disruption, including host and microbiota-derived metabolites and substrates enriched in modern diets. These ecological dynamics underpin the high and growing burden of C. difficile infection (CDI), including recurrent disease and the rising prevalence of community-associated CDI. Fecal microbiota transplantation and standardized stool-derived products consistently re-establish colonization resistance through convergent functions that include secondary bile acid restoration, nutrient niche exclusion, and suppression of opportunistic pathogens. These principles have provided a valuable roadmap for rational consortia design. In this review, we synthesize current ecological mechanisms governing C. difficile colonization, persistence, and recurrence, highlight missing dimensions in diet intervention studies and mucosal colonization by C. difficile, and propose an ecology-informed, artificial intelligence-enabled precision framework that integrates host susceptibility, exposures, diet, community function, and pathogen features to guide personalized prevention and treatment.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Clostridioides difficile/physiology/pathogenicity/growth & development
*Clostridium Infections/microbiology/prevention & control
Fecal Microbiota Transplantation
*Diet
Animals
Gastrointestinal Microbiome
Microbiota
Feces/microbiology
Biofilms/growth & development
RevDate: 2026-07-08
CmpDate: 2026-07-08
Engineering commensal microbes for host health.
Cell host & microbe, 34(7):1241-1261.
Engineered live biotherapeutic products (eLBPs) represent an emerging class of programmable microbial therapies capable of sensing and responding to host physiology. Advances in microbiome science and synthetic biology have driven the development of engineered bacteria that deliver therapeutic molecules, modulate host metabolism, or detect disease-associated signals. In this review, we summarize recent progress in the development of eLBPs across diverse disease indications, including inflammatory diseases, metabolic disorders, cancer, and infectious diseases. We highlight key factors that drive successful eLBP design, including chassis selection, methods for DNA delivery, approaches for tuning therapeutic expression, and genetic systems for biocontainment. Although early clinical studies demonstrate promising safety profiles, challenges remain in achieving predictable colonization, durable therapeutic activity, and robust biocontainment in vivo. By synthesizing advances across these areas, we propose a framework for the rational design of next-generation eLBPs that can more reliably translate from experimental systems to clinical application.
Additional Links: PMID-42419270
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PubMed:
Citation:
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@article {pmid42419270,
year = {2026},
author = {Brown, EA and Brevi, A and Zong, DM and Zarrinpar, A},
title = {Engineering commensal microbes for host health.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1241-1261},
doi = {10.1016/j.chom.2026.05.025},
pmid = {42419270},
issn = {1934-6069},
mesh = {Humans ; Animals ; Synthetic Biology ; Bacteria/genetics/metabolism ; *Genetic Engineering ; *Microbiota ; *Biological Therapy/methods ; *Microorganisms, Genetically-Modified/genetics ; Neoplasms/therapy ; Metabolic Diseases/therapy ; },
abstract = {Engineered live biotherapeutic products (eLBPs) represent an emerging class of programmable microbial therapies capable of sensing and responding to host physiology. Advances in microbiome science and synthetic biology have driven the development of engineered bacteria that deliver therapeutic molecules, modulate host metabolism, or detect disease-associated signals. In this review, we summarize recent progress in the development of eLBPs across diverse disease indications, including inflammatory diseases, metabolic disorders, cancer, and infectious diseases. We highlight key factors that drive successful eLBP design, including chassis selection, methods for DNA delivery, approaches for tuning therapeutic expression, and genetic systems for biocontainment. Although early clinical studies demonstrate promising safety profiles, challenges remain in achieving predictable colonization, durable therapeutic activity, and robust biocontainment in vivo. By synthesizing advances across these areas, we propose a framework for the rational design of next-generation eLBPs that can more reliably translate from experimental systems to clinical application.},
}
MeSH Terms:
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Humans
Animals
Synthetic Biology
Bacteria/genetics/metabolism
*Genetic Engineering
*Microbiota
*Biological Therapy/methods
*Microorganisms, Genetically-Modified/genetics
Neoplasms/therapy
Metabolic Diseases/therapy
RevDate: 2026-07-08
CmpDate: 2026-07-08
Feeding microbial allies to fight cancer.
Cell host & microbe, 34(7):1386-1388.
In a recent Immunity paper, Lobel and colleagues integrate cross-cohort human microbiome meta-analyses with mechanistic studies in mice to uncover a dietary sulfur amino acid-microbiota-immune axis that enhances anti-tumor immunity. Sulfur amino acids expand the mucus-associated bacterium Mucispirillum schaedleri and trigger an NKT-cDC1 immune circuit.
Additional Links: PMID-42419275
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PubMed:
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@article {pmid42419275,
year = {2026},
author = {Zhang, L and Tian, X and Wu, M},
title = {Feeding microbial allies to fight cancer.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1386-1388},
doi = {10.1016/j.chom.2026.06.008},
pmid = {42419275},
issn = {1934-6069},
mesh = {Humans ; Animals ; *Neoplasms/immunology/therapy/microbiology ; Mice ; *Microbiota/immunology ; },
abstract = {In a recent Immunity paper, Lobel and colleagues integrate cross-cohort human microbiome meta-analyses with mechanistic studies in mice to uncover a dietary sulfur amino acid-microbiota-immune axis that enhances anti-tumor immunity. Sulfur amino acids expand the mucus-associated bacterium Mucispirillum schaedleri and trigger an NKT-cDC1 immune circuit.},
}
MeSH Terms:
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Humans
Animals
*Neoplasms/immunology/therapy/microbiology
Mice
*Microbiota/immunology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Following Ariadne's thread through microbiome-based biomarker discovery in CRC.
Cell host & microbe, 34(7):1395-1397.
Colorectal cancer (CRC) carries a microbial fingerprint, but how does it generalize across age, geography, and sequencing platforms? In this issue of Cell Host & Microbe, Pekel and colleagues stitch together large-scale stool and tumor data to reveal a universal signal while exposing where stool-based biomarkers fall short.
Additional Links: PMID-42419278
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PubMed:
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@article {pmid42419278,
year = {2026},
author = {Kang, JX and Wong, SH},
title = {Following Ariadne's thread through microbiome-based biomarker discovery in CRC.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1395-1397},
doi = {10.1016/j.chom.2026.06.003},
pmid = {42419278},
issn = {1934-6069},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/diagnosis ; Feces/microbiology ; *Microbiota ; *Biomarkers, Tumor/analysis ; *Gastrointestinal Microbiome ; Biomarkers/analysis ; },
abstract = {Colorectal cancer (CRC) carries a microbial fingerprint, but how does it generalize across age, geography, and sequencing platforms? In this issue of Cell Host & Microbe, Pekel and colleagues stitch together large-scale stool and tumor data to reveal a universal signal while exposing where stool-based biomarkers fall short.},
}
MeSH Terms:
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Humans
*Colorectal Neoplasms/microbiology/diagnosis
Feces/microbiology
*Microbiota
*Biomarkers, Tumor/analysis
*Gastrointestinal Microbiome
Biomarkers/analysis
RevDate: 2026-07-08
Cyanobacteria-based seed coatings differentially modulate rhizosphere bacterial community and predicted functional profiles in direct-seeded and transplanted rice.
Gene pii:S0378-1119(26)00319-7 [Epub ahead of print].
Direct-seeded (DSR) and transplanted (TPR) rice impose contrasting ecological filters on rhizosphere bacterial communities, yet the influence of cyanobacteria in these systems remain poorly resolved. 16 s rRNA amplicon sequencing was used to explore how a cyanobacterial consortium (BF1-4) and a multispecies biofilm (An-Tr-PW5), applied as seed coatings in DSR and TPR, reshape the taxonomic composition of rhizosphere microbiome, to facilitate correlation with soil metabolic and crop-associated traits. Cultivation mode was predicted as the dominant driver of community structure, accounting for 69.5 and 62.4% of phylum-level of genus-level variance respectively. Coatings superimposed distinct secondary shifts, associated with enriched copiotrophic phyla (Actinomycetota, Pseudomonadota, Bacteroidota, Cyanobacteriota) and diminished oligotrophic groups (Acidobacteriota, Chloroflexota). Seed coatings were associated with increased abundance of Sphingomonas, Lysobacter, Flavisolibacter and Gemmatiomonas linked to strong positive correlations (|ρ| ≥ 0.4, p_adj ≤ 0.05) with soil organic carbon, available N, nitrogen-fixation (ARA), urease and dehydrogenase activities, biomass, grain micronutrient content and harvest indices. Network analysis predicted these genera as central hubs positively associated with nutrient-cycling and plant performance, whereas control-associated taxa (Gaiella, Nitrospira, Microvirga) were negatively associated. Predictive functional analysis suggested system-dependent responses: in DSR, coatings were associated with enrichment of KEGG orthologs for carbohydrate metabolism, nitrogen assimilation, lipid activation and energy-generation pathway. TPR was affiliated with modulation of signal-transduction and chemotaxis-related functions. Both cyanobacteria-based interventions were associated with rewiring of dominance indices (higher Simpson, reduced Fisher's α), favouring enrichment of putatively competitive taxa. Overall, the cyanobacteria-based seed coatings were associated with shifts towards beneficial bacterial communities involved in effective nutrient-cycling.
Additional Links: PMID-42419435
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PubMed:
Citation:
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@article {pmid42419435,
year = {2026},
author = {Tayade, A and Prasanna, R and Kumari, S and Varsha, D and Shivay, YS},
title = {Cyanobacteria-based seed coatings differentially modulate rhizosphere bacterial community and predicted functional profiles in direct-seeded and transplanted rice.},
journal = {Gene},
volume = {},
number = {},
pages = {150309},
doi = {10.1016/j.gene.2026.150309},
pmid = {42419435},
issn = {1879-0038},
abstract = {Direct-seeded (DSR) and transplanted (TPR) rice impose contrasting ecological filters on rhizosphere bacterial communities, yet the influence of cyanobacteria in these systems remain poorly resolved. 16 s rRNA amplicon sequencing was used to explore how a cyanobacterial consortium (BF1-4) and a multispecies biofilm (An-Tr-PW5), applied as seed coatings in DSR and TPR, reshape the taxonomic composition of rhizosphere microbiome, to facilitate correlation with soil metabolic and crop-associated traits. Cultivation mode was predicted as the dominant driver of community structure, accounting for 69.5 and 62.4% of phylum-level of genus-level variance respectively. Coatings superimposed distinct secondary shifts, associated with enriched copiotrophic phyla (Actinomycetota, Pseudomonadota, Bacteroidota, Cyanobacteriota) and diminished oligotrophic groups (Acidobacteriota, Chloroflexota). Seed coatings were associated with increased abundance of Sphingomonas, Lysobacter, Flavisolibacter and Gemmatiomonas linked to strong positive correlations (|ρ| ≥ 0.4, p_adj ≤ 0.05) with soil organic carbon, available N, nitrogen-fixation (ARA), urease and dehydrogenase activities, biomass, grain micronutrient content and harvest indices. Network analysis predicted these genera as central hubs positively associated with nutrient-cycling and plant performance, whereas control-associated taxa (Gaiella, Nitrospira, Microvirga) were negatively associated. Predictive functional analysis suggested system-dependent responses: in DSR, coatings were associated with enrichment of KEGG orthologs for carbohydrate metabolism, nitrogen assimilation, lipid activation and energy-generation pathway. TPR was affiliated with modulation of signal-transduction and chemotaxis-related functions. Both cyanobacteria-based interventions were associated with rewiring of dominance indices (higher Simpson, reduced Fisher's α), favouring enrichment of putatively competitive taxa. Overall, the cyanobacteria-based seed coatings were associated with shifts towards beneficial bacterial communities involved in effective nutrient-cycling.},
}
RevDate: 2026-07-08
Editorial: Immunotherapy in the view of microbiome.
Additional Links: PMID-42419461
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@article {pmid42419461,
year = {2026},
author = {Bu, LL and Hu, Q},
title = {Editorial: Immunotherapy in the view of microbiome.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2026.07.001},
pmid = {42419461},
issn = {1096-3650},
}
RevDate: 2026-07-08
Oral Sodium Butyrate Supplementation, Gut Microbiome Modulation, and Reduced Acute Graft-versus-Host Disease After Allogeneic Hematopoietic Stem Cell Transplantation.
Transplantation and cellular therapy pii:S2666-6367(26)00536-1 [Epub ahead of print].
BACKGROUND: Acute graft-versus-host disease (aGVHD) remains a major cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Disruption of the gut microbiome during transplantation has been implicated in the pathogenesis of aGVHD, yet clinically applicable strategies to modulate the microbiome in immunocompromised patients remain limited.
OBJECTIVES: To evaluate the association between oral sodium butyrate supplementation and the incidence and severity of aGVHD, and to investigate its impact on gut microbiome recovery following allo-HSCT.
STUDY DESIGN: In this prospective, single-center study, 39 consecutive patients undergoing allo-HSCT received oral sodium butyrate (1,200 mg/day) from neutrophil engraftment to day +100. Outcomes were compared with 18 historical controls treated at the same institution without butyrate supplementation. The primary endpoint was the cumulative incidence of grade II-IV aGVHD by day +100. Secondary endpoints included lower gastrointestinal aGVHD and microbiome characteristics assessed using shotgun metagenomic sequencing. Competing risk analyses were performed to account for death as a competing event.
RESULTS: Butyrate supplementation was associated with a lower incidence of grade II-IV aGVHD (30% vs 53%, p=0.028) and grade III-IV aGVHD (5% vs 34%, p=0.002). Lower gastrointestinal aGVHD occurred in 5% of the butyrate group compared with 40% of historical controls (p<0.001). In multivariable competing risk analysis, butyrate supplementation remained independently associated with reduced grade II-IV aGVHD (adjusted HR 0.31, 95% CI 0.11-0.89; p=0.029) and lower gastrointestinal aGVHD (adjusted HR 0.07, 95% CI 0.02-0.30; p<0.001). Microbiome analysis demonstrated improved recovery of gut microbial diversity at day +100 in the butyrate group, with enrichment of commensal taxa and restoration of fecal butyrate levels.
CONCLUSIONS: Oral sodium butyrate supplementation was associated with reduced incidence and severity of aGVHD, particularly involving the gastrointestinal tract, along with improved microbiome recovery. These findings suggest a potential role for postbiotic-based microbiome modulation in GVHD prevention and warrant validation in randomized controlled trials.
Additional Links: PMID-42419591
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PubMed:
Citation:
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@article {pmid42419591,
year = {2026},
author = {Kim, S and Seo, H and Jo, S and Rahim, MA and Hossain, MS and Shuvo, MSH and Jeong, SY and Lee, MY and Kim, KH and Lee, N and Won, JH and Song, HY and Yoon, SY},
title = {Oral Sodium Butyrate Supplementation, Gut Microbiome Modulation, and Reduced Acute Graft-versus-Host Disease After Allogeneic Hematopoietic Stem Cell Transplantation.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.07.006},
pmid = {42419591},
issn = {2666-6367},
abstract = {BACKGROUND: Acute graft-versus-host disease (aGVHD) remains a major cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Disruption of the gut microbiome during transplantation has been implicated in the pathogenesis of aGVHD, yet clinically applicable strategies to modulate the microbiome in immunocompromised patients remain limited.
OBJECTIVES: To evaluate the association between oral sodium butyrate supplementation and the incidence and severity of aGVHD, and to investigate its impact on gut microbiome recovery following allo-HSCT.
STUDY DESIGN: In this prospective, single-center study, 39 consecutive patients undergoing allo-HSCT received oral sodium butyrate (1,200 mg/day) from neutrophil engraftment to day +100. Outcomes were compared with 18 historical controls treated at the same institution without butyrate supplementation. The primary endpoint was the cumulative incidence of grade II-IV aGVHD by day +100. Secondary endpoints included lower gastrointestinal aGVHD and microbiome characteristics assessed using shotgun metagenomic sequencing. Competing risk analyses were performed to account for death as a competing event.
RESULTS: Butyrate supplementation was associated with a lower incidence of grade II-IV aGVHD (30% vs 53%, p=0.028) and grade III-IV aGVHD (5% vs 34%, p=0.002). Lower gastrointestinal aGVHD occurred in 5% of the butyrate group compared with 40% of historical controls (p<0.001). In multivariable competing risk analysis, butyrate supplementation remained independently associated with reduced grade II-IV aGVHD (adjusted HR 0.31, 95% CI 0.11-0.89; p=0.029) and lower gastrointestinal aGVHD (adjusted HR 0.07, 95% CI 0.02-0.30; p<0.001). Microbiome analysis demonstrated improved recovery of gut microbial diversity at day +100 in the butyrate group, with enrichment of commensal taxa and restoration of fecal butyrate levels.
CONCLUSIONS: Oral sodium butyrate supplementation was associated with reduced incidence and severity of aGVHD, particularly involving the gastrointestinal tract, along with improved microbiome recovery. These findings suggest a potential role for postbiotic-based microbiome modulation in GVHD prevention and warrant validation in randomized controlled trials.},
}
RevDate: 2026-07-08
Enzyme-Based Mouthwashes for Oral Wound Healing and Xerostomia.
European journal of dentistry [Epub ahead of print].
ABSTRACT: Saliva plays an essential role in maintaining oral health by providing antimicrobial protection, regulating inflammation, and supporting tissue repair. Salivary enzymes such as lactoperoxidase, lysozyme, and lactoferrin are central to these protective functions. Conditions associated with reduced salivary flow, including xerostomia and postoperative states, impair these mechanisms and may result in delayed wound healing, microbial imbalance, discomfort, and increased susceptibility to infection. Conventional antiseptic mouthwashes, particularly chlorhexidine, are effective in controlling oral microorganisms but are frequently associated with adverse effects, including mucosal irritation, taste alteration, tooth discoloration, and concerns about long-term use. This structured review summarizes current evidence on natural enzyme-based mouthwashes, focusing on their mechanisms of action, potential benefits for oral wound healing and xerostomia management, and antimicrobial effects, and compares their efficacy and safety with conventional antiseptic agents.
ABSTRACT: A focused literature search was conducted using PubMed, Scopus, and Web of Science from database inception to December 2025, supplemented by manual screening of reference lists. Peer-reviewed English-language studies, including clinical, experimental, observational, and in vitro research addressing enzyme-based mouthwashes, were considered.
ABSTRACT: The available literature suggests that enzyme-based mouthwashes exert selective antimicrobial effects by reducing pathogenic microorganisms and biofilm formation while largely preserving the commensal oral microbiota. Lactoperoxidase contributes to antimicrobial activity through hypothiocyanite generation, lysozyme disrupts bacterial cell walls, lactoferrin limits microbial growth through iron sequestration and immunomodulatory effects, and glucose oxidase supports sustained enzymatic activity. Clinical studies report improvements in oral wound healing, relief of xerostomia-related symptoms, enhanced oral comfort, and good tolerability when compared with conventional antiseptic mouthwashes. However, limitations include variability in enzyme stability, a narrower antimicrobial spectrum, and a limited number of long-term clinical trials.
ABSTRACT: In conclusion, enzyme-based mouthwashes appear to be safe and biocompatible adjuncts for supporting oral wound healing and managing xerostomia. By mimicking natural salivary defense mechanisms, they offer a microbiome-friendly, non-antibiotic alternative to conventional antiseptics in selected clinical situations. Further well-designed randomized clinical trials with standardized formulations and long-term follow-up are required to clarify their effectiveness and optimal clinical indications.
Additional Links: PMID-42419704
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PubMed:
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@article {pmid42419704,
year = {2026},
author = {Reza, N and Qader, OAJA and Al-Rawas, M and Omar, M and Abdullah, JY and Urmi, SY},
title = {Enzyme-Based Mouthwashes for Oral Wound Healing and Xerostomia.},
journal = {European journal of dentistry},
volume = {},
number = {},
pages = {},
doi = {10.1055/s-0046-1822668},
pmid = {42419704},
issn = {1305-7456},
abstract = {ABSTRACT: Saliva plays an essential role in maintaining oral health by providing antimicrobial protection, regulating inflammation, and supporting tissue repair. Salivary enzymes such as lactoperoxidase, lysozyme, and lactoferrin are central to these protective functions. Conditions associated with reduced salivary flow, including xerostomia and postoperative states, impair these mechanisms and may result in delayed wound healing, microbial imbalance, discomfort, and increased susceptibility to infection. Conventional antiseptic mouthwashes, particularly chlorhexidine, are effective in controlling oral microorganisms but are frequently associated with adverse effects, including mucosal irritation, taste alteration, tooth discoloration, and concerns about long-term use. This structured review summarizes current evidence on natural enzyme-based mouthwashes, focusing on their mechanisms of action, potential benefits for oral wound healing and xerostomia management, and antimicrobial effects, and compares their efficacy and safety with conventional antiseptic agents.
ABSTRACT: A focused literature search was conducted using PubMed, Scopus, and Web of Science from database inception to December 2025, supplemented by manual screening of reference lists. Peer-reviewed English-language studies, including clinical, experimental, observational, and in vitro research addressing enzyme-based mouthwashes, were considered.
ABSTRACT: The available literature suggests that enzyme-based mouthwashes exert selective antimicrobial effects by reducing pathogenic microorganisms and biofilm formation while largely preserving the commensal oral microbiota. Lactoperoxidase contributes to antimicrobial activity through hypothiocyanite generation, lysozyme disrupts bacterial cell walls, lactoferrin limits microbial growth through iron sequestration and immunomodulatory effects, and glucose oxidase supports sustained enzymatic activity. Clinical studies report improvements in oral wound healing, relief of xerostomia-related symptoms, enhanced oral comfort, and good tolerability when compared with conventional antiseptic mouthwashes. However, limitations include variability in enzyme stability, a narrower antimicrobial spectrum, and a limited number of long-term clinical trials.
ABSTRACT: In conclusion, enzyme-based mouthwashes appear to be safe and biocompatible adjuncts for supporting oral wound healing and managing xerostomia. By mimicking natural salivary defense mechanisms, they offer a microbiome-friendly, non-antibiotic alternative to conventional antiseptics in selected clinical situations. Further well-designed randomized clinical trials with standardized formulations and long-term follow-up are required to clarify their effectiveness and optimal clinical indications.},
}
RevDate: 2026-07-08
Comment on: "Association of Fontan Circulation With Gut Microbiome Derived Straight and Branched Short Chain Fatty Acids" by Shah et al.
Additional Links: PMID-42419729
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PubMed:
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@article {pmid42419729,
year = {2026},
author = {Haq, IU and Shah, W and Ijaz, H},
title = {Comment on: "Association of Fontan Circulation With Gut Microbiome Derived Straight and Branched Short Chain Fatty Acids" by Shah et al.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70557},
pmid = {42419729},
issn = {1440-1746},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Leaf Fungal Microbiome Is Modulated by Interspecific Hybridization Events Between Coffea Species.
Physiologia plantarum, 178(4):e71016.
Increasing attention has been given to the host phylogeny and domestication roles in shaping plant-associated microbiomes. However, the interspecific effects of hybridization on microbial communities remain poorly understood. We investigated the effects of interspecific hybridization on the composition, diversity, ecological organization, and co-occurrence patterns of leaf-associated fungal communities in five Coffea species and hybrids between C. arabica and the other four species in the same habitat. Beta-diversity analyses showed a differentiation among host genotypes. Assignment of fungal genera to guilds indicated that fungal communities were dominated by pathogen-saprotrophs. Interestingly, Coffea stenophylla, a genetically distinct species within the same broader evolutionary clade, exhibited a higher relative abundance of pigmented yeasts and saprotrophs compared to C. arabica and other Coffea species analyzed. Fungal communities associated with hybrids were more similar to those of C. arabica than to the other parental species, indicating asymmetric contributions of parental traits to the colonization of the hybrids' phylloplane. A co-occurrence network revealed that neutral associations were more prevalent in Coffea hybrids than in Coffea species. These results indicate that while dominant fungal taxa are largely conserved across Coffea species and hybrids, interspecific hybridization is associated with the reorganization of the ecological relations in a fungal community. Overall, host genetics and hybridization-related traits influence the assembly and ecological organization of leaf-associated fungal communities in Coffea.
Additional Links: PMID-42419769
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PubMed:
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@article {pmid42419769,
year = {2026},
author = {de Sousa, LP and Dos Passos E Silva, L and Passos, MP and Mayer, JLS and Brandão, MM and Guerreiro-Filho, O and Mondego, JMC},
title = {Leaf Fungal Microbiome Is Modulated by Interspecific Hybridization Events Between Coffea Species.},
journal = {Physiologia plantarum},
volume = {178},
number = {4},
pages = {e71016},
doi = {10.1111/ppl.71016},
pmid = {42419769},
issn = {1399-3054},
support = {//São Paulo Research Foundation/ ; //Coordination for the Improvement of Higher Education Personnel/ ; //National Council for Scientific and Technological Development/ ; },
mesh = {*Plant Leaves/microbiology ; *Hybridization, Genetic ; *Coffea/microbiology/genetics ; *Fungi/physiology/genetics ; Phylogeny ; *Microbiota/genetics ; *Mycobiome/genetics ; Species Specificity ; },
abstract = {Increasing attention has been given to the host phylogeny and domestication roles in shaping plant-associated microbiomes. However, the interspecific effects of hybridization on microbial communities remain poorly understood. We investigated the effects of interspecific hybridization on the composition, diversity, ecological organization, and co-occurrence patterns of leaf-associated fungal communities in five Coffea species and hybrids between C. arabica and the other four species in the same habitat. Beta-diversity analyses showed a differentiation among host genotypes. Assignment of fungal genera to guilds indicated that fungal communities were dominated by pathogen-saprotrophs. Interestingly, Coffea stenophylla, a genetically distinct species within the same broader evolutionary clade, exhibited a higher relative abundance of pigmented yeasts and saprotrophs compared to C. arabica and other Coffea species analyzed. Fungal communities associated with hybrids were more similar to those of C. arabica than to the other parental species, indicating asymmetric contributions of parental traits to the colonization of the hybrids' phylloplane. A co-occurrence network revealed that neutral associations were more prevalent in Coffea hybrids than in Coffea species. These results indicate that while dominant fungal taxa are largely conserved across Coffea species and hybrids, interspecific hybridization is associated with the reorganization of the ecological relations in a fungal community. Overall, host genetics and hybridization-related traits influence the assembly and ecological organization of leaf-associated fungal communities in Coffea.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Plant Leaves/microbiology
*Hybridization, Genetic
*Coffea/microbiology/genetics
*Fungi/physiology/genetics
Phylogeny
*Microbiota/genetics
*Mycobiome/genetics
Species Specificity
RevDate: 2026-07-08
Decoding the host-microbiome dialogue with biological foundation models.
EBioMedicine, 129:106394.
Additional Links: PMID-42419827
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PubMed:
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@article {pmid42419827,
year = {2026},
author = {eBioMedicine, },
title = {Decoding the host-microbiome dialogue with biological foundation models.},
journal = {EBioMedicine},
volume = {129},
number = {},
pages = {106394},
doi = {10.1016/j.ebiom.2026.106394},
pmid = {42419827},
issn = {2352-3964},
}
RevDate: 2026-07-08
CmpDate: 2026-07-08
Factors influencing the head and neck microbiome.
Advances in immunology, 169:111-126.
The head and neck microbiome comprises a diverse and complex community of microorganisms, including bacteria, archaea, fungi, and viruses. It contributes to oral homeostasis by maintaining a harmonious balance within the oral environment. Disruptions in the balance of the oral microbiota, known as dysbiosis, can lead to the development of various oral health conditions and may extend their effect beyond the oral cavity and influence the initiation or worsening of systemic diseases. Changes in the head and neck microbiome are attributed to interactions between the host, the environment, and the resident microbial ecology. Host-related factors, including genetic background, immune competence, age and physiological status interact closely to mould the microbial colonization across different anatomical sites within the head and neck region. Anatomical and local environmental factors create discrete ecological niches that further support site-specific microbial populations. Microbial communities interact with one another through cooperative and competitive mechanisms. In healthy conditions, the oral microbiome maintains a favorable commensal relationship with its environment. However, in certain circumstances, opportunistic microorganisms within the oral microbiome may undergo a shift and become pathogenic, thereby influencing the stability, resilience, and pathogenic potential of microbiome. Microbial changes within the head and neck region are highly dynamic and respond to both short term, transient influences such as dietary intake and oral hygiene practices, as well as long term, chronic exposures, systemic disease, and sustained immune dysregulation Host related, environmental, and microbial influencing factors therefore exhibit a complex interplay in both health and disease, such that alterations in one component are capable of inducing shifts across the entire microbial ecosystem.
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PubMed:
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@article {pmid42419828,
year = {2026},
author = {Ekanayaka, R and Chaurasia, A},
title = {Factors influencing the head and neck microbiome.},
journal = {Advances in immunology},
volume = {169},
number = {},
pages = {111-126},
doi = {10.1016/bs.ai.2026.03.009},
pmid = {42419828},
issn = {1557-8445},
mesh = {Humans ; *Microbiota/immunology ; *Neck/microbiology ; *Head/microbiology ; *Dysbiosis/microbiology/immunology ; *Mouth/microbiology ; Animals ; Bacteria ; Host Microbial Interactions ; },
abstract = {The head and neck microbiome comprises a diverse and complex community of microorganisms, including bacteria, archaea, fungi, and viruses. It contributes to oral homeostasis by maintaining a harmonious balance within the oral environment. Disruptions in the balance of the oral microbiota, known as dysbiosis, can lead to the development of various oral health conditions and may extend their effect beyond the oral cavity and influence the initiation or worsening of systemic diseases. Changes in the head and neck microbiome are attributed to interactions between the host, the environment, and the resident microbial ecology. Host-related factors, including genetic background, immune competence, age and physiological status interact closely to mould the microbial colonization across different anatomical sites within the head and neck region. Anatomical and local environmental factors create discrete ecological niches that further support site-specific microbial populations. Microbial communities interact with one another through cooperative and competitive mechanisms. In healthy conditions, the oral microbiome maintains a favorable commensal relationship with its environment. However, in certain circumstances, opportunistic microorganisms within the oral microbiome may undergo a shift and become pathogenic, thereby influencing the stability, resilience, and pathogenic potential of microbiome. Microbial changes within the head and neck region are highly dynamic and respond to both short term, transient influences such as dietary intake and oral hygiene practices, as well as long term, chronic exposures, systemic disease, and sustained immune dysregulation Host related, environmental, and microbial influencing factors therefore exhibit a complex interplay in both health and disease, such that alterations in one component are capable of inducing shifts across the entire microbial ecosystem.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Microbiota/immunology
*Neck/microbiology
*Head/microbiology
*Dysbiosis/microbiology/immunology
*Mouth/microbiology
Animals
Bacteria
Host Microbial Interactions
RevDate: 2026-07-08
CmpDate: 2026-07-08
Mechanistic pathways of dysbiosis in oral cancer development.
Advances in immunology, 169:127-171.
Head and neck cancers develop within a complex microenvironment shaped by both host genetic alterations and microbial communities. Accumulating evidence demonstrates that microbial dysbiosis actively contributes to carcinogenesis by modulating immune responses, inducing chronic inflammation, and promoting immune evasion. Specific microbes can trigger oncogenic signaling pathways-including JAK/STAT, PI3K/AKT, and NF-κB-that drive cell proliferation, survival, and invasiveness. Microbiome-derived metabolites and co-carcinogens further promote DNA damage, epigenetic reprogramming, and metabolic shifts, reinforcing tumor progression and therapy resistance. This chapter reviews the molecular and cellular mechanisms linking the microbiome to tumor initiation and progression, emphasizing interactions between microbes, immune modulation, intracellular signaling, metabolic dysregulation, as well as induced DNA damages.
Additional Links: PMID-42419829
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PubMed:
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@article {pmid42419829,
year = {2026},
author = {Niu, L and Al-Ahmad, A and Scholz, K and Cieplik, F and Wolf, M},
title = {Mechanistic pathways of dysbiosis in oral cancer development.},
journal = {Advances in immunology},
volume = {169},
number = {},
pages = {127-171},
doi = {10.1016/bs.ai.2026.04.001},
pmid = {42419829},
issn = {1557-8445},
mesh = {Humans ; *Dysbiosis/immunology/microbiology ; Signal Transduction ; *Microbiota/immunology ; *Mouth Neoplasms/microbiology/immunology/metabolism/etiology/pathology ; Animals ; DNA Damage ; Tumor Microenvironment/immunology ; Carcinogenesis/immunology ; },
abstract = {Head and neck cancers develop within a complex microenvironment shaped by both host genetic alterations and microbial communities. Accumulating evidence demonstrates that microbial dysbiosis actively contributes to carcinogenesis by modulating immune responses, inducing chronic inflammation, and promoting immune evasion. Specific microbes can trigger oncogenic signaling pathways-including JAK/STAT, PI3K/AKT, and NF-κB-that drive cell proliferation, survival, and invasiveness. Microbiome-derived metabolites and co-carcinogens further promote DNA damage, epigenetic reprogramming, and metabolic shifts, reinforcing tumor progression and therapy resistance. This chapter reviews the molecular and cellular mechanisms linking the microbiome to tumor initiation and progression, emphasizing interactions between microbes, immune modulation, intracellular signaling, metabolic dysregulation, as well as induced DNA damages.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Dysbiosis/immunology/microbiology
Signal Transduction
*Microbiota/immunology
*Mouth Neoplasms/microbiology/immunology/metabolism/etiology/pathology
Animals
DNA Damage
Tumor Microenvironment/immunology
Carcinogenesis/immunology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Microbial biomarkers for OPMD progression.
Advances in immunology, 169:193-212.
Oral potentially malignant disorders (OPMDs) present a heterogeneous risk of progression to oral squamous cell carcinoma (OSCC), underscoring the need for reliable, non-invasive biomarkers to aid in clinical stratification. This chapter evaluates the utility of the oral microbiome as a source of predictive biomarkers for OPMD progression. Current evidence indicates that OPMDs and OSCC are frequently associated with microbial dysbiosis, characterized by a shift toward anaerobic, periodontal-associated taxa, such as Fusobacterium and Porphyromonas, and a concomitant depletion of health-associated Streptococcus. However, translating these taxonomic signatures into clinical practice is hindered by overlapping community structures across healthy, premalignant, and malignant mucosal states, alongside significant confounding from periodontal inflammation and lifestyle exposures. Furthermore, the field remains divided on whether this dysbiosis acts as an upstream driver of carcinogenesis or a downstream consequence of tumor-associated microenvironmental selection. To overcome these methodological and biological limitations, this chapter advocates for an ecology-driven, multi-omics approach. By integrating taxonomic profiling with functional readouts like metabolomics and metaproteomics, and contextualizing these signals within host microenvironmental strata (e.g., hypoxia and inflammation), researchers can achieve greater mechanistic interpretability and robustness. Ultimately, microbiome-informed tools are best positioned not as standalone diagnostic tests, but as adjunctive instruments for clinical triage and risk enrichment, provided they are rigorously validated in prospective, longitudinal converter/non-converter cohorts.
Additional Links: PMID-42419831
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PubMed:
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@article {pmid42419831,
year = {2026},
author = {Li, JW and Wang, Y and Chaurasia, A},
title = {Microbial biomarkers for OPMD progression.},
journal = {Advances in immunology},
volume = {169},
number = {},
pages = {193-212},
doi = {10.1016/bs.ai.2026.03.001},
pmid = {42419831},
issn = {1557-8445},
mesh = {Humans ; *Microbiota ; Disease Progression ; *Mouth Neoplasms/microbiology/diagnosis ; *Dysbiosis/microbiology ; Biomarkers ; *Carcinoma, Squamous Cell/microbiology/diagnosis ; *Biomarkers, Tumor ; *Precancerous Conditions/microbiology ; Metabolomics ; Multiomics ; },
abstract = {Oral potentially malignant disorders (OPMDs) present a heterogeneous risk of progression to oral squamous cell carcinoma (OSCC), underscoring the need for reliable, non-invasive biomarkers to aid in clinical stratification. This chapter evaluates the utility of the oral microbiome as a source of predictive biomarkers for OPMD progression. Current evidence indicates that OPMDs and OSCC are frequently associated with microbial dysbiosis, characterized by a shift toward anaerobic, periodontal-associated taxa, such as Fusobacterium and Porphyromonas, and a concomitant depletion of health-associated Streptococcus. However, translating these taxonomic signatures into clinical practice is hindered by overlapping community structures across healthy, premalignant, and malignant mucosal states, alongside significant confounding from periodontal inflammation and lifestyle exposures. Furthermore, the field remains divided on whether this dysbiosis acts as an upstream driver of carcinogenesis or a downstream consequence of tumor-associated microenvironmental selection. To overcome these methodological and biological limitations, this chapter advocates for an ecology-driven, multi-omics approach. By integrating taxonomic profiling with functional readouts like metabolomics and metaproteomics, and contextualizing these signals within host microenvironmental strata (e.g., hypoxia and inflammation), researchers can achieve greater mechanistic interpretability and robustness. Ultimately, microbiome-informed tools are best positioned not as standalone diagnostic tests, but as adjunctive instruments for clinical triage and risk enrichment, provided they are rigorously validated in prospective, longitudinal converter/non-converter cohorts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
Disease Progression
*Mouth Neoplasms/microbiology/diagnosis
*Dysbiosis/microbiology
Biomarkers
*Carcinoma, Squamous Cell/microbiology/diagnosis
*Biomarkers, Tumor
*Precancerous Conditions/microbiology
Metabolomics
Multiomics
RevDate: 2026-07-08
CmpDate: 2026-07-08
The microbiome of the head and neck region.
Advances in immunology, 169:25-51.
The head and neck region is a host to a diverse and complex microbiome, comprising of very specific microbial communities across different anatomical niches such as the oral cavity, nasal sinuses, pharynx, larynx, salivary glands, and middle ear. The existence of these communities is determined by various factors such as physicochemical conditions, local environment and host genetics playing a critical role in maintaining mucosal integrity, immune modulation, colonization resistance, and thereby achieving metabolic homeostasis. As the human ages, the microbiome constantly evolves, influenced by diet, hormonal changes, and lifestyle even causing disruptions such as dysbiosis linked to diseases like head and neck squamous cell carcinoma (HNSCC). This chapter attempts to explore the anatomical and ecological diversity, site-specific microbial compositions, functional roles, developmental trajectories, and the challenges in understanding these microbial communities. Even though there were significant advances in sequencing technologies helping in identifying the microbial protective and pathogenic potential, hurdles like sampling difficulties and low biomass contamination tend to complicate the research process. Therefore it is of utmost importance to understand the baseline microbiome thereby helping in laying a foundation for studying its role in HNSCC, creating a pathway for microbial diagnostics and curative therapies.
Additional Links: PMID-42419832
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PubMed:
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@article {pmid42419832,
year = {2026},
author = {Chaurasia, A and Ponangi, K},
title = {The microbiome of the head and neck region.},
journal = {Advances in immunology},
volume = {169},
number = {},
pages = {25-51},
doi = {10.1016/bs.ai.2026.03.002},
pmid = {42419832},
issn = {1557-8445},
mesh = {Humans ; *Microbiota/immunology ; *Dysbiosis/immunology/microbiology ; *Head and Neck Neoplasms/microbiology/immunology ; Animals ; *Head/microbiology ; *Squamous Cell Carcinoma of Head and Neck/microbiology/immunology ; },
abstract = {The head and neck region is a host to a diverse and complex microbiome, comprising of very specific microbial communities across different anatomical niches such as the oral cavity, nasal sinuses, pharynx, larynx, salivary glands, and middle ear. The existence of these communities is determined by various factors such as physicochemical conditions, local environment and host genetics playing a critical role in maintaining mucosal integrity, immune modulation, colonization resistance, and thereby achieving metabolic homeostasis. As the human ages, the microbiome constantly evolves, influenced by diet, hormonal changes, and lifestyle even causing disruptions such as dysbiosis linked to diseases like head and neck squamous cell carcinoma (HNSCC). This chapter attempts to explore the anatomical and ecological diversity, site-specific microbial compositions, functional roles, developmental trajectories, and the challenges in understanding these microbial communities. Even though there were significant advances in sequencing technologies helping in identifying the microbial protective and pathogenic potential, hurdles like sampling difficulties and low biomass contamination tend to complicate the research process. Therefore it is of utmost importance to understand the baseline microbiome thereby helping in laying a foundation for studying its role in HNSCC, creating a pathway for microbial diagnostics and curative therapies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota/immunology
*Dysbiosis/immunology/microbiology
*Head and Neck Neoplasms/microbiology/immunology
Animals
*Head/microbiology
*Squamous Cell Carcinoma of Head and Neck/microbiology/immunology
RevDate: 2026-07-08
CmpDate: 2026-07-08
Introduction.
Advances in immunology, 169:3-23.
Microorganisms colonize nearly all anatomical sites of the human body, with the oral cavity hosting one of the most diverse, accessible, and densely populated microbial ecosystems. The oral microbiome comprises a complex consortium of bacteria, fungi, viruses, archaea, and protozoa that inhabit distinct ecological niches. Each niche provides unique physicochemical conditions that shape microbial composition, structure, and function. In addition to oral and dental sites, oral biofilms frequently develop on dental materials, appliances, and prostheses, where surface characteristics such as roughness, hydrophobicity, and chemical composition further influence microbial adhesion and biofilm maturation, leading to marked differences at species and strain levels. Advances in culture-independent molecular technologies, particularly 16S rRNA gene sequencing, shotgun metagenomics, and other multi-omics approaches, have greatly enhanced understanding of oral microbial diversity, functional capacity, and host-microbe interactions beyond the limitations of conventional culture-based methods. In health, the oral microbiome exists in a state of dynamic equilibrium, or eubiosis, which contributes to local and systemic homeostasis. This balance is modulated by host factors such as saliva composition, immune responses, and oral hygiene practices, as well as environmental influences including diet, tobacco use, and alcohol consumption. Disruption of this equilibrium, termed dysbiosis, has been increasingly implicated in the pathogenesis of head and neck cancers. Emerging evidence suggests that microbial dysbiosis may promote carcinogenesis through chronic inflammation, immune modulation, production of carcinogenic metabolites, and direct interactions with epithelial cells. Understanding the microbiology of head and neck cancer therefore provides critical insights into disease initiation, progression, and potential diagnostic and therapeutic strategies.
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PubMed:
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@article {pmid42419833,
year = {2026},
author = {Jams, J and Jayasinghe, RD},
title = {Introduction.},
journal = {Advances in immunology},
volume = {169},
number = {},
pages = {3-23},
doi = {10.1016/bs.ai.2026.03.005},
pmid = {42419833},
issn = {1557-8445},
mesh = {Humans ; *Microbiota ; *Dysbiosis/microbiology/immunology ; *Mouth/microbiology ; Biofilms ; Animals ; *Head and Neck Neoplasms/microbiology/etiology/immunology ; Host Microbial Interactions ; Host-Pathogen Interactions ; },
abstract = {Microorganisms colonize nearly all anatomical sites of the human body, with the oral cavity hosting one of the most diverse, accessible, and densely populated microbial ecosystems. The oral microbiome comprises a complex consortium of bacteria, fungi, viruses, archaea, and protozoa that inhabit distinct ecological niches. Each niche provides unique physicochemical conditions that shape microbial composition, structure, and function. In addition to oral and dental sites, oral biofilms frequently develop on dental materials, appliances, and prostheses, where surface characteristics such as roughness, hydrophobicity, and chemical composition further influence microbial adhesion and biofilm maturation, leading to marked differences at species and strain levels. Advances in culture-independent molecular technologies, particularly 16S rRNA gene sequencing, shotgun metagenomics, and other multi-omics approaches, have greatly enhanced understanding of oral microbial diversity, functional capacity, and host-microbe interactions beyond the limitations of conventional culture-based methods. In health, the oral microbiome exists in a state of dynamic equilibrium, or eubiosis, which contributes to local and systemic homeostasis. This balance is modulated by host factors such as saliva composition, immune responses, and oral hygiene practices, as well as environmental influences including diet, tobacco use, and alcohol consumption. Disruption of this equilibrium, termed dysbiosis, has been increasingly implicated in the pathogenesis of head and neck cancers. Emerging evidence suggests that microbial dysbiosis may promote carcinogenesis through chronic inflammation, immune modulation, production of carcinogenic metabolites, and direct interactions with epithelial cells. Understanding the microbiology of head and neck cancer therefore provides critical insights into disease initiation, progression, and potential diagnostic and therapeutic strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
*Dysbiosis/microbiology/immunology
*Mouth/microbiology
Biofilms
Animals
*Head and Neck Neoplasms/microbiology/etiology/immunology
Host Microbial Interactions
Host-Pathogen Interactions
RevDate: 2026-07-08
CmpDate: 2026-07-08
Overview of head & neck microbiota.
Advances in immunology, 169:53-109.
The human oral cavity and upper aerodigestive tract harbor one of the most complex microbial ecosystems in the body, comprising bacteria, fungi, archaea, and viruses that coexist in a finely regulated state of eubiosis. These multi-kingdom communities play fundamental roles in maintaining mucosal homeostasis through colonization resistance, metabolic activity, immune modulation, and epithelial protection. However, disruption of this equilibrium results in dysbiosis, characterized by altered microbial composition, reduced diversity, and functional reprogramming, which collectively promote chronic inflammation, epithelial damage, and carcinogenic processes. Increasing evidence links site-specific microbial alterations in the oral cavity, oropharynx, hypopharynx, nasopharynx, larynx, sinonasal tract, and saliva with the initiation and progression of head and neck squamous cell carcinomas. Rather than single pathogens, complex microbial consortia appear to shape a pro-tumorigenic microenvironment through immune dysregulation, metabolic carcinogen production, activation of oncogenic signaling pathways, and facilitation of tumor immune evasion. This chapter provides a comprehensive overview of the composition, spatial organization, and functional roles of head and neck microbiota, with particular emphasis on their involvement in cancer-associated dysbiosis. Understanding these microbial ecosystems offers a critical framework for developing microbiome-based diagnostic biomarkers, preventive strategies, and therapeutic interventions in head and neck oncology.
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PubMed:
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@article {pmid42419834,
year = {2026},
author = {Jayasinghe, RD and Gunawardhana, KSND and Senevirathna, K},
title = {Overview of head & neck microbiota.},
journal = {Advances in immunology},
volume = {169},
number = {},
pages = {53-109},
doi = {10.1016/bs.ai.2026.04.003},
pmid = {42419834},
issn = {1557-8445},
mesh = {Humans ; *Microbiota/immunology ; *Dysbiosis/immunology/microbiology ; *Head and Neck Neoplasms/microbiology/immunology ; Animals ; *Mouth/microbiology ; Tumor Microenvironment/immunology ; },
abstract = {The human oral cavity and upper aerodigestive tract harbor one of the most complex microbial ecosystems in the body, comprising bacteria, fungi, archaea, and viruses that coexist in a finely regulated state of eubiosis. These multi-kingdom communities play fundamental roles in maintaining mucosal homeostasis through colonization resistance, metabolic activity, immune modulation, and epithelial protection. However, disruption of this equilibrium results in dysbiosis, characterized by altered microbial composition, reduced diversity, and functional reprogramming, which collectively promote chronic inflammation, epithelial damage, and carcinogenic processes. Increasing evidence links site-specific microbial alterations in the oral cavity, oropharynx, hypopharynx, nasopharynx, larynx, sinonasal tract, and saliva with the initiation and progression of head and neck squamous cell carcinomas. Rather than single pathogens, complex microbial consortia appear to shape a pro-tumorigenic microenvironment through immune dysregulation, metabolic carcinogen production, activation of oncogenic signaling pathways, and facilitation of tumor immune evasion. This chapter provides a comprehensive overview of the composition, spatial organization, and functional roles of head and neck microbiota, with particular emphasis on their involvement in cancer-associated dysbiosis. Understanding these microbial ecosystems offers a critical framework for developing microbiome-based diagnostic biomarkers, preventive strategies, and therapeutic interventions in head and neck oncology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota/immunology
*Dysbiosis/immunology/microbiology
*Head and Neck Neoplasms/microbiology/immunology
Animals
*Mouth/microbiology
Tumor Microenvironment/immunology
RevDate: 2026-07-07
Endophytic Microbiome Diversity in Citrus Leaves and the Biocontrol Potential Bacteria against Xanthomonas citri subsp. citri.
Plant disease [Epub ahead of print].
Citrus is a pivotal economic crop in southern China, while citrus canker caused by Xanthomonas citri subsp. citri (Xcc) is a devastating quarantine disease that severely threatens the sustainability of the citrus industry. Endophytic bacteria represent a promising sustainable alternative for disease management, yet systematic exploration of their potential against Xcc in citrus leaves remains limited. To address this, we characterized the leaf endophytic microbiome from major citrus-growing regions in southern China via high-throughput sequencing, revealing significant differences in the endophytic bacterial community structure between symptomatic and asymptomatic citrus leaves, with a significantly elevated relative abundance of Proteobacteria and prominent enrichment of the genera Xanthomonas, Enterobacter, and Pseudomonas in symptomatic tissues. Furthermore, symptomatic leaves harbored significantly higher endophytic bacterial diversity than asymptomatic leaves from the same production region, and the Xanthomonas abundance in the samples was highly consistent with the actual field disease severity. From 519 bacterial isolates, four strains-A1 (Bacillus altitudinis), A3 (Bacillus velezensis), A6 (Pseudomonas parafulva), and A7 (Delftia tsuruhatensis) demonstrated strong in vitro and detached-leaf antagonism against Xcc. Strain-specific fermentation parameters were optimized, and all four strains were successfully formulated into wettable powders. In a field trial, these formulations achieved control efficacies ranging from 25.8% to 53.5%, with strain A1 showing the highest and most sustained activity. Strains A3, A6, and A7 also exhibited broad-spectrum antibacterial activity against several other phytopathogenic bacteria. This study not only elucidates shifts in the endophytic microbiome associated with citrus canker but also provides novel, efficacious biocontrol resources and a practical development pipeline for sustainable disease management.
Additional Links: PMID-42410687
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PubMed:
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@article {pmid42410687,
year = {2026},
author = {Li, Y and Chen, D and Huang, K and Yi, J and Yu, H and Zhu, Y and Chang, C and Liao, L},
title = {Endophytic Microbiome Diversity in Citrus Leaves and the Biocontrol Potential Bacteria against Xanthomonas citri subsp. citri.},
journal = {Plant disease},
volume = {},
number = {},
pages = {},
doi = {10.1094/PDIS-05-26-0960-RE},
pmid = {42410687},
issn = {0191-2917},
abstract = {Citrus is a pivotal economic crop in southern China, while citrus canker caused by Xanthomonas citri subsp. citri (Xcc) is a devastating quarantine disease that severely threatens the sustainability of the citrus industry. Endophytic bacteria represent a promising sustainable alternative for disease management, yet systematic exploration of their potential against Xcc in citrus leaves remains limited. To address this, we characterized the leaf endophytic microbiome from major citrus-growing regions in southern China via high-throughput sequencing, revealing significant differences in the endophytic bacterial community structure between symptomatic and asymptomatic citrus leaves, with a significantly elevated relative abundance of Proteobacteria and prominent enrichment of the genera Xanthomonas, Enterobacter, and Pseudomonas in symptomatic tissues. Furthermore, symptomatic leaves harbored significantly higher endophytic bacterial diversity than asymptomatic leaves from the same production region, and the Xanthomonas abundance in the samples was highly consistent with the actual field disease severity. From 519 bacterial isolates, four strains-A1 (Bacillus altitudinis), A3 (Bacillus velezensis), A6 (Pseudomonas parafulva), and A7 (Delftia tsuruhatensis) demonstrated strong in vitro and detached-leaf antagonism against Xcc. Strain-specific fermentation parameters were optimized, and all four strains were successfully formulated into wettable powders. In a field trial, these formulations achieved control efficacies ranging from 25.8% to 53.5%, with strain A1 showing the highest and most sustained activity. Strains A3, A6, and A7 also exhibited broad-spectrum antibacterial activity against several other phytopathogenic bacteria. This study not only elucidates shifts in the endophytic microbiome associated with citrus canker but also provides novel, efficacious biocontrol resources and a practical development pipeline for sustainable disease management.},
}
RevDate: 2026-07-07
Estimation of postmortem submersion interval based on microbial community composition in human remains recovered from aquatic environments.
Journal of forensic sciences [Epub ahead of print].
Estimating the postmortem submersion interval (PMSI) remains a major challenge in forensic science. Although microbiome-based approaches to postmortem interval estimation have advanced considerably in recent years, studies focusing specifically on aquatic environments, particularly involving human remains and region-specific conditions, remain limited. This study aimed to investigate microbial community composition in human remains recovered from freshwater ecosystems using 16S rRNA gene sequencing and to evaluate the potential use of stage-associated microbial community patterns for estimating PMSI. Gut swabs and rib bones were collected to study the changes in the bacterial community with time. To estimate PMSI, we established regression models using random forest algorithms based on postmortem microbial community composition. The full model, incorporating 1129 bacterial genera, explained 40.4% of the variance in PMSI estimation. Furthermore, we identified 15 key genera and aquatic-specific biomarkers to construct a simplified predictive model, which significantly improved performance, explaining 81.8% of the variance with a mean absolute error of 2.66 days. To our knowledge, this study represents one of the first investigations in India to characterize microbial community composition in human cadavers recovered from freshwater environments. This research provides evidence that microbial community composition and stage-associated bacterial patterns serve as valuable biological markers for estimating PMSI in corpses recovered from aquatic habitats, offering a robust tool for forensic investigations involving submerged remains.
Additional Links: PMID-42410746
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PubMed:
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@article {pmid42410746,
year = {2026},
author = {Jangid, C and Kumari, K and Joshi, R and Hamza, M and Dalal, J},
title = {Estimation of postmortem submersion interval based on microbial community composition in human remains recovered from aquatic environments.},
journal = {Journal of forensic sciences},
volume = {},
number = {},
pages = {},
doi = {10.1111/1556-4029.70399},
pmid = {42410746},
issn = {1556-4029},
support = {200510192313//University Grants Commission/ ; },
abstract = {Estimating the postmortem submersion interval (PMSI) remains a major challenge in forensic science. Although microbiome-based approaches to postmortem interval estimation have advanced considerably in recent years, studies focusing specifically on aquatic environments, particularly involving human remains and region-specific conditions, remain limited. This study aimed to investigate microbial community composition in human remains recovered from freshwater ecosystems using 16S rRNA gene sequencing and to evaluate the potential use of stage-associated microbial community patterns for estimating PMSI. Gut swabs and rib bones were collected to study the changes in the bacterial community with time. To estimate PMSI, we established regression models using random forest algorithms based on postmortem microbial community composition. The full model, incorporating 1129 bacterial genera, explained 40.4% of the variance in PMSI estimation. Furthermore, we identified 15 key genera and aquatic-specific biomarkers to construct a simplified predictive model, which significantly improved performance, explaining 81.8% of the variance with a mean absolute error of 2.66 days. To our knowledge, this study represents one of the first investigations in India to characterize microbial community composition in human cadavers recovered from freshwater environments. This research provides evidence that microbial community composition and stage-associated bacterial patterns serve as valuable biological markers for estimating PMSI in corpses recovered from aquatic habitats, offering a robust tool for forensic investigations involving submerged remains.},
}
RevDate: 2026-07-07
CmpDate: 2026-07-07
Mendelian randomization analysis on the dissecting causal relationships between gut microbiota, circulating metabolites, and colorectal cancer: Insights from the latest evidence.
Medicine, 105(27):e49390.
The gut microbiota (GM) plays a direct role in colorectal cancer (CRC), but much of the epidemiological evidence linking the gut microbiome to CRC risk stems from observational studies. It remains unclear whether the observed microbial changes are causes or consequences of CRC development, and the role of metabolites as potential mediators is also uncertain. We conducted bidirectional Mendelian randomization (MR) using aggregated GWAS data on GM and circulating metabolites to explore causal relationships with CRC. Additionally, mediation analyses, 2-step MR, and multivariate MR were conducted to identify potential mediating factors of circulating metabolites in this relationship. We identified 12 positive and 15 negative causal effects between GM and CRC, and 4 positive and 3 negative causal effects between circulating metabolites and CRC. Notably, Succinivibrionaceae protected against CRC by increasing the CLA/FA ratio (CLA/FA; odds ratio [OR]: 1.045, 95% confidence interval [CI]: 1.006-1.086, P = .025), while Peptococcus increased CRC risk by raising the cholesterol esters to total lipids ratio in chylomicrons and extremely large VLDL (XXL-VLDL-CE_percent; OR: 1.098, 95% CI: 1.004-1.201, P = .04). This MR study provides new evidence supporting causal relationships between specific GM and CRC, along with potential new mediating metabolites.
Additional Links: PMID-42410827
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PubMed:
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@article {pmid42410827,
year = {2026},
author = {Chen, M and Dong, X and Zhang, H and Zhong, W and Wang, B},
title = {Mendelian randomization analysis on the dissecting causal relationships between gut microbiota, circulating metabolites, and colorectal cancer: Insights from the latest evidence.},
journal = {Medicine},
volume = {105},
number = {27},
pages = {e49390},
doi = {10.1097/MD.0000000000049390},
pmid = {42410827},
issn = {1536-5964},
support = {2022YFC2504004//National Key R&D Program of China/ ; },
mesh = {*Colorectal Neoplasms/genetics/microbiology/blood ; Humans ; *Mendelian Randomization Analysis ; *Gastrointestinal Microbiome/genetics ; Genome-Wide Association Study ; },
abstract = {The gut microbiota (GM) plays a direct role in colorectal cancer (CRC), but much of the epidemiological evidence linking the gut microbiome to CRC risk stems from observational studies. It remains unclear whether the observed microbial changes are causes or consequences of CRC development, and the role of metabolites as potential mediators is also uncertain. We conducted bidirectional Mendelian randomization (MR) using aggregated GWAS data on GM and circulating metabolites to explore causal relationships with CRC. Additionally, mediation analyses, 2-step MR, and multivariate MR were conducted to identify potential mediating factors of circulating metabolites in this relationship. We identified 12 positive and 15 negative causal effects between GM and CRC, and 4 positive and 3 negative causal effects between circulating metabolites and CRC. Notably, Succinivibrionaceae protected against CRC by increasing the CLA/FA ratio (CLA/FA; odds ratio [OR]: 1.045, 95% confidence interval [CI]: 1.006-1.086, P = .025), while Peptococcus increased CRC risk by raising the cholesterol esters to total lipids ratio in chylomicrons and extremely large VLDL (XXL-VLDL-CE_percent; OR: 1.098, 95% CI: 1.004-1.201, P = .04). This MR study provides new evidence supporting causal relationships between specific GM and CRC, along with potential new mediating metabolites.},
}
MeSH Terms:
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hide MeSH Terms
*Colorectal Neoplasms/genetics/microbiology/blood
Humans
*Mendelian Randomization Analysis
*Gastrointestinal Microbiome/genetics
Genome-Wide Association Study
RevDate: 2026-07-07
CmpDate: 2026-07-07
Causal relationships between gut microbiota, C-reactive protein levels and colorectal cancer: A Mendelian randomization study.
Medicine, 105(27):e49652.
Gut microbiota have been associated with C-reactive protein (CRP) levels and colorectal cancer (CRC), but their causal relationships in humans remain unclear. We performed Mendelian randomization (MR) analyses to investigate causal relationships among gut microbiota, CRP, and CRC using genome-wide association studies (GWAS) summary data. The inverse variance weighted method was prespecified as the primary estimator, with complementary MR methods and sensitivity analyses used to assess robustness. Multiple-testing correction was applied across 209 gut microbial taxa. External validation and targeted replication were conducted using independent CRC GWAS datasets. An exploratory prerequisite-based analysis evaluated whether CRP might represent a potential inflammatory pathway linking CRC-associated gut microbial taxa to CRC. Five gut microbial taxa showed nominal associations with CRC. Genus Eubacterium brachy group id.11296 (odds ratio [OR] = 1.13, 95% confidence intervals [CI] = 1.04-1.22, P = .002) and genus Ruminococcaceae UCG004 id.11362 (OR = 1.15, 95% CI = 1.03-1.29, P = .016) were positively associated with CRC risk. Family Enterobacteriaceae id.3469 (OR = 0.83, 95% CI = 0.69-1.00, P = .048), genus Oscillibacter id.2063 (OR = 0.88, 95% CI = 0.77-1.00, P = .045), and order Enterobacteriales id.3468 (OR = 0.83, 95% CI = 0.69-1.00, P = .048) showed inverse associations. However, none survived Bonferroni or Benjamini-Hochberg false discovery rate correction. Targeted replication provided partial support in BioBank Japan, with 3 taxa showing nominal replication, whereas no nominal replication was observed in FinnGen. For CRP, the weighted median method suggested a nominal inverse association with CRC risk, but this was not supported by the primary inverse variance weighting analysis or other complementary methods. The exploratory pathway analysis did not support CRP as a mediator linking the identified microbial taxa to CRC. This MR study identified 5 gut microbial taxa showing nominal associations with CRC risk, but these findings did not survive multiple-testing correction and should be interpreted as suggestive. Current evidence did not support a robust direct causal effect of CRP on CRC or a CRP-mediated microbiota-CRC pathway. Larger ancestry-matched GWAS datasets, strain-resolved microbiome analyses, and experimental studies are needed.
Additional Links: PMID-42410831
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@article {pmid42410831,
year = {2026},
author = {Xing, Z and Gong, W and Xu, Y and Wu, Y and Xu, X and Qin, S and Jiao, Y and Wang, L},
title = {Causal relationships between gut microbiota, C-reactive protein levels and colorectal cancer: A Mendelian randomization study.},
journal = {Medicine},
volume = {105},
number = {27},
pages = {e49652},
doi = {10.1097/MD.0000000000049652},
pmid = {42410831},
issn = {1536-5964},
mesh = {Humans ; *Colorectal Neoplasms/genetics/microbiology ; *C-Reactive Protein/metabolism/analysis/genetics ; Mendelian Randomization Analysis ; Genome-Wide Association Study ; *Gastrointestinal Microbiome/genetics ; },
abstract = {Gut microbiota have been associated with C-reactive protein (CRP) levels and colorectal cancer (CRC), but their causal relationships in humans remain unclear. We performed Mendelian randomization (MR) analyses to investigate causal relationships among gut microbiota, CRP, and CRC using genome-wide association studies (GWAS) summary data. The inverse variance weighted method was prespecified as the primary estimator, with complementary MR methods and sensitivity analyses used to assess robustness. Multiple-testing correction was applied across 209 gut microbial taxa. External validation and targeted replication were conducted using independent CRC GWAS datasets. An exploratory prerequisite-based analysis evaluated whether CRP might represent a potential inflammatory pathway linking CRC-associated gut microbial taxa to CRC. Five gut microbial taxa showed nominal associations with CRC. Genus Eubacterium brachy group id.11296 (odds ratio [OR] = 1.13, 95% confidence intervals [CI] = 1.04-1.22, P = .002) and genus Ruminococcaceae UCG004 id.11362 (OR = 1.15, 95% CI = 1.03-1.29, P = .016) were positively associated with CRC risk. Family Enterobacteriaceae id.3469 (OR = 0.83, 95% CI = 0.69-1.00, P = .048), genus Oscillibacter id.2063 (OR = 0.88, 95% CI = 0.77-1.00, P = .045), and order Enterobacteriales id.3468 (OR = 0.83, 95% CI = 0.69-1.00, P = .048) showed inverse associations. However, none survived Bonferroni or Benjamini-Hochberg false discovery rate correction. Targeted replication provided partial support in BioBank Japan, with 3 taxa showing nominal replication, whereas no nominal replication was observed in FinnGen. For CRP, the weighted median method suggested a nominal inverse association with CRC risk, but this was not supported by the primary inverse variance weighting analysis or other complementary methods. The exploratory pathway analysis did not support CRP as a mediator linking the identified microbial taxa to CRC. This MR study identified 5 gut microbial taxa showing nominal associations with CRC risk, but these findings did not survive multiple-testing correction and should be interpreted as suggestive. Current evidence did not support a robust direct causal effect of CRP on CRC or a CRP-mediated microbiota-CRC pathway. Larger ancestry-matched GWAS datasets, strain-resolved microbiome analyses, and experimental studies are needed.},
}
MeSH Terms:
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Humans
*Colorectal Neoplasms/genetics/microbiology
*C-Reactive Protein/metabolism/analysis/genetics
Mendelian Randomization Analysis
Genome-Wide Association Study
*Gastrointestinal Microbiome/genetics
RevDate: 2026-07-07
CmpDate: 2026-07-07
Association between oral microbiome diversity and cardiovascular-kidney-metabolic syndrome in US adults: Analysis of NHANES 2009 to 2012.
Medicine, 105(27):e49530.
The present study aimed to examine the association between oral microbiome alpha diversity and the severity of cardiovascular-kidney-metabolic (CKM) syndrome among US adults. Emerging evidence suggests that the oral microbiome may influence systemic cardiometabolic health; however, its relationship with integrated CKM syndrome remains unclear. We conducted a cross-sectional analysis of adults aged ≥20 years from the 2009 to 2012 National Health and Nutrition Examination Survey, a nationally representative survey of the US population, including participants with available oral microbiome data (n = 4834). Alpha diversity was assessed using observed amplicon sequence variants richness, Faith's phylogenetic diversity Shannon index, and Simpson index. CKM syndrome was classified into 5 stages (0-4), with advanced CKM defined as stages 3-4, representing subclinical or clinical cardiovascular disease and/or significant kidney involvement. Weighted multivariable logistic regression models were used to estimate odds ratios and 95% confidence intervals. Higher oral microbiome diversity was consistently associated with lower odds of advanced CKM. In fully adjusted models, each unit increase in observed amplicon sequence variants was associated with a 2% lower odds of advanced CKM (odds ratio = 0.98, 95% confidence interval = 0.97-1.00). Participants in the highest tertile of diversity had 10% to 12% lower odds of advanced CKM compared with the lowest tertile across diversity indices, with significant trends. Associations were consistent across demographic and clinical subgroups. Greater oral microbial diversity was inversely associated with advanced CKM syndrome in US adults. These findings support a potential association between oral microbial ecology and integrated cardiometabolic-renal health, although longitudinal and mechanistic studies are required to clarify temporality and causality.
Additional Links: PMID-42410848
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PubMed:
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@article {pmid42410848,
year = {2026},
author = {Huang, X and Gao, Y and Sun, J and Shi, L},
title = {Association between oral microbiome diversity and cardiovascular-kidney-metabolic syndrome in US adults: Analysis of NHANES 2009 to 2012.},
journal = {Medicine},
volume = {105},
number = {27},
pages = {e49530},
doi = {10.1097/MD.0000000000049530},
pmid = {42410848},
issn = {1536-5964},
mesh = {Humans ; *Microbiota/genetics ; *Metabolic Syndrome/epidemiology/microbiology ; United States/epidemiology ; Nutrition Surveys ; Female ; Cross-Sectional Studies ; Male ; Adult ; *Cardiovascular Diseases/epidemiology/microbiology ; *Mouth/microbiology ; Middle Aged ; *Kidney Diseases/epidemiology/microbiology ; },
abstract = {The present study aimed to examine the association between oral microbiome alpha diversity and the severity of cardiovascular-kidney-metabolic (CKM) syndrome among US adults. Emerging evidence suggests that the oral microbiome may influence systemic cardiometabolic health; however, its relationship with integrated CKM syndrome remains unclear. We conducted a cross-sectional analysis of adults aged ≥20 years from the 2009 to 2012 National Health and Nutrition Examination Survey, a nationally representative survey of the US population, including participants with available oral microbiome data (n = 4834). Alpha diversity was assessed using observed amplicon sequence variants richness, Faith's phylogenetic diversity Shannon index, and Simpson index. CKM syndrome was classified into 5 stages (0-4), with advanced CKM defined as stages 3-4, representing subclinical or clinical cardiovascular disease and/or significant kidney involvement. Weighted multivariable logistic regression models were used to estimate odds ratios and 95% confidence intervals. Higher oral microbiome diversity was consistently associated with lower odds of advanced CKM. In fully adjusted models, each unit increase in observed amplicon sequence variants was associated with a 2% lower odds of advanced CKM (odds ratio = 0.98, 95% confidence interval = 0.97-1.00). Participants in the highest tertile of diversity had 10% to 12% lower odds of advanced CKM compared with the lowest tertile across diversity indices, with significant trends. Associations were consistent across demographic and clinical subgroups. Greater oral microbial diversity was inversely associated with advanced CKM syndrome in US adults. These findings support a potential association between oral microbial ecology and integrated cardiometabolic-renal health, although longitudinal and mechanistic studies are required to clarify temporality and causality.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota/genetics
*Metabolic Syndrome/epidemiology/microbiology
United States/epidemiology
Nutrition Surveys
Female
Cross-Sectional Studies
Male
Adult
*Cardiovascular Diseases/epidemiology/microbiology
*Mouth/microbiology
Middle Aged
*Kidney Diseases/epidemiology/microbiology
RevDate: 2026-07-07
Organ-Specific Human Microbiomes and Dysbiosis: Mechanistic Links to Disease and Emerging Therapeutic Strategies.
Journal of clinical laboratory analysis [Epub ahead of print].
BACKGROUND: The human microbiome is a dynamic and diverse community of microorganisms that affects susceptibility to illness and promotes wellness. Dysbiosis, or disruption of this delicately regulated microbial ecology, has been identified as a major factor in the emergence and development of systemic and organ-specific disorders.
OBJECTIVE: With an emphasis on dysbiosis-driven illness processes and therapeutic intervention implications, this study attempts to critically analyze host-microbiome interactions across key human organ systems.
METHODS: Using predetermined microbiome-related keywords, a systematic literature search (2001-2025) was carried out in PubMed, Scopus, Web of Science, and Google Scholar. To assess microbiome formation, organ-specific distribution, disease correlations, and therapeutic implications, English-language peer-reviewed original papers, meta-analyses, and clinical or validated animal studies were chosen and methodically compiled.
RESULTS: Microbiome dysbiosis is linked to cardiovascular, metabolic, inflammatory, neurological, hepatic, renal, and cancer-related illnesses by interfering with immune modulation, metabolic balance, and epithelial barrier integrity, according to evidence from human and verified animal research. Modified production of short-chain fatty acids, immunological signaling imbalance, chronic inflammation, and communication between the gut-organ axis are examples of mechanistic linkages. Immune and metabolic indicators improved condition-specifically with interventions such as probiotics, fecal microbiota transplantation, and diet-based regulation.
CONCLUSION: Collectively, current evidence supports the microbiome as a modifiable determinant of disease risk and therapeutic response, underscoring its translational potential for precision medicine.
Additional Links: PMID-42410982
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@article {pmid42410982,
year = {2026},
author = {Alanazi, A},
title = {Organ-Specific Human Microbiomes and Dysbiosis: Mechanistic Links to Disease and Emerging Therapeutic Strategies.},
journal = {Journal of clinical laboratory analysis},
volume = {},
number = {},
pages = {e70307},
doi = {10.1002/jcla.70307},
pmid = {42410982},
issn = {1098-2825},
abstract = {BACKGROUND: The human microbiome is a dynamic and diverse community of microorganisms that affects susceptibility to illness and promotes wellness. Dysbiosis, or disruption of this delicately regulated microbial ecology, has been identified as a major factor in the emergence and development of systemic and organ-specific disorders.
OBJECTIVE: With an emphasis on dysbiosis-driven illness processes and therapeutic intervention implications, this study attempts to critically analyze host-microbiome interactions across key human organ systems.
METHODS: Using predetermined microbiome-related keywords, a systematic literature search (2001-2025) was carried out in PubMed, Scopus, Web of Science, and Google Scholar. To assess microbiome formation, organ-specific distribution, disease correlations, and therapeutic implications, English-language peer-reviewed original papers, meta-analyses, and clinical or validated animal studies were chosen and methodically compiled.
RESULTS: Microbiome dysbiosis is linked to cardiovascular, metabolic, inflammatory, neurological, hepatic, renal, and cancer-related illnesses by interfering with immune modulation, metabolic balance, and epithelial barrier integrity, according to evidence from human and verified animal research. Modified production of short-chain fatty acids, immunological signaling imbalance, chronic inflammation, and communication between the gut-organ axis are examples of mechanistic linkages. Immune and metabolic indicators improved condition-specifically with interventions such as probiotics, fecal microbiota transplantation, and diet-based regulation.
CONCLUSION: Collectively, current evidence supports the microbiome as a modifiable determinant of disease risk and therapeutic response, underscoring its translational potential for precision medicine.},
}
RevDate: 2026-07-07
Consistent root microbiomes across contrasting habitats in a wild perennial vine.
Plant biology (Stuttgart, Germany) [Epub ahead of print].
While we are beginning to understand that the plant microbiome is important for plant health, we still lack information about how plant microbiomes are shaped across environments and how they influence plant performance, in particular, in wild study species. Here, we examined the root microbiota of the perennial vine Solanum dulcamara, a wild relative of potato with an unusually wide ecological amplitude. Using amplicon sequencing, we characterized root communities of bacteria, fungi, and arbuscular mycorrhizal fungi in eight populations across four habitat types (beach, forest, rural, urban) and investigated the link with habitat and plant performance. We found significant differences in the composition and diversity of the root microbiota across habitats and populations, but a core set of taxa (61% of all bacterial and 73% of all fungal) made up the majority of the root microbiome. The microbiome composition was connected to soil pH and plant nutrients. Even though the investigated populations differed in herbivory and plant performance, the association between plant performance and microbial composition was weak. In conclusion, our results suggest that wild species can have similar root microbiomes across widely different habitats, and that plant performance is not always directly linked to the plant microbiome.
Additional Links: PMID-42410992
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PubMed:
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@article {pmid42410992,
year = {2026},
author = {Aleklett, K and Karlsson Green, K and Andersen, CB and Ramirez, N and Kadish, D and Grenville-Briggs, L and Lankinen, Å},
title = {Consistent root microbiomes across contrasting habitats in a wild perennial vine.},
journal = {Plant biology (Stuttgart, Germany)},
volume = {},
number = {},
pages = {},
doi = {10.1111/plb.70245},
pmid = {42410992},
issn = {1438-8677},
support = {//Svenska Forskningsrådet Formas/ ; //the Martha and Dagny Larsson foundation/ ; //Carl Tryggers Stiftelse för Vetenskaplig Forskning/ ; //Vetenskapsrådet/ ; },
abstract = {While we are beginning to understand that the plant microbiome is important for plant health, we still lack information about how plant microbiomes are shaped across environments and how they influence plant performance, in particular, in wild study species. Here, we examined the root microbiota of the perennial vine Solanum dulcamara, a wild relative of potato with an unusually wide ecological amplitude. Using amplicon sequencing, we characterized root communities of bacteria, fungi, and arbuscular mycorrhizal fungi in eight populations across four habitat types (beach, forest, rural, urban) and investigated the link with habitat and plant performance. We found significant differences in the composition and diversity of the root microbiota across habitats and populations, but a core set of taxa (61% of all bacterial and 73% of all fungal) made up the majority of the root microbiome. The microbiome composition was connected to soil pH and plant nutrients. Even though the investigated populations differed in herbivory and plant performance, the association between plant performance and microbial composition was weak. In conclusion, our results suggest that wild species can have similar root microbiomes across widely different habitats, and that plant performance is not always directly linked to the plant microbiome.},
}
RevDate: 2026-07-07
CmpDate: 2026-07-07
Multi-Omics Framework Integrating Genetics, Microbiome, Metabolism, and Immunity for Deciphering Ulcerative Colitis Pathogenesis and Diagnostic Biomarker Discovery.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 40(13):e72122.
Ulcerative colitis (UC) is an inflammatory bowel disease involving complex interactions between genetics, gut microbiota, metabolism, and immunity. This study aimed to systematically evaluate multi-omics factors potentially associated with UC susceptibility and identify reliable diagnostic biomarkers. A two-sample Mendelian randomization (MR) framework assessed potential causal associations between gut microbiome, circulating metabolites, immune cell phenotypes, and UC susceptibility. Significant MR findings were integrated with multiple transcriptomic datasets to identify differentially expressed candidate genes. Immune infiltration analysis, machine learning modeling, and external validation were subsequently performed. Single-cell and spatial transcriptomics were used to localize key genes and to explore their potential cell type-specific functions within the tissue microenvironment, followed by qRT-PCR validation in independent clinical tissues and siRNA-mediated IFITM2 knockdown in THP-1-derived macrophages. MR analyses identified potential causal associations for specific microbiota, sphingomyelin-related metabolites, and immune cell phenotypes with UC susceptibility. Integrative analysis prioritized four core signature genes: SAG, WDR48, IFITM2, and SIRPA. A random forest model achieved an AUC of 0.964 and identified a four-gene signature with strong diagnostic performance. Single-cell and spatial transcriptomics localized IFITM2 upregulation mainly to myeloid cells, particularly Neutrophil_IFITM2. CellChat suggested a potential CD4_Tem_IL7R-ANXA1-FPR1-Neutrophil_IFITM2 axis. qRT-PCR supported the expression directions of the four genes, and IFITM2 knockdown in THP-1-derived macrophages reduced TNF-α, IL-6, and IL-1β mRNA expression. This multi-omics framework supports the potential roles of specific microbiota, sphingolipid metabolism, and immune phenotypes in UC pathogenesis. The four-gene signature and characterization of Neutrophil_IFITM2, supported by independent qRT-PCR validation and preliminary IFITM2 knockdown experiments, may provide a framework for precision diagnosis and future mechanistic studies in UC.
Additional Links: PMID-42411190
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PubMed:
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@article {pmid42411190,
year = {2026},
author = {Wang, Y and Tian, Y and Cui, H and Chang, S and Tang, T and Chang, Y},
title = {Multi-Omics Framework Integrating Genetics, Microbiome, Metabolism, and Immunity for Deciphering Ulcerative Colitis Pathogenesis and Diagnostic Biomarker Discovery.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {13},
pages = {e72122},
doi = {10.1096/fj.202601379R},
pmid = {42411190},
issn = {1530-6860},
mesh = {Humans ; *Colitis, Ulcerative/genetics/metabolism/diagnosis/microbiology/immunology ; Multiomics ; *Biomarkers/metabolism ; *Gastrointestinal Microbiome ; Transcriptome ; },
abstract = {Ulcerative colitis (UC) is an inflammatory bowel disease involving complex interactions between genetics, gut microbiota, metabolism, and immunity. This study aimed to systematically evaluate multi-omics factors potentially associated with UC susceptibility and identify reliable diagnostic biomarkers. A two-sample Mendelian randomization (MR) framework assessed potential causal associations between gut microbiome, circulating metabolites, immune cell phenotypes, and UC susceptibility. Significant MR findings were integrated with multiple transcriptomic datasets to identify differentially expressed candidate genes. Immune infiltration analysis, machine learning modeling, and external validation were subsequently performed. Single-cell and spatial transcriptomics were used to localize key genes and to explore their potential cell type-specific functions within the tissue microenvironment, followed by qRT-PCR validation in independent clinical tissues and siRNA-mediated IFITM2 knockdown in THP-1-derived macrophages. MR analyses identified potential causal associations for specific microbiota, sphingomyelin-related metabolites, and immune cell phenotypes with UC susceptibility. Integrative analysis prioritized four core signature genes: SAG, WDR48, IFITM2, and SIRPA. A random forest model achieved an AUC of 0.964 and identified a four-gene signature with strong diagnostic performance. Single-cell and spatial transcriptomics localized IFITM2 upregulation mainly to myeloid cells, particularly Neutrophil_IFITM2. CellChat suggested a potential CD4_Tem_IL7R-ANXA1-FPR1-Neutrophil_IFITM2 axis. qRT-PCR supported the expression directions of the four genes, and IFITM2 knockdown in THP-1-derived macrophages reduced TNF-α, IL-6, and IL-1β mRNA expression. This multi-omics framework supports the potential roles of specific microbiota, sphingolipid metabolism, and immune phenotypes in UC pathogenesis. The four-gene signature and characterization of Neutrophil_IFITM2, supported by independent qRT-PCR validation and preliminary IFITM2 knockdown experiments, may provide a framework for precision diagnosis and future mechanistic studies in UC.},
}
MeSH Terms:
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Humans
*Colitis, Ulcerative/genetics/metabolism/diagnosis/microbiology/immunology
Multiomics
*Biomarkers/metabolism
*Gastrointestinal Microbiome
Transcriptome
RevDate: 2026-07-07
Disruption of the Gut Microbiome and Mental Health Effects Connected to Environmental Pollutants via the Gut-Brain Axis.
Current neuropharmacology pii:CN-EPUB-156886 [Epub ahead of print].
Environmental pollutants, including heavy metals, endocrine-disrupting chemicals, persistent organic pollutants, microplastics, and particulate matter, are increasingly recognized as key modifiers of the gut microbiome. These exposures can induce dysbiosis, disrupting the microbiota-gut-brain axis and influencing neurodevelopment, neurotransmission, immune regulation, and behavior. Mechanistically, pollutant-induced alterations in microbial metabolites (e.g., short-chain fatty acids, indoles, and bile acids), intestinal permeability, neuroinflammation, vagal signaling, and activation of the hypothalamic-pituitary-adrenal axis contribute to adverse neurobehavioral outcomes. Evidence from human cohort studies and animal models supports associations between pollutant exposure, microbial functional changes, and cognitive or mental health effects. This review synthesizes current mechanistic insights, highlighting advances in exposomic, microbial xenobiotic metabolism, and microbiome-targeted interventions to mitigate neurotoxicity. While these findings offer promising directions for risk assessment and therapeutic development, human evidence remains limited, and quantitative links between microbiome alterations and neurobehavioral outcomes require further investigation.
Additional Links: PMID-42411211
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PubMed:
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@article {pmid42411211,
year = {2026},
author = {Sivamaruthi, BS and Kesika, P and Chaiyasut, C and Varman, DR},
title = {Disruption of the Gut Microbiome and Mental Health Effects Connected to Environmental Pollutants via the Gut-Brain Axis.},
journal = {Current neuropharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/011570159X478499260630105121},
pmid = {42411211},
issn = {1875-6190},
abstract = {Environmental pollutants, including heavy metals, endocrine-disrupting chemicals, persistent organic pollutants, microplastics, and particulate matter, are increasingly recognized as key modifiers of the gut microbiome. These exposures can induce dysbiosis, disrupting the microbiota-gut-brain axis and influencing neurodevelopment, neurotransmission, immune regulation, and behavior. Mechanistically, pollutant-induced alterations in microbial metabolites (e.g., short-chain fatty acids, indoles, and bile acids), intestinal permeability, neuroinflammation, vagal signaling, and activation of the hypothalamic-pituitary-adrenal axis contribute to adverse neurobehavioral outcomes. Evidence from human cohort studies and animal models supports associations between pollutant exposure, microbial functional changes, and cognitive or mental health effects. This review synthesizes current mechanistic insights, highlighting advances in exposomic, microbial xenobiotic metabolism, and microbiome-targeted interventions to mitigate neurotoxicity. While these findings offer promising directions for risk assessment and therapeutic development, human evidence remains limited, and quantitative links between microbiome alterations and neurobehavioral outcomes require further investigation.},
}
RevDate: 2026-07-07
CmpDate: 2026-07-07
Isolation of Bacteria and Fungi from Human Pancreatic Tumors and Duodenum.
Gut microbes, 18(1):2695522.
Pancreatic ductal adenocarcinoma has a unique tumor microbiome, and the depletion of gut bacteria or fungi using antibiotic/antifungal cocktails has been shown to decrease pancreatic tumor burden in mice. However, functional studies evaluating the role of tumor-associated microbes are few due to the limited availability of clinically relevant microbiota. Here, we describe in detail an effective workflow for the isolation of bacteria and fungi from the duodenum and tumor of pancreatic cancer patients, specifically optimized for cryopreserved, low biomass samples. Using this workflow we also isolated microbiota from normal pancreatic tissue and duodenum from organ donors, and we confirmed the presence of bacteria and fungi isolated from tissue samples with 16S and ITS sequencing analysis. Isolation and sequencing results show distinct similarities between the pancreatic and duodenal microbiomes and highlight unique bacterial strains that survive in the tumor microenvironment. As a proof of concept, we characterized a select Klebsiella oxytoca strain (UMKO1) isolated from a pancreatic tumor, using whole genome sequencing, metabolomics, and ex- vivo tumor cultures to determine its potential impact on the pancreatic tumor microenvironment. In summary, this optimized workflow allows for the isolation of a variety of bacteria and fungi from low biomass, cryopreserved pancreatic and duodenal tissues, which can then be used for functional studies characterizing clinically relevant tumor-associated microbiota.
Additional Links: PMID-42411381
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PubMed:
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@article {pmid42411381,
year = {2026},
author = {Awad, D and Attebury, H and Hong, R and Kim, K and Zhang, L and Bischoff, A and Achi, S and denDekker, A and Lesniak, N and The, S and Nieto Carrion, JA and Nelson, NS and Strayhorn, C and Griffith, BD and Watkoske, HR and Espinoza, CE and Peterson, N and Lenard, M and Muir, A and Sahai, V and Li, G and Frankel, TL and Pasca di Magliano, M and Lyssiotis, CA and Schmidt, TM and Daley, D},
title = {Isolation of Bacteria and Fungi from Human Pancreatic Tumors and Duodenum.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2695522},
doi = {10.1080/19490976.2026.2695522},
pmid = {42411381},
issn = {1949-0984},
mesh = {Humans ; *Bacteria/isolation & purification/classification/genetics ; *Fungi/isolation & purification/classification/genetics ; *Pancreatic Neoplasms/microbiology ; *Duodenum/microbiology ; Gastrointestinal Microbiome ; *Carcinoma, Pancreatic Ductal/microbiology ; Pancreas/microbiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Pancreatic ductal adenocarcinoma has a unique tumor microbiome, and the depletion of gut bacteria or fungi using antibiotic/antifungal cocktails has been shown to decrease pancreatic tumor burden in mice. However, functional studies evaluating the role of tumor-associated microbes are few due to the limited availability of clinically relevant microbiota. Here, we describe in detail an effective workflow for the isolation of bacteria and fungi from the duodenum and tumor of pancreatic cancer patients, specifically optimized for cryopreserved, low biomass samples. Using this workflow we also isolated microbiota from normal pancreatic tissue and duodenum from organ donors, and we confirmed the presence of bacteria and fungi isolated from tissue samples with 16S and ITS sequencing analysis. Isolation and sequencing results show distinct similarities between the pancreatic and duodenal microbiomes and highlight unique bacterial strains that survive in the tumor microenvironment. As a proof of concept, we characterized a select Klebsiella oxytoca strain (UMKO1) isolated from a pancreatic tumor, using whole genome sequencing, metabolomics, and ex- vivo tumor cultures to determine its potential impact on the pancreatic tumor microenvironment. In summary, this optimized workflow allows for the isolation of a variety of bacteria and fungi from low biomass, cryopreserved pancreatic and duodenal tissues, which can then be used for functional studies characterizing clinically relevant tumor-associated microbiota.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Bacteria/isolation & purification/classification/genetics
*Fungi/isolation & purification/classification/genetics
*Pancreatic Neoplasms/microbiology
*Duodenum/microbiology
Gastrointestinal Microbiome
*Carcinoma, Pancreatic Ductal/microbiology
Pancreas/microbiology
RNA, Ribosomal, 16S/genetics
RevDate: 2026-07-07
CmpDate: 2026-07-07
Exploring the Microbiome-Kynurenine Axis in Mild Cognitive Impairment: From Gut to Brain.
Journal of integrative neuroscience, 25(6):48660.
Mild cognitive impairment (MCI) represents a critical prodromal stage of Alzheimer's disease. This review synthesizes current evidence to present a coherent pathological cascade driving MCI progression: gut microbiota dysbiosis (e.g., enrichment of Prevotella and depletion of Akkermansia) triggers a butyrate deficit and compromise of intestinal integrity, leading to systemic inflammation. This inflammatory milieu upregulates indoleamine 2,3-dioxygenase 1 (IDO1), shifting tryptophan metabolism toward the kynurenine pathway and resulting in the dominance of neurotoxic branches (3-hydroxykynurenine [3-HK], quinolinic acid [QUIN]) over neuroprotective kynurenic acid (KYNA). This metabolic imbalance promotes N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity, oxidative stress, and neuroinflammation, which collectively precipitate synaptic dysfunction and cognitive decline. We explicitly highlight this "gut-immune-metabolic" vicious cycle as the core framework of MCI pathology. Targeting this cycle through a dual strategy-restoring microbial diversity and pharmacologically inhibiting the IDO1/kynurenine 3-monooxygenase (KMO) enzymes-represents a promising therapeutic approach to delay the transition from MCI to dementia.
Additional Links: PMID-42411439
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PubMed:
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@article {pmid42411439,
year = {2026},
author = {Zhu, J and Xie, H and Ouyang, Y and Zhu, T and Liu, Q and Liu, W and Xiong, S and Liu, M},
title = {Exploring the Microbiome-Kynurenine Axis in Mild Cognitive Impairment: From Gut to Brain.},
journal = {Journal of integrative neuroscience},
volume = {25},
number = {6},
pages = {48660},
doi = {10.31083/JIN48660},
pmid = {42411439},
issn = {0219-6352},
support = {2024JK2132//Projects of the science and technology innovation Program of Hunan Province/ ; 2024RC1061//Projects of the science and technology innovation Program of Hunan Province/ ; 20257637//Scientific Research Project of Hunan Provincial Health Commission/ ; [2022] 256//State Administration of Traditional Chinese Medicine 2022 Youth Qihuang Scholars Training Program (National Letter of Traditional Chinese Medicine Education)/ ; [2022] 357//Hunan Provincial Graduate Joint Cultivation Base for Acupuncture-Moxibustion and Tuina of Hunan University of Chinese Medicine (Hunan Provincial Department of Education Notice)/ ; [2021] 356//Acupuncture Bioinformation and Smart Wellness Innovation and Entrepreneurship Education Center of Hunan University of Chinese Medicine (Hunan Provincial Department of Education Notice)/ ; [2020] 19//Innovative Graduate Cultivation Base for Chinese Medicine Sub-health of Hunan University of Chinese Medicine (University Administrative Research Document)/ ; },
mesh = {Humans ; *Kynurenine/metabolism ; *Gastrointestinal Microbiome/physiology ; *Cognitive Dysfunction/metabolism/microbiology/immunology ; Animals ; *Brain/metabolism ; *Dysbiosis/metabolism/immunology ; },
abstract = {Mild cognitive impairment (MCI) represents a critical prodromal stage of Alzheimer's disease. This review synthesizes current evidence to present a coherent pathological cascade driving MCI progression: gut microbiota dysbiosis (e.g., enrichment of Prevotella and depletion of Akkermansia) triggers a butyrate deficit and compromise of intestinal integrity, leading to systemic inflammation. This inflammatory milieu upregulates indoleamine 2,3-dioxygenase 1 (IDO1), shifting tryptophan metabolism toward the kynurenine pathway and resulting in the dominance of neurotoxic branches (3-hydroxykynurenine [3-HK], quinolinic acid [QUIN]) over neuroprotective kynurenic acid (KYNA). This metabolic imbalance promotes N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity, oxidative stress, and neuroinflammation, which collectively precipitate synaptic dysfunction and cognitive decline. We explicitly highlight this "gut-immune-metabolic" vicious cycle as the core framework of MCI pathology. Targeting this cycle through a dual strategy-restoring microbial diversity and pharmacologically inhibiting the IDO1/kynurenine 3-monooxygenase (KMO) enzymes-represents a promising therapeutic approach to delay the transition from MCI to dementia.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Kynurenine/metabolism
*Gastrointestinal Microbiome/physiology
*Cognitive Dysfunction/metabolism/microbiology/immunology
Animals
*Brain/metabolism
*Dysbiosis/metabolism/immunology
RevDate: 2026-07-07
CmpDate: 2026-07-07
Amyotrophic Lateral Sclerosis as a Systemic Disease: Why Integrative and Microbiome-Focused Approaches Deserve Re-Evaluation.
Frontiers in bioscience (Landmark edition), 31(6):52497.
Despite decades of intensive research, therapeutic advances in amyotrophic lateral sclerosis (ALS) remain limited. Increasing evidence suggests that ALS is a multisystem disorder involving motor neuron degeneration, immune dysregulation, skeletal muscle pathology, and gastrointestinal dysfunction, thereby challenging the adequacy of current therapeutic strategies. Complementary and alternative medicine (CAM) approaches are widely used by patients with ALS. However, their efficacy remains controversial owing to limited clinical evidence and methodological limitations. The multicomponent herbal medicine and system-level characteristics of CAM conceptually align with the emerging view of ALS as a multisystemic disease. The involvement of gut microbiome dysbiosis in the pathophysiology of ALS has provided a unifying biological framework linking the peripheral, metabolic, and neuroinflammatory processes. These findings suggest that the combination of CAM and conventional therapy may serve as a potential integrative approach to target gut-brain-muscle interactions and systemic disease pathways. This article highlights critical gaps in the existing evidence and proposes that microbiome-focused, biomarker-driven clinical trials are essential to thoroughly evaluate CAM-based interventions in ALS. Embracing a system-oriented therapeutic framework may help address the complexity of ALS beyond traditional neuron-centered approaches.
Additional Links: PMID-42411482
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PubMed:
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@article {pmid42411482,
year = {2026},
author = {Yang, EJ},
title = {Amyotrophic Lateral Sclerosis as a Systemic Disease: Why Integrative and Microbiome-Focused Approaches Deserve Re-Evaluation.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {31},
number = {6},
pages = {52497},
doi = {10.31083/FBL52497},
pmid = {42411482},
issn = {2768-6698},
support = {KSN2225011//KIOM/ ; },
mesh = {Humans ; *Amyotrophic Lateral Sclerosis/therapy/microbiology/physiopathology ; *Complementary Therapies/methods ; *Gastrointestinal Microbiome ; Animals ; Dysbiosis/microbiology ; },
abstract = {Despite decades of intensive research, therapeutic advances in amyotrophic lateral sclerosis (ALS) remain limited. Increasing evidence suggests that ALS is a multisystem disorder involving motor neuron degeneration, immune dysregulation, skeletal muscle pathology, and gastrointestinal dysfunction, thereby challenging the adequacy of current therapeutic strategies. Complementary and alternative medicine (CAM) approaches are widely used by patients with ALS. However, their efficacy remains controversial owing to limited clinical evidence and methodological limitations. The multicomponent herbal medicine and system-level characteristics of CAM conceptually align with the emerging view of ALS as a multisystemic disease. The involvement of gut microbiome dysbiosis in the pathophysiology of ALS has provided a unifying biological framework linking the peripheral, metabolic, and neuroinflammatory processes. These findings suggest that the combination of CAM and conventional therapy may serve as a potential integrative approach to target gut-brain-muscle interactions and systemic disease pathways. This article highlights critical gaps in the existing evidence and proposes that microbiome-focused, biomarker-driven clinical trials are essential to thoroughly evaluate CAM-based interventions in ALS. Embracing a system-oriented therapeutic framework may help address the complexity of ALS beyond traditional neuron-centered approaches.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Amyotrophic Lateral Sclerosis/therapy/microbiology/physiopathology
*Complementary Therapies/methods
*Gastrointestinal Microbiome
Animals
Dysbiosis/microbiology
RevDate: 2026-07-07
CmpDate: 2026-07-07
Beyond Amyloid: Evolutionary and Immune-Metabolic Perspectives on Alzheimer's Disease.
Frontiers in bioscience (Landmark edition), 31(6):53859.
Alzheimer's disease (AD) is increasingly recognized as a multifactorial and systems-level disorder that extends beyond the classical amyloid cascade hypothesis. Rather than dismissing established concepts such as tau pathology, synaptic dysfunction, vascular compromise, mitochondrial abnormalities, and impaired proteostasis, emerging evidence suggests that these processes may interact dynamically with chronic immune activation, microbial signaling, and systemic metabolic stress. Recent studies examining the microbiome-gut-brain axis, chronic infection, innate immunity, and systemic immune-metabolic dysfunction have broadened the conceptual framework of AD pathogenesis. Importantly, amyloid-β (Aβ) is now understood to possess evolutionarily conserved antimicrobial and immunomodulatory properties, suggesting that amyloid deposition may initially represent a protective host-defense response rather than solely a toxic pathological event. This perspective does not overturn the amyloid cascade model but instead reframes amyloid biology within a broader adaptive evolutionary context in which chronic or dysregulated activation becomes maladaptive during aging. The present opinion article integrates these converging concepts into a unified framework in which AD emerges from the prolonged interaction among immune responses, microbial exposures, metabolic disturbances, mitochondrial dysfunction, vascular injury, and age-associated failures in proteostatic resilience. This integrative interpretation seeks to humanize the disease process by viewing neurodegeneration not simply as isolated protein accumulation, but as the gradual exhaustion of ancient host-defense and energy-regulatory systems that were originally evolutionarily advantageous for survival.
Additional Links: PMID-42411493
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PubMed:
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@article {pmid42411493,
year = {2026},
author = {Stefano, GB},
title = {Beyond Amyloid: Evolutionary and Immune-Metabolic Perspectives on Alzheimer's Disease.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {31},
number = {6},
pages = {53859},
doi = {10.31083/FBL53859},
pmid = {42411493},
issn = {2768-6698},
mesh = {Humans ; *Alzheimer Disease/metabolism/immunology/pathology ; Animals ; *Amyloid beta-Peptides/metabolism/immunology ; Immunity, Innate ; Brain/metabolism/immunology/pathology ; Mitochondria/metabolism ; Biological Evolution ; Gastrointestinal Microbiome ; },
abstract = {Alzheimer's disease (AD) is increasingly recognized as a multifactorial and systems-level disorder that extends beyond the classical amyloid cascade hypothesis. Rather than dismissing established concepts such as tau pathology, synaptic dysfunction, vascular compromise, mitochondrial abnormalities, and impaired proteostasis, emerging evidence suggests that these processes may interact dynamically with chronic immune activation, microbial signaling, and systemic metabolic stress. Recent studies examining the microbiome-gut-brain axis, chronic infection, innate immunity, and systemic immune-metabolic dysfunction have broadened the conceptual framework of AD pathogenesis. Importantly, amyloid-β (Aβ) is now understood to possess evolutionarily conserved antimicrobial and immunomodulatory properties, suggesting that amyloid deposition may initially represent a protective host-defense response rather than solely a toxic pathological event. This perspective does not overturn the amyloid cascade model but instead reframes amyloid biology within a broader adaptive evolutionary context in which chronic or dysregulated activation becomes maladaptive during aging. The present opinion article integrates these converging concepts into a unified framework in which AD emerges from the prolonged interaction among immune responses, microbial exposures, metabolic disturbances, mitochondrial dysfunction, vascular injury, and age-associated failures in proteostatic resilience. This integrative interpretation seeks to humanize the disease process by viewing neurodegeneration not simply as isolated protein accumulation, but as the gradual exhaustion of ancient host-defense and energy-regulatory systems that were originally evolutionarily advantageous for survival.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/metabolism/immunology/pathology
Animals
*Amyloid beta-Peptides/metabolism/immunology
Immunity, Innate
Brain/metabolism/immunology/pathology
Mitochondria/metabolism
Biological Evolution
Gastrointestinal Microbiome
RevDate: 2026-07-07
CmpDate: 2026-07-07
Microbiome-Derived Effectors and Convergent Host Pathways in Organ Injury and Fibrosis.
Frontiers in bioscience (Landmark edition), 31(6):51062.
The human microbiome functions as an endocrine-like biochemical network that generates metabolites, structural ligands, and peptides capable of shaping host physiology. Under physiological conditions, these microbiome-derived effectors contribute to epithelial integrity, immune homeostasis, metabolic regulation, and tissue resilience. During dysbiosis, however, the composition and systemic distribution of these effectors are altered, shifting host responses toward injury. Despite their chemical diversity, microbiome-derived signals converge on a limited set of host pathways, including pattern-recognition receptor activation, mitochondrial dysfunction, apoptosis and senescence, inflammatory amplification, and fibrosis, which collectively determine tissue vulnerability across organ systems. This framework links gut imbalance to disorders such as pulmonary fibrosis, acute lung injury, chronic kidney disease, and hepatobiliary inflammation. Microbial peptides represent an emerging layer of regulation. Among these peptides, corisin exemplifies how discrete microbial effectors can directly engage intracellular targets and amplify tissue injury. Together, these observations reframe microbiome-associated disease as a disorder of microbial chemistry and host pathway activation, thereby providing a foundation for mechanism-based biomarkers and targeted therapeutic strategies.
Additional Links: PMID-42411494
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PubMed:
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@article {pmid42411494,
year = {2026},
author = {D'Alessandro, VF and Fujimoto, H and D'Alessandro-Gabazza, CN and Toda, M and Shah, R and Nishihama, K and Hataji, O and Gabazza, EC and Leckband, D and Cann, I and Kobayashi, T and Yasuma, T},
title = {Microbiome-Derived Effectors and Convergent Host Pathways in Organ Injury and Fibrosis.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {31},
number = {6},
pages = {51062},
doi = {10.31083/FBL51062},
pmid = {42411494},
issn = {2768-6698},
support = {JPMJFR2216//Japan Science and Technology Agency (JST)/ ; 22K08280//Japan Society for the Promotion of Science/ ; 25K18797//Japan Society for the Promotion of Science/ ; //2022 Takeda Science Foundation/ ; //2023 Takeda Science Foundation/ ; //2025-2026 MSD Life Science Foundation/ ; //2025-2026 TERUMO Life Science Foundation/ ; //Daiwa Security Foundation 2024/ ; },
mesh = {Humans ; Animals ; *Microbiota ; Fibrosis/microbiology ; *Dysbiosis/microbiology/metabolism ; *Gastrointestinal Microbiome ; },
abstract = {The human microbiome functions as an endocrine-like biochemical network that generates metabolites, structural ligands, and peptides capable of shaping host physiology. Under physiological conditions, these microbiome-derived effectors contribute to epithelial integrity, immune homeostasis, metabolic regulation, and tissue resilience. During dysbiosis, however, the composition and systemic distribution of these effectors are altered, shifting host responses toward injury. Despite their chemical diversity, microbiome-derived signals converge on a limited set of host pathways, including pattern-recognition receptor activation, mitochondrial dysfunction, apoptosis and senescence, inflammatory amplification, and fibrosis, which collectively determine tissue vulnerability across organ systems. This framework links gut imbalance to disorders such as pulmonary fibrosis, acute lung injury, chronic kidney disease, and hepatobiliary inflammation. Microbial peptides represent an emerging layer of regulation. Among these peptides, corisin exemplifies how discrete microbial effectors can directly engage intracellular targets and amplify tissue injury. Together, these observations reframe microbiome-associated disease as a disorder of microbial chemistry and host pathway activation, thereby providing a foundation for mechanism-based biomarkers and targeted therapeutic strategies.},
}
MeSH Terms:
show MeSH Terms
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Humans
Animals
*Microbiota
Fibrosis/microbiology
*Dysbiosis/microbiology/metabolism
*Gastrointestinal Microbiome
RevDate: 2026-07-07
CmpDate: 2026-07-07
Non-Antibiotic Prophylaxis for Recurrent Urinary Tract Infection: A Narrative Review & Clinical Guide for Primary and Hospital Care.
British journal of hospital medicine (London, England : 2005), 87(6):49956.
Recurrent urinary tract infection (rUTI) is a common and distressing condition disproportionately affecting females. It also accounts for a substantial proportion of antibiotic prescribing in primary care. Repeated antibiotic exposure contributes to adverse effects, disruption of the urogenital microbiome and the accelerating global threat of antimicrobial resistance. Consequently, contemporary clinical guidelines increasingly emphasise non-antibiotic prophylactic strategies as a core component of rUTI management. This narrative review synthesises contemporary evidence and guideline recommendations from the European Association of Urology (EAU), the National Institute for Health and Care Excellence (NICE), and the American Urological Association (AUA) on non-antibiotic prophylaxis for rUTI. It places particular focus on practical implementation in primary care. Behavioural and risk-factor optimisation, methenamine hippurate, topical estrogen, D-mannose, probiotics, cranberry products, immunoactive prophylaxis and intravesical therapies are reviewed. These are appraised with respect to efficacy, safety, tolerability, accessibility and quality of evidence. This review highlights key differences in guideline positioning and identifies areas of ongoing uncertainty and future research. Additionally, this review explores the central role of general practitioners in confirming diagnosis and initiating first-line non-antibiotic prophylaxis. Moreover, their role in supporting shared decision-making and managing timely specialist referral, where appropriate, is highlighted. Considerations for both men and women with rUTI are discussed. To support the translation of evidence into practice, this article includes pragmatic clinical tools, such as a shared decision-making aid, a stepwise treatment algorithm, and a structured risk-factor checklist. By integrating evidence-based non-antibiotic strategies into routine care, clinicians can reduce antibiotic exposure, improve patient outcomes, and respond proactively to the global challenge of antimicrobial resistance.
Additional Links: PMID-42411541
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PubMed:
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@article {pmid42411541,
year = {2026},
author = {Antoniou, V and Somani, B},
title = {Non-Antibiotic Prophylaxis for Recurrent Urinary Tract Infection: A Narrative Review & Clinical Guide for Primary and Hospital Care.},
journal = {British journal of hospital medicine (London, England : 2005)},
volume = {87},
number = {6},
pages = {49956},
doi = {10.31083/BJHM49956},
pmid = {42411541},
issn = {1759-7390},
mesh = {Humans ; *Urinary Tract Infections/prevention & control/drug therapy ; Primary Health Care ; Probiotics/therapeutic use ; Practice Guidelines as Topic ; Estrogens/therapeutic use ; Female ; Recurrence ; Methenamine/therapeutic use/analogs & derivatives ; Vaccinium macrocarpon ; Anti-Bacterial Agents ; Risk Factors ; Hippurates ; },
abstract = {Recurrent urinary tract infection (rUTI) is a common and distressing condition disproportionately affecting females. It also accounts for a substantial proportion of antibiotic prescribing in primary care. Repeated antibiotic exposure contributes to adverse effects, disruption of the urogenital microbiome and the accelerating global threat of antimicrobial resistance. Consequently, contemporary clinical guidelines increasingly emphasise non-antibiotic prophylactic strategies as a core component of rUTI management. This narrative review synthesises contemporary evidence and guideline recommendations from the European Association of Urology (EAU), the National Institute for Health and Care Excellence (NICE), and the American Urological Association (AUA) on non-antibiotic prophylaxis for rUTI. It places particular focus on practical implementation in primary care. Behavioural and risk-factor optimisation, methenamine hippurate, topical estrogen, D-mannose, probiotics, cranberry products, immunoactive prophylaxis and intravesical therapies are reviewed. These are appraised with respect to efficacy, safety, tolerability, accessibility and quality of evidence. This review highlights key differences in guideline positioning and identifies areas of ongoing uncertainty and future research. Additionally, this review explores the central role of general practitioners in confirming diagnosis and initiating first-line non-antibiotic prophylaxis. Moreover, their role in supporting shared decision-making and managing timely specialist referral, where appropriate, is highlighted. Considerations for both men and women with rUTI are discussed. To support the translation of evidence into practice, this article includes pragmatic clinical tools, such as a shared decision-making aid, a stepwise treatment algorithm, and a structured risk-factor checklist. By integrating evidence-based non-antibiotic strategies into routine care, clinicians can reduce antibiotic exposure, improve patient outcomes, and respond proactively to the global challenge of antimicrobial resistance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Urinary Tract Infections/prevention & control/drug therapy
Primary Health Care
Probiotics/therapeutic use
Practice Guidelines as Topic
Estrogens/therapeutic use
Female
Recurrence
Methenamine/therapeutic use/analogs & derivatives
Vaccinium macrocarpon
Anti-Bacterial Agents
Risk Factors
Hippurates
RevDate: 2026-07-07
CmpDate: 2026-07-07
The Role of the Microbiome in the Development of an Autoimmune Reaction in Rheumatoid Arthritis.
Frontiers in bioscience (Scholar edition), 18(2):44236.
Patients with rheumatoid arthritis (RA), a chronic inflammatory illness, have joint inflammation, increasing tissue damage, and severe disability, all of which negatively impact quality of life. While the precise mechanisms behind RA remain unknown, there is growing evidence that both the onset and development of the illness are closely linked to an imbalance in the intestinal microbiota. Variations in the microbial content of RA patients and healthy people suggest that the gut microbiota plays a part in regulating immunological responses and fostering inflammation. Thus, therapies aimed at restoring the microbiome to its original state have demonstrated encouraging results in terms of increasing therapeutic efficacy, improving patient outcomes, and delaying the progression of disease. However, more research is needed to clarify the intricate interactions between the intestinal microbiota and autoimmunity mechanisms in RA.
Additional Links: PMID-42411656
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PubMed:
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@article {pmid42411656,
year = {2026},
author = {Blagov, A and Vatlin, AA and Pavshintsev, VV and Mitkin, NA and Maltseva, ON and Orekhov, AN},
title = {The Role of the Microbiome in the Development of an Autoimmune Reaction in Rheumatoid Arthritis.},
journal = {Frontiers in bioscience (Scholar edition)},
volume = {18},
number = {2},
pages = {44236},
doi = {10.31083/FBS44236},
pmid = {42411656},
issn = {1945-0524},
support = {202760-2-000//RUDN University Scientific Projects Grant System/ ; },
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology ; *Autoimmunity ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/immunology/microbiology ; Animals ; },
abstract = {Patients with rheumatoid arthritis (RA), a chronic inflammatory illness, have joint inflammation, increasing tissue damage, and severe disability, all of which negatively impact quality of life. While the precise mechanisms behind RA remain unknown, there is growing evidence that both the onset and development of the illness are closely linked to an imbalance in the intestinal microbiota. Variations in the microbial content of RA patients and healthy people suggest that the gut microbiota plays a part in regulating immunological responses and fostering inflammation. Thus, therapies aimed at restoring the microbiome to its original state have demonstrated encouraging results in terms of increasing therapeutic efficacy, improving patient outcomes, and delaying the progression of disease. However, more research is needed to clarify the intricate interactions between the intestinal microbiota and autoimmunity mechanisms in RA.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Arthritis, Rheumatoid/immunology/microbiology
*Autoimmunity
*Gastrointestinal Microbiome/immunology
*Dysbiosis/immunology/microbiology
Animals
RevDate: 2026-07-07
CmpDate: 2026-07-07
Systematic Review and Meta-Analysis of the Efficacy of Fecal Microbiota Transplantation in Parkinson's Disease: An Exploration Based on UPDRS and Cognitive Scores.
Revista de neurologia, 81(6):50106.
BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disorder that has been increasingly linked to gut-brain axis dysfunction. Fecal microbiota transplantation (FMT), a microbiome-targeted intervention, has shown theoretical and preliminary clinical potential in PD, but randomized clinical evidence remains limited. This review aimed to systematically evaluate the effects of FMT on motor, non-motor, and cognitive outcomes in patients with PD.
METHODS: A Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)-compliant systematic review and meta-analysis of randomized controlled trials (RCTs) comparing FMT with placebo or conventional care in PD was conducted. Two reviewers independently screened studies, extracted data, and assessed risk of bias. Pooled analyses were performed using a random-effects model, and the certainty of evidence was evaluated using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach.
RESULTS: Five RCTs involving 226 participants were included. No statistically significant differences were observed between the FMT and control groups in Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Parts I-III, Montreal Cognitive Assessment (MoCA), or Mini-Mental State Examination (MMSE) scores at any assessed follow-up time, with heterogeneity generally low to moderate across outcomes.
CONCLUSIONS: Based on current evidence from five small RCTs, FMT did not demonstrate a statistically significant benefit for motor, daily living, or cognitive outcomes in PD. However, these findings should be interpreted cautiously, given the limited sample size, short follow-up duration, and between-study differences in intervention protocols. Larger, well-designed RCTs with standardized FMT protocols and longer follow-up are needed. The PROSPERO Registration: This systematic review was registered in the PROSPERO database under registration number CRD420251121443, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251121443.
Additional Links: PMID-42411731
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PubMed:
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@article {pmid42411731,
year = {2026},
author = {Liang, B and Zou, J and Mao, X and Xie, N and Liang, Z},
title = {Systematic Review and Meta-Analysis of the Efficacy of Fecal Microbiota Transplantation in Parkinson's Disease: An Exploration Based on UPDRS and Cognitive Scores.},
journal = {Revista de neurologia},
volume = {81},
number = {6},
pages = {50106},
doi = {10.31083/RN50106},
pmid = {42411731},
issn = {1576-6578},
mesh = {Humans ; *Parkinson Disease/therapy/psychology ; *Fecal Microbiota Transplantation ; Randomized Controlled Trials as Topic ; Treatment Outcome ; Cognition ; Severity of Illness Index ; },
abstract = {BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disorder that has been increasingly linked to gut-brain axis dysfunction. Fecal microbiota transplantation (FMT), a microbiome-targeted intervention, has shown theoretical and preliminary clinical potential in PD, but randomized clinical evidence remains limited. This review aimed to systematically evaluate the effects of FMT on motor, non-motor, and cognitive outcomes in patients with PD.
METHODS: A Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)-compliant systematic review and meta-analysis of randomized controlled trials (RCTs) comparing FMT with placebo or conventional care in PD was conducted. Two reviewers independently screened studies, extracted data, and assessed risk of bias. Pooled analyses were performed using a random-effects model, and the certainty of evidence was evaluated using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach.
RESULTS: Five RCTs involving 226 participants were included. No statistically significant differences were observed between the FMT and control groups in Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Parts I-III, Montreal Cognitive Assessment (MoCA), or Mini-Mental State Examination (MMSE) scores at any assessed follow-up time, with heterogeneity generally low to moderate across outcomes.
CONCLUSIONS: Based on current evidence from five small RCTs, FMT did not demonstrate a statistically significant benefit for motor, daily living, or cognitive outcomes in PD. However, these findings should be interpreted cautiously, given the limited sample size, short follow-up duration, and between-study differences in intervention protocols. Larger, well-designed RCTs with standardized FMT protocols and longer follow-up are needed. The PROSPERO Registration: This systematic review was registered in the PROSPERO database under registration number CRD420251121443, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251121443.},
}
MeSH Terms:
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Humans
*Parkinson Disease/therapy/psychology
*Fecal Microbiota Transplantation
Randomized Controlled Trials as Topic
Treatment Outcome
Cognition
Severity of Illness Index
RevDate: 2026-07-07
Short-chain fatty acid-producing taxa enriched by competitive exclusion cultures can drive resistance to non-typhoidal Salmonella colonization in broilers.
Journal of applied microbiology pii:8726157 [Epub ahead of print].
AIMS: This study evaluated the efficacy of three Competitive Exclusion (CE) products, formulated under aerobic (AER), anaerobic (ANA), and combined (MIS) conditions, in controlling Salmonella Heidelberg (SH) and Salmonella Infantis (SI) in experimentally challenged broiler chicks.
METHODS AND RESULTS: Birds were inoculated with CE on the first day of life and challenged with Salmonella (SH or SI) 24 h later. Cecal colonization, fecal shedding, and microbiota modulation were monitored up to 21 days post-infection (DPI). The combined treatment (MIS) produced the most consistent results, yielding the greatest reductions in both cecal and fecal Salmonella counts. Beta diversity analyses revealed significant community restructuring across all time points (P = 0.036). CE accelerated microbial maturation, promoting early establishment of beneficial anaerobes such as Bacteroides and Subdoligranulum. Differential abundance analysis (LEfSe) confirmed strong modulatory effects, particularly enhancing key genera linked to intestinal health, including Bacteroides, Subdoligranulum, and Faecalibacterium.
CONCLUSIONS: Competitive Exclusion cultures are effective in reducing Salmonella colonization in broiler chickens and represent a promising alternative to antimicrobials. The combined CE formulation (MIS) improved the performance of standard anaerobic products and enhanced the establishment of beneficial microbiota associated with colonization resistance.
Additional Links: PMID-42411845
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PubMed:
Citation:
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@article {pmid42411845,
year = {2026},
author = {Kolososki, IMM and Rodrigues, HLS and Ferreira, VA and Rabelo, ALC and Santos, MCB and Nascimento, CF and Lima, TS and Benevides, VP and Campos, IC and Almeida, AM and Funnicelli, MIG and Barrow, PA and Olsen, JE and Junior, AB and Saraiva, MMS},
title = {Short-chain fatty acid-producing taxa enriched by competitive exclusion cultures can drive resistance to non-typhoidal Salmonella colonization in broilers.},
journal = {Journal of applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jambio/lxag168},
pmid = {42411845},
issn = {1365-2672},
abstract = {AIMS: This study evaluated the efficacy of three Competitive Exclusion (CE) products, formulated under aerobic (AER), anaerobic (ANA), and combined (MIS) conditions, in controlling Salmonella Heidelberg (SH) and Salmonella Infantis (SI) in experimentally challenged broiler chicks.
METHODS AND RESULTS: Birds were inoculated with CE on the first day of life and challenged with Salmonella (SH or SI) 24 h later. Cecal colonization, fecal shedding, and microbiota modulation were monitored up to 21 days post-infection (DPI). The combined treatment (MIS) produced the most consistent results, yielding the greatest reductions in both cecal and fecal Salmonella counts. Beta diversity analyses revealed significant community restructuring across all time points (P = 0.036). CE accelerated microbial maturation, promoting early establishment of beneficial anaerobes such as Bacteroides and Subdoligranulum. Differential abundance analysis (LEfSe) confirmed strong modulatory effects, particularly enhancing key genera linked to intestinal health, including Bacteroides, Subdoligranulum, and Faecalibacterium.
CONCLUSIONS: Competitive Exclusion cultures are effective in reducing Salmonella colonization in broiler chickens and represent a promising alternative to antimicrobials. The combined CE formulation (MIS) improved the performance of standard anaerobic products and enhanced the establishment of beneficial microbiota associated with colonization resistance.},
}
RevDate: 2026-07-07
IUJ Special Collection on the Microbiome, Urinary Tract Infection and Bladder Pain: A Field in Transition.
Additional Links: PMID-42412129
Publisher:
PubMed:
Citation:
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@article {pmid42412129,
year = {2026},
author = {Horsley, H},
title = {IUJ Special Collection on the Microbiome, Urinary Tract Infection and Bladder Pain: A Field in Transition.},
journal = {International urogynecology journal},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00192-026-06743-z},
pmid = {42412129},
issn = {1433-3023},
}
RevDate: 2026-07-07
Gut microbiome profile and inflammatory response in pelvic organ prolapse: A pilot study.
International urogynecology journal [Epub ahead of print].
INTRODUCTION AND HYPOTHESIS: Pelvic organ prolapse (POP) is a common condition with poorly understood mechanisms. Metabolic endotoxemia and gut microbiome dysbiosis may impair connective tissue integrity, contributing to POP. We hypothesized that women with POP have a distinct gut microbiome and greater systemic inflammation than controls.
METHODS: This prospective cohort study enrolled patients undergoing hysterectomy for benign indications from February 2023 to February 2024. Stool, blood, and uterosacral ligament (USL) biopsies were collected. Gut microbiome composition, including alpha and beta diversity and differential abundance of bacterial taxa, was assessed. In addition, plasma inflammatory markers and histologic inflammation were also evaluated.
RESULTS: Eighty-six patients were analyzed. Alpha diversity was higher in POP patients by observed features (p = 0.048) and increased with prolapse stage, but these associations did not persist after adjusting for age. Beta diversity showed no distinct patterns. Clostridia vadinBB60 group, Eubacteriales, and Rhodospirillales increased with advancing stage, persisting after age adjustment. Plasma lipopolysaccharide-binding protein (LBP) and histologic inflammation were significantly higher in POP patients, while lipopolysaccharide (LPS) and zonulin were comparable.
CONCLUSIONS: Women with POP exhibited modest gut microbiome differences. Greater microbial richness paralleled prolapse severity but was largely attributable to age. In contrast, stage-associated enrichment of Clostridia vadinBB60 group, Eubacteriales, and Rhodospirillales persisted after age adjustment, suggesting taxonomic shifts specific to prolapse rather than aging alone. Elevated histologic inflammation and plasma LBP suggest a systemic inflammatory response consistent with an inflamm-aging framework. Together, these findings support a possible gut-pelvic floor axis and may provide groundwork for microbiome- and inflammation-targeted therapies.
Additional Links: PMID-42412132
PubMed:
Citation:
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@article {pmid42412132,
year = {2026},
author = {Hilton, AE and Asmar, DM and Orlicky, DJ and Arruda, JS and Rascoff, LG and Colas, JAH and Yang, I and Guess, MK and Johnson, J and Connell, KA},
title = {Gut microbiome profile and inflammatory response in pelvic organ prolapse: A pilot study.},
journal = {International urogynecology journal},
volume = {},
number = {},
pages = {},
pmid = {42412132},
issn = {1433-3023},
abstract = {INTRODUCTION AND HYPOTHESIS: Pelvic organ prolapse (POP) is a common condition with poorly understood mechanisms. Metabolic endotoxemia and gut microbiome dysbiosis may impair connective tissue integrity, contributing to POP. We hypothesized that women with POP have a distinct gut microbiome and greater systemic inflammation than controls.
METHODS: This prospective cohort study enrolled patients undergoing hysterectomy for benign indications from February 2023 to February 2024. Stool, blood, and uterosacral ligament (USL) biopsies were collected. Gut microbiome composition, including alpha and beta diversity and differential abundance of bacterial taxa, was assessed. In addition, plasma inflammatory markers and histologic inflammation were also evaluated.
RESULTS: Eighty-six patients were analyzed. Alpha diversity was higher in POP patients by observed features (p = 0.048) and increased with prolapse stage, but these associations did not persist after adjusting for age. Beta diversity showed no distinct patterns. Clostridia vadinBB60 group, Eubacteriales, and Rhodospirillales increased with advancing stage, persisting after age adjustment. Plasma lipopolysaccharide-binding protein (LBP) and histologic inflammation were significantly higher in POP patients, while lipopolysaccharide (LPS) and zonulin were comparable.
CONCLUSIONS: Women with POP exhibited modest gut microbiome differences. Greater microbial richness paralleled prolapse severity but was largely attributable to age. In contrast, stage-associated enrichment of Clostridia vadinBB60 group, Eubacteriales, and Rhodospirillales persisted after age adjustment, suggesting taxonomic shifts specific to prolapse rather than aging alone. Elevated histologic inflammation and plasma LBP suggest a systemic inflammatory response consistent with an inflamm-aging framework. Together, these findings support a possible gut-pelvic floor axis and may provide groundwork for microbiome- and inflammation-targeted therapies.},
}
RevDate: 2026-07-07
Resolution Failure in Periodontal Diseases: Dysregulated Pro-resolving Mechanisms in Chronic Inflammation and Tissue Breakdown.
Current topics in microbiology and immunology [Epub ahead of print].
Periodontitis is a highly prevalent chronic inflammatory disease characterized by irreversible destruction of the tooth-supporting tissues. Although classically interpreted as the consequence of excessive inflammation that drives microbial dysbiosis, accumulating experimental and clinical evidence indicates that periodontitis can be more precisely described as a disorder of failed inflammatory resolution. In periodontal tissues-constantly exposed to microbial challenge-resolution is not a terminal event but a constitutive biological requirement essential for maintaining tissue homeostasis. This chapter examines the molecular and cellular mechanisms through which pro-resolving pathways become dysregulated in periodontitis, with particular emphasis on imbalances in lipid mediator networks, defective biosynthetic class switching, impaired receptor-mediated signaling, altered leukocyte fate decisions, and disruption of osteoimmune coupling. We further discuss how these resolution defects are functionally expressed across immune, stromal, and bone compartments, and how they reshape the inflammatory microenvironment and host-microbiome interactions. Finally, we evaluate the implications of these mechanisms for resolution pharmacology, highlighting how restoration of endogenous termination and repair programs-rather than suppression of inflammatory initiation-offers a biologically grounded therapeutic paradigm. Collectively, this chapter positions periodontitis as both a disease-specific manifestation of resolution failure and a tractable translational model for advancing resolution-based therapeutic strategies with potential relevance beyond oral tissues.
Additional Links: PMID-42412215
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PubMed:
Citation:
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@article {pmid42412215,
year = {2026},
author = {Baima, G and Mehrnia, N and Romandini, M and Van Dyke, TE},
title = {Resolution Failure in Periodontal Diseases: Dysregulated Pro-resolving Mechanisms in Chronic Inflammation and Tissue Breakdown.},
journal = {Current topics in microbiology and immunology},
volume = {},
number = {},
pages = {},
doi = {10.1007/82_2026_347},
pmid = {42412215},
issn = {0070-217X},
abstract = {Periodontitis is a highly prevalent chronic inflammatory disease characterized by irreversible destruction of the tooth-supporting tissues. Although classically interpreted as the consequence of excessive inflammation that drives microbial dysbiosis, accumulating experimental and clinical evidence indicates that periodontitis can be more precisely described as a disorder of failed inflammatory resolution. In periodontal tissues-constantly exposed to microbial challenge-resolution is not a terminal event but a constitutive biological requirement essential for maintaining tissue homeostasis. This chapter examines the molecular and cellular mechanisms through which pro-resolving pathways become dysregulated in periodontitis, with particular emphasis on imbalances in lipid mediator networks, defective biosynthetic class switching, impaired receptor-mediated signaling, altered leukocyte fate decisions, and disruption of osteoimmune coupling. We further discuss how these resolution defects are functionally expressed across immune, stromal, and bone compartments, and how they reshape the inflammatory microenvironment and host-microbiome interactions. Finally, we evaluate the implications of these mechanisms for resolution pharmacology, highlighting how restoration of endogenous termination and repair programs-rather than suppression of inflammatory initiation-offers a biologically grounded therapeutic paradigm. Collectively, this chapter positions periodontitis as both a disease-specific manifestation of resolution failure and a tractable translational model for advancing resolution-based therapeutic strategies with potential relevance beyond oral tissues.},
}
RevDate: 2026-07-07
Targeting the Gut-Heart Axis in Atherosclerosis: Microbial Metabolites, Molecular Mechanisms, and Precision Therapeutics.
Probiotics and antimicrobial proteins [Epub ahead of print].
Despite advances in lipid-lowering and anti-inflammatory medications, atherosclerotic cardiovascular disease (ASCVD) continues to be the leading cause of morbidity and mortality worldwide. Recent studies have identified the gut microbiota as a key modulator of cardiovascular health via the gut-heart axis. This review investigates the molecular processes by which microbial metabolites affect atherogenesis. Proatherogenic substances like trimethylamine-N-oxide (TMAO), which are produced from dietary precursors through gut microbial and hepatic metabolism, aggravate foam cell production, platelet aggregation, and vascular inflammation. Short chain fatty acids (SCFAs), such as butyrate and propionate, have been shown to protect against atherosclerosis by activating G-protein-coupled receptors, regulating gene expression, and improving endothelial function. Additionally, secondary bile acids, tryptophan derivatives, and phenylacetylglutamine have emerged as important microbial metabolites involved in vascular disease. The review also summarizes various therapeutic strategies such as use of probiotics, prebiotics, postbiotics, precision microbiome editing (using bacteriophages and CRISPR-Cas systems), and fecal microbiota transplantation (FMT) for targeting gut-heart axis. Multi-omic systems combined with artificial intelligence can now detect disease-specific microbial signatures, improving risk stratification and paving the way for precision microbiome-based therapeutics. However, challenges such as determining causality, regulatory intricacies, and inter-individual variability in host-microbiome interactions remain. Despite these obstacles, the gut-heart axis provides a disruptive paradigm in preventive cardiology by emphasizing tailored microbiome therapies as a complement to traditional ASCVD care.
Additional Links: PMID-42412324
PubMed:
Citation:
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@article {pmid42412324,
year = {2026},
author = {Adiga, U and Vasishta, S and Adiga, S and Augustine, AJ},
title = {Targeting the Gut-Heart Axis in Atherosclerosis: Microbial Metabolites, Molecular Mechanisms, and Precision Therapeutics.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42412324},
issn = {1867-1314},
abstract = {Despite advances in lipid-lowering and anti-inflammatory medications, atherosclerotic cardiovascular disease (ASCVD) continues to be the leading cause of morbidity and mortality worldwide. Recent studies have identified the gut microbiota as a key modulator of cardiovascular health via the gut-heart axis. This review investigates the molecular processes by which microbial metabolites affect atherogenesis. Proatherogenic substances like trimethylamine-N-oxide (TMAO), which are produced from dietary precursors through gut microbial and hepatic metabolism, aggravate foam cell production, platelet aggregation, and vascular inflammation. Short chain fatty acids (SCFAs), such as butyrate and propionate, have been shown to protect against atherosclerosis by activating G-protein-coupled receptors, regulating gene expression, and improving endothelial function. Additionally, secondary bile acids, tryptophan derivatives, and phenylacetylglutamine have emerged as important microbial metabolites involved in vascular disease. The review also summarizes various therapeutic strategies such as use of probiotics, prebiotics, postbiotics, precision microbiome editing (using bacteriophages and CRISPR-Cas systems), and fecal microbiota transplantation (FMT) for targeting gut-heart axis. Multi-omic systems combined with artificial intelligence can now detect disease-specific microbial signatures, improving risk stratification and paving the way for precision microbiome-based therapeutics. However, challenges such as determining causality, regulatory intricacies, and inter-individual variability in host-microbiome interactions remain. Despite these obstacles, the gut-heart axis provides a disruptive paradigm in preventive cardiology by emphasizing tailored microbiome therapies as a complement to traditional ASCVD care.},
}
RevDate: 2026-07-07
Combining genotoxic gut bacterial strains increases tumor burden and accelerates onset in a germ-free mouse model of colon carcinogenesis.
Cell reports, 45(7):117645 pii:S2211-1247(26)00723-0 [Epub ahead of print].
To identify causal links between gut microbes and tumorigenesis, we colonized germ-free, colon tumor-susceptible mice (Apc[Min/+];Il10[-/-]) with 19 cultured human fecal microbiotas from healthy individuals and patients with inflammatory bowel disease or colorectal cancer. Colonic tumor counts vary by donor microbiota but not by donor health status. In vitro screens of host cell proliferation, genotoxicity, and inflammation in bacteria-mammalian cell co-cultures reveal that genotoxicity best predicts tumorigenic microbes in vivo, with genotoxic microbes present in all tested individuals. The genotoxic subset of strains from each donor induces more tumors than the complete community-even when the complete community is not tumorigenic. Combining genotoxic microbes from multiple sources increases tumor number and decreases time to tumor onset. Together, these results suggest that most individuals harbor genotoxic bacterial strains and that the balance of genotoxic to protective strains determines the timing and severity of tumorigenesis in vivo.
Additional Links: PMID-42412611
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PubMed:
Citation:
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@article {pmid42412611,
year = {2026},
author = {Plitt, T and Piessevaux, A and Rajpal, U and Fischer, J and Spindler, MP and Ruprecht, C and Li, Z and Mogno, I and Yang, Y and Desch, AN and Chu, G and Jiang, Z and Wang, J and Gevers, D and Pocalyko, D and Geis, AL and Jobin, C and Bachman, KE and Sears, CL and Britton, GJ and San Mateo, LR and Faith, JJ},
title = {Combining genotoxic gut bacterial strains increases tumor burden and accelerates onset in a germ-free mouse model of colon carcinogenesis.},
journal = {Cell reports},
volume = {45},
number = {7},
pages = {117645},
doi = {10.1016/j.celrep.2026.117645},
pmid = {42412611},
issn = {2211-1247},
abstract = {To identify causal links between gut microbes and tumorigenesis, we colonized germ-free, colon tumor-susceptible mice (Apc[Min/+];Il10[-/-]) with 19 cultured human fecal microbiotas from healthy individuals and patients with inflammatory bowel disease or colorectal cancer. Colonic tumor counts vary by donor microbiota but not by donor health status. In vitro screens of host cell proliferation, genotoxicity, and inflammation in bacteria-mammalian cell co-cultures reveal that genotoxicity best predicts tumorigenic microbes in vivo, with genotoxic microbes present in all tested individuals. The genotoxic subset of strains from each donor induces more tumors than the complete community-even when the complete community is not tumorigenic. Combining genotoxic microbes from multiple sources increases tumor number and decreases time to tumor onset. Together, these results suggest that most individuals harbor genotoxic bacterial strains and that the balance of genotoxic to protective strains determines the timing and severity of tumorigenesis in vivo.},
}
RevDate: 2026-07-07
CmpDate: 2026-07-07
[Possible mechanisms of action of electroconvulsive therapy].
Psychiatria Hungarica : A Magyar Pszichiatriai Tarsasag tudomanyos folyoirata, 40(3-4):328-337.
Electroconvulsive therapy (ECT) remains one of the most effective biological treatment methods in psychiatry. The development of convulsive treatment methods was based on a theory of its mechanism of action, namely the presumed biological antagonism between schizophrenia and epilepsy. Later studies did not confirm this antagonistic diseases theory, but intensive research started to clarify ECT's mechanism of action. In early studies on ECT, attention was drawn to the anticonvulsant effect , its impact on cerebral circulation and the change of permeability of the blood-brain barrier. Later research focused on the effect of ECT on the neurotransmitter and neurohormonal systems. The inflammatory theory of the mechanism of action was based on the improvement of the laboratory findings observed in conditions that responded well to ECT. With the development of the imaging techniques, the volume reduction of certain brain areas in depression and schizophrenia came into focus. These changes turned out to be reversible with ECT which provided the basis of the neuroplasticity theory of ECT's mechanism of action. The network theory explanation of the effect of ECT was based on the correction of the abnormal circuits of the brain's electrical networks. Finally, in recent years, increasing attention has been paid to the microbiome-gut-brain axis, which, according to preliminary findings, is also affected by ECT. However, the extent to which this is responsible for the therapeutic effects of ECT in psychiatric disorders needs further investigations. Keywords: electroconvulsive therapy; mechanism of action; neuroplasticity; network theory; microbiome.
Additional Links: PMID-42412649
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@article {pmid42412649,
year = {2025},
author = {Gazdag, G and Girasek, H and Takács, R},
title = {[Possible mechanisms of action of electroconvulsive therapy].},
journal = {Psychiatria Hungarica : A Magyar Pszichiatriai Tarsasag tudomanyos folyoirata},
volume = {40},
number = {3-4},
pages = {328-337},
pmid = {42412649},
issn = {0237-7896},
mesh = {Humans ; *Electroconvulsive Therapy/methods ; *Schizophrenia/therapy/physiopathology ; Neuronal Plasticity ; *Brain/physiopathology/metabolism ; Blood-Brain Barrier ; Epilepsy/therapy ; Neurotransmitter Agents/metabolism ; },
abstract = {Electroconvulsive therapy (ECT) remains one of the most effective biological treatment methods in psychiatry. The development of convulsive treatment methods was based on a theory of its mechanism of action, namely the presumed biological antagonism between schizophrenia and epilepsy. Later studies did not confirm this antagonistic diseases theory, but intensive research started to clarify ECT's mechanism of action. In early studies on ECT, attention was drawn to the anticonvulsant effect , its impact on cerebral circulation and the change of permeability of the blood-brain barrier. Later research focused on the effect of ECT on the neurotransmitter and neurohormonal systems. The inflammatory theory of the mechanism of action was based on the improvement of the laboratory findings observed in conditions that responded well to ECT. With the development of the imaging techniques, the volume reduction of certain brain areas in depression and schizophrenia came into focus. These changes turned out to be reversible with ECT which provided the basis of the neuroplasticity theory of ECT's mechanism of action. The network theory explanation of the effect of ECT was based on the correction of the abnormal circuits of the brain's electrical networks. Finally, in recent years, increasing attention has been paid to the microbiome-gut-brain axis, which, according to preliminary findings, is also affected by ECT. However, the extent to which this is responsible for the therapeutic effects of ECT in psychiatric disorders needs further investigations. Keywords: electroconvulsive therapy; mechanism of action; neuroplasticity; network theory; microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Electroconvulsive Therapy/methods
*Schizophrenia/therapy/physiopathology
Neuronal Plasticity
*Brain/physiopathology/metabolism
Blood-Brain Barrier
Epilepsy/therapy
Neurotransmitter Agents/metabolism
RevDate: 2026-07-07
CmpDate: 2026-07-07
Genotype-specific root morphology and metabolic traits shape bacterial communities and tolerance to Fusarium root rot in wheat.
PloS one, 21(7):e0349952 pii:PONE-D-25-60791.
Plant genotype plays a critical role in shaping root-associated microbiota and in modulating plant tolerance to soilborne diseases such as Fusarium root rot (FRR). In this study, we investigated how four wheat (Triticum aestivum) varieties, with differing tolerance to FRR, influence the composition and structure of bacterial communities in the rhizosphere and root endosphere. In the current study evaluated root traits that may contribute to the genotype-specific assembly of bacterial communities across the four wheat genotypes. The variety Concret exhibited the highest FRR tolerance, whereas Pilier was the most susceptible. Analyses of root morphology revealed significant genotype-dependent differences in root length and volume. Notably, traits associated with the tolerant genotype were positively correlated with the abundance of key beneficial bacterial genera in the rhizosphere, including Bacillus, Lysobacter, and Sphingomonas. Untargeted metabolomics identified 879 features, with 20 key metabolites distinguishing the wheat genotypes, including alkaloids, benzoate derivatives, and benzoxazinoid-derived compounds. Correlation analysis revealed significant relationships between these root metabolites and key bacterial taxa. This findings demonstrate that wheat genotypes influence the assembly of the root microbiota through genotype-based morphological and metabolic traits, providing valuable insights into the specific root traits that wheat genotypes can leverage to modulate the plant microbiome and enhance disease resistance.
Additional Links: PMID-42412762
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PubMed:
Citation:
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@article {pmid42412762,
year = {2026},
author = {Hafidi, O and Simonin, M and Magot, F and Munakata, Y and Kergunteuil, A and Larbat, R and Grosjean, J and Hehn, A and Barret, M and Slezack, S},
title = {Genotype-specific root morphology and metabolic traits shape bacterial communities and tolerance to Fusarium root rot in wheat.},
journal = {PloS one},
volume = {21},
number = {7},
pages = {e0349952},
doi = {10.1371/journal.pone.0349952},
pmid = {42412762},
issn = {1932-6203},
mesh = {*Triticum/microbiology/genetics/metabolism/anatomy & histology ; *Plant Roots/microbiology/metabolism/anatomy & histology/genetics ; *Fusarium/pathogenicity/physiology ; Genotype ; Rhizosphere ; *Plant Diseases/microbiology/genetics ; *Microbiota ; Bacteria/genetics/classification ; Soil Microbiology ; },
abstract = {Plant genotype plays a critical role in shaping root-associated microbiota and in modulating plant tolerance to soilborne diseases such as Fusarium root rot (FRR). In this study, we investigated how four wheat (Triticum aestivum) varieties, with differing tolerance to FRR, influence the composition and structure of bacterial communities in the rhizosphere and root endosphere. In the current study evaluated root traits that may contribute to the genotype-specific assembly of bacterial communities across the four wheat genotypes. The variety Concret exhibited the highest FRR tolerance, whereas Pilier was the most susceptible. Analyses of root morphology revealed significant genotype-dependent differences in root length and volume. Notably, traits associated with the tolerant genotype were positively correlated with the abundance of key beneficial bacterial genera in the rhizosphere, including Bacillus, Lysobacter, and Sphingomonas. Untargeted metabolomics identified 879 features, with 20 key metabolites distinguishing the wheat genotypes, including alkaloids, benzoate derivatives, and benzoxazinoid-derived compounds. Correlation analysis revealed significant relationships between these root metabolites and key bacterial taxa. This findings demonstrate that wheat genotypes influence the assembly of the root microbiota through genotype-based morphological and metabolic traits, providing valuable insights into the specific root traits that wheat genotypes can leverage to modulate the plant microbiome and enhance disease resistance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Triticum/microbiology/genetics/metabolism/anatomy & histology
*Plant Roots/microbiology/metabolism/anatomy & histology/genetics
*Fusarium/pathogenicity/physiology
Genotype
Rhizosphere
*Plant Diseases/microbiology/genetics
*Microbiota
Bacteria/genetics/classification
Soil Microbiology
RevDate: 2026-07-07
CmpDate: 2026-07-07
A novel transformer model of protein domains for viral taxonomy classification.
Bioinformatics (Oxford, England), 42(Supplement_1):.
MOTIVATION: Viruses with carefully curated taxonomic assignments (such as those in the ICTV taxonomy) still represent only a small fraction of viruses identified through sequencing data from virome or microbiome projects. It is therefore critical to develop methods that can assign viruses at multiple taxonomic ranks, so that a virus deemed novel at a given rank may still be placed into a higher-level taxon. Sequence-similarity-based approaches can classify viruses that share substantial genomic similarity with known viruses (e.g. those belonging to the same species or genus); however, their performance drops significantly when applied to more divergent viruses. Recent deep learning models, such as ViTax, which utilize DNA language models, aim to address these limitations, but their performance also degrades when applied to novel viruses lacking genus-level similarity to known references. Proteins are more conserved than genomic sequences, and the multiple proteins encoded by a virus can be leveraged to reveal evolutionary relationships among viruses.
RESULTS: We propose a new tool, D2T (Domain-to-Taxonomy), that leverages recent advances in protein language models to improve viral taxonomic assignment. D2T represents a virus as a sequence of protein domain tokens and learns a transformer-based model for taxonomic classification. Experiments on multiple closed-set and open-set datasets show that D2T excels at assigning higher-level taxonomic labels (family and above). Furthermore, by combining D2T with Kraken2, which performs well at the genus level, the hybrid method (K+D2T) achieves accurate viral taxonomic classification across multiple taxonomic ranks.
D2T is available as a GitHub repository at https://github.com/mgtools/D2T.
Additional Links: PMID-42412789
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@article {pmid42412789,
year = {2026},
author = {Shin, J and Xiao, Q and Ye, Y},
title = {A novel transformer model of protein domains for viral taxonomy classification.},
journal = {Bioinformatics (Oxford, England)},
volume = {42},
number = {Supplement_1},
pages = {},
doi = {10.1093/bioinformatics/btag291},
pmid = {42412789},
issn = {1367-4811},
support = {R01AI143254/GF/NIH HHS/United States ; EF-2025451//NSF/ ; },
mesh = {*Viruses/classification/genetics ; *Protein Domains ; *Viral Proteins/chemistry/genetics ; *Computational Biology/methods ; },
abstract = {MOTIVATION: Viruses with carefully curated taxonomic assignments (such as those in the ICTV taxonomy) still represent only a small fraction of viruses identified through sequencing data from virome or microbiome projects. It is therefore critical to develop methods that can assign viruses at multiple taxonomic ranks, so that a virus deemed novel at a given rank may still be placed into a higher-level taxon. Sequence-similarity-based approaches can classify viruses that share substantial genomic similarity with known viruses (e.g. those belonging to the same species or genus); however, their performance drops significantly when applied to more divergent viruses. Recent deep learning models, such as ViTax, which utilize DNA language models, aim to address these limitations, but their performance also degrades when applied to novel viruses lacking genus-level similarity to known references. Proteins are more conserved than genomic sequences, and the multiple proteins encoded by a virus can be leveraged to reveal evolutionary relationships among viruses.
RESULTS: We propose a new tool, D2T (Domain-to-Taxonomy), that leverages recent advances in protein language models to improve viral taxonomic assignment. D2T represents a virus as a sequence of protein domain tokens and learns a transformer-based model for taxonomic classification. Experiments on multiple closed-set and open-set datasets show that D2T excels at assigning higher-level taxonomic labels (family and above). Furthermore, by combining D2T with Kraken2, which performs well at the genus level, the hybrid method (K+D2T) achieves accurate viral taxonomic classification across multiple taxonomic ranks.
D2T is available as a GitHub repository at https://github.com/mgtools/D2T.},
}
MeSH Terms:
show MeSH Terms
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*Viruses/classification/genetics
*Protein Domains
*Viral Proteins/chemistry/genetics
*Computational Biology/methods
RevDate: 2026-07-07
CmpDate: 2026-07-07
Recurrent urinary tract infections in older adults: A systematic review of current challenges and emerging therapeutic strategies.
Acta pharmaceutica (Zagreb, Croatia), 76(2):1-25 pii:acph-2026-0017.
As global life expectancy continues to rise, urinary tract infections (UTIs) have become an increasing concern in older adults. The higher prevalence in this population is attributed to anatomical and physiological changes of the urinary tract, hormonal imbalances, immunosenescence, and the presence of comorbidities. These factors, combined with a distinct microbiological profile and rising antimicrobial resistance, create significant clinical challenges in diagnosis and treatment. We conducted a systematic review of clinical trials and observational studies on the epidemiology, pathogenesis, diagnosis, and management of recurrent urinary tract infections (rUTIs) in older adults. The prevalence of rUTIs increases with age, disproportionately affecting women, with 53 % of those over 55 years experiencing recurrences within one year. Healthcare-associated UTIs (HAUTIs) account for 20-30 % of nosocomial infections, primarily impacting older adults. The host microbiome seemed crucial in UTI pathogenesis, with Escherichia coli being the leading causative agent due to its ability to adhere, colonise, and evade the immune response. In elderly patients, atypical presentations - such as delirium, functional decline, or nonspecific abdominal symptoms - complicate diagnosis, underscoring the critical need to differentiate symptomatic infections from asymptomatic bacteriuria (ASB) to prevent misdiagnosis and overtreatment. Effective management requires accurate diagnosis, appropriate antibiotic selection, and careful monitoring of adverse effects, especially in patients with comorbidities. Emerging therapies, including faecal microbiota transplantation, bacteriophages, probiotics, and proanthocyanidins, offer promising adjuncts. While long-term antibiotic prophylaxis is effective, it increases the risk of bacterial resistance, particularly in catheterised patients. Behavioural modifications, such as increased fluid intake, aid pathogen clearance, and topical estrogen therapy in postmenopausal women provides additional preventive benefit. Managing recurrent UTIs in ageing populations requires addressing microbiological, diagnostic, and antimicrobial resistance challenges. Despite resistance levels, the first-line treatment, nitrofurantoin, remains a viable therapeutic option, particularly in developed countries. An integrated approach combining individualised care, healthcare provider training, and rational antimicrobial use is essential to improving patient outcomes and quality of life. Future strategies should focus on novel antimicrobials targeting bacterial virulence factors, vaccines against uropathogens, and advanced diagnostic technologies.
Additional Links: PMID-42412955
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PubMed:
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@article {pmid42412955,
year = {2026},
author = {Lv, J and Waza, AA},
title = {Recurrent urinary tract infections in older adults: A systematic review of current challenges and emerging therapeutic strategies.},
journal = {Acta pharmaceutica (Zagreb, Croatia)},
volume = {76},
number = {2},
pages = {1-25},
doi = {10.2478/acph-2026-0017},
pmid = {42412955},
issn = {1846-9558},
mesh = {Humans ; *Urinary Tract Infections/diagnosis/epidemiology/therapy/microbiology/drug therapy ; Aged ; Recurrence ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; Female ; Prevalence ; Age Factors ; Risk Factors ; },
abstract = {As global life expectancy continues to rise, urinary tract infections (UTIs) have become an increasing concern in older adults. The higher prevalence in this population is attributed to anatomical and physiological changes of the urinary tract, hormonal imbalances, immunosenescence, and the presence of comorbidities. These factors, combined with a distinct microbiological profile and rising antimicrobial resistance, create significant clinical challenges in diagnosis and treatment. We conducted a systematic review of clinical trials and observational studies on the epidemiology, pathogenesis, diagnosis, and management of recurrent urinary tract infections (rUTIs) in older adults. The prevalence of rUTIs increases with age, disproportionately affecting women, with 53 % of those over 55 years experiencing recurrences within one year. Healthcare-associated UTIs (HAUTIs) account for 20-30 % of nosocomial infections, primarily impacting older adults. The host microbiome seemed crucial in UTI pathogenesis, with Escherichia coli being the leading causative agent due to its ability to adhere, colonise, and evade the immune response. In elderly patients, atypical presentations - such as delirium, functional decline, or nonspecific abdominal symptoms - complicate diagnosis, underscoring the critical need to differentiate symptomatic infections from asymptomatic bacteriuria (ASB) to prevent misdiagnosis and overtreatment. Effective management requires accurate diagnosis, appropriate antibiotic selection, and careful monitoring of adverse effects, especially in patients with comorbidities. Emerging therapies, including faecal microbiota transplantation, bacteriophages, probiotics, and proanthocyanidins, offer promising adjuncts. While long-term antibiotic prophylaxis is effective, it increases the risk of bacterial resistance, particularly in catheterised patients. Behavioural modifications, such as increased fluid intake, aid pathogen clearance, and topical estrogen therapy in postmenopausal women provides additional preventive benefit. Managing recurrent UTIs in ageing populations requires addressing microbiological, diagnostic, and antimicrobial resistance challenges. Despite resistance levels, the first-line treatment, nitrofurantoin, remains a viable therapeutic option, particularly in developed countries. An integrated approach combining individualised care, healthcare provider training, and rational antimicrobial use is essential to improving patient outcomes and quality of life. Future strategies should focus on novel antimicrobials targeting bacterial virulence factors, vaccines against uropathogens, and advanced diagnostic technologies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Urinary Tract Infections/diagnosis/epidemiology/therapy/microbiology/drug therapy
Aged
Recurrence
*Anti-Bacterial Agents/therapeutic use/administration & dosage
Female
Prevalence
Age Factors
Risk Factors
RevDate: 2026-07-07
Crop domestication, selective breeding, and the seed microbiome: a call for further research.
Canadian journal of microbiology [Epub ahead of print].
Plants have been domesticated for thousands of years and subject to human derived selection for desirable traits such as improved yield, disease tolerance, nutrient content, and palatability.Advancements in high-throughput DNA sequencing advancements have allowed researchers to study the diversity of the seed microbiome. We reviewed the literature and identified articles that investigated the impact of domestication on seed microbiome diversity of various plant species.The resultant analysis suggests that the impacts of domestication and selective breeding on seed microbiome diversity are variable and inconclusive due to the low number of independent studies per species and the limited diversity of domesticated species examined. Based upon our analysis we suggest a need for standardized methodology and bioinformatic analysis to accompany further research on seed development of domesticated crop species. Understanding the mechanisms that influence plantmicrobe interactions, such as microbial colonization during seed development, and their applications in sustainable crop improvement is the next step towards innovative and scalable advances in agricultural practice.
Additional Links: PMID-42413113
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@article {pmid42413113,
year = {2026},
author = {Farago, GC and Grajales, RD and Yost, CK},
title = {Crop domestication, selective breeding, and the seed microbiome: a call for further research.},
journal = {Canadian journal of microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1139/cjm-2026-0018},
pmid = {42413113},
issn = {1480-3275},
abstract = {Plants have been domesticated for thousands of years and subject to human derived selection for desirable traits such as improved yield, disease tolerance, nutrient content, and palatability.Advancements in high-throughput DNA sequencing advancements have allowed researchers to study the diversity of the seed microbiome. We reviewed the literature and identified articles that investigated the impact of domestication on seed microbiome diversity of various plant species.The resultant analysis suggests that the impacts of domestication and selective breeding on seed microbiome diversity are variable and inconclusive due to the low number of independent studies per species and the limited diversity of domesticated species examined. Based upon our analysis we suggest a need for standardized methodology and bioinformatic analysis to accompany further research on seed development of domesticated crop species. Understanding the mechanisms that influence plantmicrobe interactions, such as microbial colonization during seed development, and their applications in sustainable crop improvement is the next step towards innovative and scalable advances in agricultural practice.},
}
RevDate: 2026-07-07
Unlocking the biotechnological potential of traditional fermented food microbiomes.
Current opinion in biotechnology, 100:103550 pii:S0958-1669(26)00115-1 [Epub ahead of print].
Fermented foods are a globally important source of dietary microbes, cultural heritage, and functional diversity, yet current microbiome research captures only a narrow fraction of this richness. Public sequencing datasets are heavily skewed toward a limited set of regions and fermentation types, leaving vast areas of geographic, substrate, and process diversity underrepresented. This imbalance constrains the discovery of novel microbial species, enzymes, and biosynthetic capacities, and risks accelerating homogenization through standardized starter cultures. We argue that coordinated, ethically grounded global efforts integrating metagenomics, multi-omics, standardized metadata, and biobanking are urgently needed to document, preserve, and responsibly leverage fermented food microbial diversity for sustainable food systems and innovation.
Additional Links: PMID-42413135
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@article {pmid42413135,
year = {2026},
author = {Hernández-Velázquez, R and Bokulich, NA},
title = {Unlocking the biotechnological potential of traditional fermented food microbiomes.},
journal = {Current opinion in biotechnology},
volume = {100},
number = {},
pages = {103550},
doi = {10.1016/j.copbio.2026.103550},
pmid = {42413135},
issn = {1879-0429},
abstract = {Fermented foods are a globally important source of dietary microbes, cultural heritage, and functional diversity, yet current microbiome research captures only a narrow fraction of this richness. Public sequencing datasets are heavily skewed toward a limited set of regions and fermentation types, leaving vast areas of geographic, substrate, and process diversity underrepresented. This imbalance constrains the discovery of novel microbial species, enzymes, and biosynthetic capacities, and risks accelerating homogenization through standardized starter cultures. We argue that coordinated, ethically grounded global efforts integrating metagenomics, multi-omics, standardized metadata, and biobanking are urgently needed to document, preserve, and responsibly leverage fermented food microbial diversity for sustainable food systems and innovation.},
}
RevDate: 2026-07-07
The effects of cold temperature on the development, microbiome, and transcriptome of the sea anemone Nematostella vectensis.
Comparative biochemistry and physiology. Part D, Genomics & proteomics, 60:101928 pii:S1744-117X(26)00187-5 [Epub ahead of print].
Thermal conditions impact essentially all aspects of the physiology for ectotherms. While the effects of high temperatures have been widely studied, cold temperature effects on aquatic invertebrates and their microbial communities have been poorly characterized. To determine the diverse effects of exposure to cold temperatures, we assessed acute and long-term impacts of ecologically relevant low temperatures on the development, microbiome, and gene expression of the sea anemone Nematostella vectensis. Two hours post fertilization, embryos were exposed to temperatures from 4°C to 35°C and development rate to the juvenile stage was quantified. We found temperature impacts the development rate of embryos, where lower temperatures extended development time and resulted in mortality below 10°C. For both microbiome and host transcriptomic responses, anemones were held at 20°C, 10°C, and 0°C and compared at 24 hours and 7 days. Extended exposures to colder temperatures caused restructuring of the host-associated microbiome, with the loss of common taxonomic groups from the class Bacteroidia and Bacilli. Lastly, cold stress induced significant changes in gene expression, which were more pronounced at the 10°C than 0°C but showed little change over time in each temperature. Interestingly, expression of genes associated with innate immunity were among the most differentially expressed genes including heat shock proteins and innate immune genes providing a potential host-imposed mechanism to explain the shift in the microbiome. Overall, cold temperatures have broad effects on many facets of this sea anemone and its microbial community and indicate the importance of cold temperature events when characterizing how ectotherms acclimate to thermal variation.
Additional Links: PMID-42413177
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PubMed:
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@article {pmid42413177,
year = {2026},
author = {Krueger, Q and Kennedy, C and Clark, J and Reitzel, AM},
title = {The effects of cold temperature on the development, microbiome, and transcriptome of the sea anemone Nematostella vectensis.},
journal = {Comparative biochemistry and physiology. Part D, Genomics & proteomics},
volume = {60},
number = {},
pages = {101928},
doi = {10.1016/j.cbd.2026.101928},
pmid = {42413177},
issn = {1878-0407},
abstract = {Thermal conditions impact essentially all aspects of the physiology for ectotherms. While the effects of high temperatures have been widely studied, cold temperature effects on aquatic invertebrates and their microbial communities have been poorly characterized. To determine the diverse effects of exposure to cold temperatures, we assessed acute and long-term impacts of ecologically relevant low temperatures on the development, microbiome, and gene expression of the sea anemone Nematostella vectensis. Two hours post fertilization, embryos were exposed to temperatures from 4°C to 35°C and development rate to the juvenile stage was quantified. We found temperature impacts the development rate of embryos, where lower temperatures extended development time and resulted in mortality below 10°C. For both microbiome and host transcriptomic responses, anemones were held at 20°C, 10°C, and 0°C and compared at 24 hours and 7 days. Extended exposures to colder temperatures caused restructuring of the host-associated microbiome, with the loss of common taxonomic groups from the class Bacteroidia and Bacilli. Lastly, cold stress induced significant changes in gene expression, which were more pronounced at the 10°C than 0°C but showed little change over time in each temperature. Interestingly, expression of genes associated with innate immunity were among the most differentially expressed genes including heat shock proteins and innate immune genes providing a potential host-imposed mechanism to explain the shift in the microbiome. Overall, cold temperatures have broad effects on many facets of this sea anemone and its microbial community and indicate the importance of cold temperature events when characterizing how ectotherms acclimate to thermal variation.},
}
RevDate: 2026-07-07
β-sitosterol and next-generation neuroprotection for multi-target strategies and the gut-brain axis in neurodegenerative diseases.
The Journal of steroid biochemistry and molecular biology, 264:107080 pii:S0960-0760(26)00146-9 [Epub ahead of print].
Neurodegenerative disorders such as Alzheimer's and Parkinson's diseases arise from complex interactions among oxidative stress, neuroinflammation, metabolic dysfunction, and dysregulated signaling networks. This review aim of the synthesize mechanistic evidence on β-sitosterol as a multi-target phytochemical and clarify how its actions connect to gut-brain axis modulation in neurodegeneration. The integrated mechanistic framework linking β-sitosterol's effects on cholesterol homeostasis, neuroinflammation, mitochondrial function, cholinergic signaling, and microbiota-barrier integrity to cognitive outcomes. Scope: preclinical and early translational evidence on β-sitosterol alone and with complementary phytochemicals, including nano-delivery strategies. Increasing evidence highlights phytochemicals as promising multi-target therapeutic agents capable of modulating these interconnected pathological processes. β-Sitosterol exhibits broad activity by regulating cholesterol metabolism, suppressing neuroinflammation, restoring redox balance, preserving mitochondrial function, and inhibiting important Alzheimer's diseases targets, including acetylcholinesterase and butyrylcholinesterase. The mechanisms action of β-sitosterol may (i) dampen microglial activation via TLR4/NF-κB signaling, (ii) activate Nrf2-dependent antioxidant responses (Nrf2/HO-1), (iii) support mitochondrial function and reduce ROS, (iv) stabilize membrane cholesterol and modulate amyloidogenic processing, and (v) inhibit acetylcholinesterase/butyrylcholinesterase to restore cholinergic tone. Complementary showing a neuroprotective effect actions of other phytochemicals such as curcumin, resveratrol, sulforaphane, and sinapic acid further enhance neuroprotection by modulating pathways like Nrf2/HO-1, TLR4/NF-κB, PI3K/Akt, and autophagy. Collectively, preclinical studies demonstrate that diverse botanical extracts significantly improve cognitive performance, reduce amyloid burden, restore cholinergic function, and attenuate neuroinflammation and oxidative damage. Emerging preclinical evidence suggests in rodent models of amyloid pathology, β-sitosterol (5-50 mg/kg) has been reported to improve memory in behavioral tests and reduce markers of neuroinflammation and oxidative stress; gut-brain effects include microbiota remodeling and enhanced barrier integrity, which correlate with reduced neuroimmune activation. Advances in nano-delivery systems and functional food formulations substantially improve phytochemical stability, bioavailability, and brain targeting. Available evidence is chiefly preclinical; clinical translation will require standardized dosing, pharmacokinetic and blood-brain barrier penetration studies, and randomized trials with microbiome and cognitive endpoints. Collectively, these findings position phytochemicals as promising candidates for multi-target disease modification and the development of next-generation neurotherapeutic strategies.
Additional Links: PMID-42413380
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PubMed:
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@article {pmid42413380,
year = {2026},
author = {Sivalingam, AM},
title = {β-sitosterol and next-generation neuroprotection for multi-target strategies and the gut-brain axis in neurodegenerative diseases.},
journal = {The Journal of steroid biochemistry and molecular biology},
volume = {264},
number = {},
pages = {107080},
doi = {10.1016/j.jsbmb.2026.107080},
pmid = {42413380},
issn = {1879-1220},
abstract = {Neurodegenerative disorders such as Alzheimer's and Parkinson's diseases arise from complex interactions among oxidative stress, neuroinflammation, metabolic dysfunction, and dysregulated signaling networks. This review aim of the synthesize mechanistic evidence on β-sitosterol as a multi-target phytochemical and clarify how its actions connect to gut-brain axis modulation in neurodegeneration. The integrated mechanistic framework linking β-sitosterol's effects on cholesterol homeostasis, neuroinflammation, mitochondrial function, cholinergic signaling, and microbiota-barrier integrity to cognitive outcomes. Scope: preclinical and early translational evidence on β-sitosterol alone and with complementary phytochemicals, including nano-delivery strategies. Increasing evidence highlights phytochemicals as promising multi-target therapeutic agents capable of modulating these interconnected pathological processes. β-Sitosterol exhibits broad activity by regulating cholesterol metabolism, suppressing neuroinflammation, restoring redox balance, preserving mitochondrial function, and inhibiting important Alzheimer's diseases targets, including acetylcholinesterase and butyrylcholinesterase. The mechanisms action of β-sitosterol may (i) dampen microglial activation via TLR4/NF-κB signaling, (ii) activate Nrf2-dependent antioxidant responses (Nrf2/HO-1), (iii) support mitochondrial function and reduce ROS, (iv) stabilize membrane cholesterol and modulate amyloidogenic processing, and (v) inhibit acetylcholinesterase/butyrylcholinesterase to restore cholinergic tone. Complementary showing a neuroprotective effect actions of other phytochemicals such as curcumin, resveratrol, sulforaphane, and sinapic acid further enhance neuroprotection by modulating pathways like Nrf2/HO-1, TLR4/NF-κB, PI3K/Akt, and autophagy. Collectively, preclinical studies demonstrate that diverse botanical extracts significantly improve cognitive performance, reduce amyloid burden, restore cholinergic function, and attenuate neuroinflammation and oxidative damage. Emerging preclinical evidence suggests in rodent models of amyloid pathology, β-sitosterol (5-50 mg/kg) has been reported to improve memory in behavioral tests and reduce markers of neuroinflammation and oxidative stress; gut-brain effects include microbiota remodeling and enhanced barrier integrity, which correlate with reduced neuroimmune activation. Advances in nano-delivery systems and functional food formulations substantially improve phytochemical stability, bioavailability, and brain targeting. Available evidence is chiefly preclinical; clinical translation will require standardized dosing, pharmacokinetic and blood-brain barrier penetration studies, and randomized trials with microbiome and cognitive endpoints. Collectively, these findings position phytochemicals as promising candidates for multi-target disease modification and the development of next-generation neurotherapeutic strategies.},
}
RevDate: 2026-07-07
Barrier restoration as a therapeutic strategy for disorders of gut-brain interaction.
The lancet. Gastroenterology & hepatology pii:S2468-1253(26)00081-6 [Epub ahead of print].
Disorders of gut-brain interaction, such as irritable bowel syndrome and functional dyspepsia, are increasingly linked to defects in gut barrier function. Mucosal disruption, encompassing alterations in the epithelial and mucus layers, leads to enhanced intestinal permeability, microbial translocation, and aberrant immune and neuronal signalling, potentially contributing to symptom severity. Despite growing recognition of barrier dysfunction in disorders of gut-brain interaction, clinical interventions remain largely symptom-based, with few therapies designed to directly restore epithelial integrity. In this Review, we examine the cellular and molecular pathways underpinning gut barrier function and highlight evidence supporting the role of diet, microbiome-targeted interventions, stress modulation, and pharmacological agents in maintaining or restoring intestinal permeability. Mechanistic insights reveal that short-chain fatty acids, amino acids (glutamine and tryptophan), and targeted probiotics can enhance tight junction integrity and mucin secretion, whereas psychological stress, low-fibre diets, and high-fat diets disrupt these pathways. We also discuss novel therapeutics, including antihistamines, mast cell stabilisers, protease inhibitors, secretagogues, and guanylate cyclase C agonists, and emerging technologies, such as vagal nerve stimulation and barrier-protective hydrogel delivery systems. Although promising, these strategies require validation in well designed clinical trials with targeted endpoints, and patient stratification based on microbial and immune phenotypes. By integrating advances in molecular biology with translational therapeutics, interventions targeting intestinal permeability could shift the treatment paradigm for disorders of gut-brain interaction from general symptom management to personalised disease modification.
Additional Links: PMID-42413530
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@article {pmid42413530,
year = {2026},
author = {Britton, TA and Grover, M},
title = {Barrier restoration as a therapeutic strategy for disorders of gut-brain interaction.},
journal = {The lancet. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/S2468-1253(26)00081-6},
pmid = {42413530},
issn = {2468-1253},
abstract = {Disorders of gut-brain interaction, such as irritable bowel syndrome and functional dyspepsia, are increasingly linked to defects in gut barrier function. Mucosal disruption, encompassing alterations in the epithelial and mucus layers, leads to enhanced intestinal permeability, microbial translocation, and aberrant immune and neuronal signalling, potentially contributing to symptom severity. Despite growing recognition of barrier dysfunction in disorders of gut-brain interaction, clinical interventions remain largely symptom-based, with few therapies designed to directly restore epithelial integrity. In this Review, we examine the cellular and molecular pathways underpinning gut barrier function and highlight evidence supporting the role of diet, microbiome-targeted interventions, stress modulation, and pharmacological agents in maintaining or restoring intestinal permeability. Mechanistic insights reveal that short-chain fatty acids, amino acids (glutamine and tryptophan), and targeted probiotics can enhance tight junction integrity and mucin secretion, whereas psychological stress, low-fibre diets, and high-fat diets disrupt these pathways. We also discuss novel therapeutics, including antihistamines, mast cell stabilisers, protease inhibitors, secretagogues, and guanylate cyclase C agonists, and emerging technologies, such as vagal nerve stimulation and barrier-protective hydrogel delivery systems. Although promising, these strategies require validation in well designed clinical trials with targeted endpoints, and patient stratification based on microbial and immune phenotypes. By integrating advances in molecular biology with translational therapeutics, interventions targeting intestinal permeability could shift the treatment paradigm for disorders of gut-brain interaction from general symptom management to personalised disease modification.},
}
RevDate: 2026-07-07
Clinical and molecular improvements in pediatric patients with atopic dermatitis treated with dupilumab: an analysis from the TREATKids registry.
The Journal of investigative dermatology pii:S0022-202X(26)02663-1 [Epub ahead of print].
Real-world evidence on clinical and molecular outcomes of systemic therapy for pediatric atopic dermatitis remains limited. Within the prospective TREATkids registry, we conducted an observational analysis of children and adolescents treated with Dupilumab in routine care. Baseline data from 200 and follow-up data from 124 patients were evaluated for clinician- and patient-/caregiver-reported outcomes, alongside with epidermal proteomic profiling using tape strips and the Olink® Explore Inflammation 384 (n=20) panel and 16S rRNA gene sequencing for skin microbiome assessment in subsets (n=48). At treatment initiation, disease burden was high (mean EASI 16.5; oSCORAD 44.9; peak itch PP-NRS 6.6). By month 3, EASI50/75/90 response rates were 87%, 60%, and 30%. Response rates at months 6 and 12 were generally consistent with those observed at month 3, with no discontinuations and conjunctivitis in 4.0%. Proteomic analyses demonstrated marked baseline upregulation of alarmins, Th2 chemokines, and tissue-remodeling markers in lesional skin, followed by downregulation of 144/161 dysregulated proteins at month 3, including CCL17/TARC, CXCL8, IL-6, IL-18, and MMPs. Microbiome profiling showed baseline dysbiosis with Staphylococcus aureus overabundance and reduced α-diversity, normalizing toward a non-lesional-like state after therapy at month 3. Overall, dupilumab was associated with rapid, sustained clinical and molecular improvement.
Additional Links: PMID-42413573
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PubMed:
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@article {pmid42413573,
year = {2026},
author = {Fonfara, M and Stölzl, D and Hartmann, J and Harder, I and Kind, B and Heinrich, L and Abraham, S and Gerdes, S and Gappa, M and Kleinheinz, A and Neustädter, I and Heratizadeh, A and Kerzel, S and Wollenberg, A and Mann, C and Asefi, M and Nemat, K and Vogelberg, C and Ott, H and Schaub, B and Werfel, T and Schmitt, J and Weidinger, S},
title = {Clinical and molecular improvements in pediatric patients with atopic dermatitis treated with dupilumab: an analysis from the TREATKids registry.},
journal = {The Journal of investigative dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jid.2026.06.1283},
pmid = {42413573},
issn = {1523-1747},
abstract = {Real-world evidence on clinical and molecular outcomes of systemic therapy for pediatric atopic dermatitis remains limited. Within the prospective TREATkids registry, we conducted an observational analysis of children and adolescents treated with Dupilumab in routine care. Baseline data from 200 and follow-up data from 124 patients were evaluated for clinician- and patient-/caregiver-reported outcomes, alongside with epidermal proteomic profiling using tape strips and the Olink® Explore Inflammation 384 (n=20) panel and 16S rRNA gene sequencing for skin microbiome assessment in subsets (n=48). At treatment initiation, disease burden was high (mean EASI 16.5; oSCORAD 44.9; peak itch PP-NRS 6.6). By month 3, EASI50/75/90 response rates were 87%, 60%, and 30%. Response rates at months 6 and 12 were generally consistent with those observed at month 3, with no discontinuations and conjunctivitis in 4.0%. Proteomic analyses demonstrated marked baseline upregulation of alarmins, Th2 chemokines, and tissue-remodeling markers in lesional skin, followed by downregulation of 144/161 dysregulated proteins at month 3, including CCL17/TARC, CXCL8, IL-6, IL-18, and MMPs. Microbiome profiling showed baseline dysbiosis with Staphylococcus aureus overabundance and reduced α-diversity, normalizing toward a non-lesional-like state after therapy at month 3. Overall, dupilumab was associated with rapid, sustained clinical and molecular improvement.},
}
RevDate: 2026-07-07
AI/ML-Enabled Multi-Omics Integration of Host Genetics, Immunity, and the Gut Microbiome in Crohn's Disease: From Diagnosis to Theranostics.
SLAS technology pii:S2472-6303(26)00066-X [Epub ahead of print].
Crohn's disease is a long-term inflammatory disorder arising from the interaction of genetic risk factors, immune system dysfunction, and alterations in gut microbiota. Variability in clinical phenotypes and lack of biomarker specificity hinder the efficiency of current traditional diagnostic and treatment approaches. This review aims to assess how AI- and ML-driven multi-omics offer comprehensive insights into pathogenicity, thereby enhancing diagnostic techniques and personalized therapeutic approaches in CD. Current studies employ integration of multi-omics like genomics, proteomics, transcriptomics, metabolomics, and microbiome analysis in CD with AI and ML for significant advancement of biomarker discovery and clinical applications. Emerging evidence reveals that CD is a multi-factorial disorder involving host genetics, immune dysfunction, and microbiome shifts. Integration of advanced AI/ML models with multi-omics data can predict disease-specific biomarkers for easy diagnosis and facilitate precision medicine to enhance therapies. For a successful clinical implementation of an AI/ML model with multi-omics in CD, a standardized data framework and large-scale validation are needed. Additionally, future research should focus on developing interpretable AI models, real-time monitoring systems, and theranostic platforms to enhance precision healthcare delivery.
Additional Links: PMID-42413620
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@article {pmid42413620,
year = {2026},
author = {Kedari, N and Dey, U and Sreenija, D and Paul, S and Shakya, S and Biswas, R and Ramaiah, S and Anbarasu, A},
title = {AI/ML-Enabled Multi-Omics Integration of Host Genetics, Immunity, and the Gut Microbiome in Crohn's Disease: From Diagnosis to Theranostics.},
journal = {SLAS technology},
volume = {},
number = {},
pages = {100452},
doi = {10.1016/j.slast.2026.100452},
pmid = {42413620},
issn = {2472-6311},
abstract = {Crohn's disease is a long-term inflammatory disorder arising from the interaction of genetic risk factors, immune system dysfunction, and alterations in gut microbiota. Variability in clinical phenotypes and lack of biomarker specificity hinder the efficiency of current traditional diagnostic and treatment approaches. This review aims to assess how AI- and ML-driven multi-omics offer comprehensive insights into pathogenicity, thereby enhancing diagnostic techniques and personalized therapeutic approaches in CD. Current studies employ integration of multi-omics like genomics, proteomics, transcriptomics, metabolomics, and microbiome analysis in CD with AI and ML for significant advancement of biomarker discovery and clinical applications. Emerging evidence reveals that CD is a multi-factorial disorder involving host genetics, immune dysfunction, and microbiome shifts. Integration of advanced AI/ML models with multi-omics data can predict disease-specific biomarkers for easy diagnosis and facilitate precision medicine to enhance therapies. For a successful clinical implementation of an AI/ML model with multi-omics in CD, a standardized data framework and large-scale validation are needed. Additionally, future research should focus on developing interpretable AI models, real-time monitoring systems, and theranostic platforms to enhance precision healthcare delivery.},
}
RevDate: 2026-07-07
Gut microbiome-mediated modulation of the glioblastoma tumor microenvironment for enhanced immunotherapy response: Mechanistic insights and future perspectives.
Cellular signalling pii:S0898-6568(26)00382-7 [Epub ahead of print].
Glioblastoma (GBM) is known to be one of the most aggressive and deadly brain tumors in adults, with a very poor prognosis. An immunosuppressive tumor microenvironment, the blood-brain barrier's (BBB's) protective nature, and genetic heterogeneity mediate resistance to conventional treatments, such as immune checkpoint inhibitors. Recent studies have shed light on the important role of the gut-brain axis in regulating GBM pathogenesis. Studies have demonstrated that patients with GBM frequently exhibit gut dysbiosis, with limited beneficial microbial populations, thereby enhancing immunosuppression and reducing the effectiveness of immune checkpoint inhibitors. This is mediated by SCFAs derived from the gut microbiota, such as acetate, propionate, and butyrate, which influence CNS immunity through direct effects on immune cells and processes, including HDAC inhibition. SCFAs can enhance the proliferation of anti-inflammatory T regulatory cells, promote pro-inflammatory responses from microglia and tumor-associated macrophages, and fortify the integrity of the BBB. Also, certain bacteria belonging to the genera Blautia and Bifidobacterium have been found to enhance the recruitment of anti-tumor CD8+ cytotoxic T lymphocytes. Thus, FMT, probiotics, prebiotics, and high-fiber diets are very promising adjuvant strategies to overcome GBM resistance by therapeutically enhancing the gut microbiome. This will aid in restoring microbial resilience, optimizing SCFA production, and potentiating anti-tumor immune responses. To validate microbial biomarkers and causative pathways, future advances in this field will integrate multi-omics data with robust clinical trials. Moreover, to examine how the gut microbiome influences the glioblastoma tumor microenvironment and the response to immunotherapy, this narrative review synthesizes existing data from studies of GBM patients, experimental models, and neuroimmunology research.
Additional Links: PMID-42413643
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PubMed:
Citation:
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@article {pmid42413643,
year = {2026},
author = {Dey, U and Madabhushi, LP and Chacko, AA and Gopalakrishnan, AV and Santhanam, R and Gajendran, B},
title = {Gut microbiome-mediated modulation of the glioblastoma tumor microenvironment for enhanced immunotherapy response: Mechanistic insights and future perspectives.},
journal = {Cellular signalling},
volume = {},
number = {},
pages = {112726},
doi = {10.1016/j.cellsig.2026.112726},
pmid = {42413643},
issn = {1873-3913},
abstract = {Glioblastoma (GBM) is known to be one of the most aggressive and deadly brain tumors in adults, with a very poor prognosis. An immunosuppressive tumor microenvironment, the blood-brain barrier's (BBB's) protective nature, and genetic heterogeneity mediate resistance to conventional treatments, such as immune checkpoint inhibitors. Recent studies have shed light on the important role of the gut-brain axis in regulating GBM pathogenesis. Studies have demonstrated that patients with GBM frequently exhibit gut dysbiosis, with limited beneficial microbial populations, thereby enhancing immunosuppression and reducing the effectiveness of immune checkpoint inhibitors. This is mediated by SCFAs derived from the gut microbiota, such as acetate, propionate, and butyrate, which influence CNS immunity through direct effects on immune cells and processes, including HDAC inhibition. SCFAs can enhance the proliferation of anti-inflammatory T regulatory cells, promote pro-inflammatory responses from microglia and tumor-associated macrophages, and fortify the integrity of the BBB. Also, certain bacteria belonging to the genera Blautia and Bifidobacterium have been found to enhance the recruitment of anti-tumor CD8+ cytotoxic T lymphocytes. Thus, FMT, probiotics, prebiotics, and high-fiber diets are very promising adjuvant strategies to overcome GBM resistance by therapeutically enhancing the gut microbiome. This will aid in restoring microbial resilience, optimizing SCFA production, and potentiating anti-tumor immune responses. To validate microbial biomarkers and causative pathways, future advances in this field will integrate multi-omics data with robust clinical trials. Moreover, to examine how the gut microbiome influences the glioblastoma tumor microenvironment and the response to immunotherapy, this narrative review synthesizes existing data from studies of GBM patients, experimental models, and neuroimmunology research.},
}
RevDate: 2026-07-07
Temporal response patterns of swine gut microbiota to arabinoxylan.
Journal of advanced research pii:S2090-1232(26)00539-4 [Epub ahead of print].
INTRODUCTION: Arabinoxylan (AX) is a major dietary fiber that is depolymerized and fermented by gut microbiota to produce short-chain fatty acids (SCFAs), thereby influencing host energy harvest and gut homeostasis. However, it remains unclear how baseline differences in the gut microbiota among individuals shape the temporal dynamics and metabolic outcomes of AX fermentation.
OBJECTIVES: This study aimed to investigate how preexisting variation in swine gut microbial ecosystems affects the utilization of AX.
METHODS: We employed an in vitro fermentation model inoculated with fecal microbiota from two genetically divergent pig breeds: Jinhua (JH, a native breed) and Duroc × Landrace × Yorkshire (DLY, a commercial crossbred). Microbial succession was characterized by 16S rRNA gene amplicon sequencing coupled with time-series clustering, co-occurrence network reconstruction, and co-abundance response groups (CARGs) analysis. We used PICRUSt2 to predict the functional potential of the microbial communities and assessed fermentation outputs by measuring pH, SCFA concentrations, and key enzyme activities.
RESULTS: JH and DLY maintained distinct baseline community structures and displayed pronounced, stage-dependent succession during AX fermentation, with most structural changes occurring within 24 h. The JH microbiota consistently exhibited higher α-diversity than DLY, driven by enrichment of fiber-degrading bacteria. Functional prediction identified the pentose and glucuronate interconversion pathways as key functional differences between the two microbial ecosystems. CARG analysis revealed a consortium of Limosilactobacillus species (L. mucosae, L. balticus, L. agrestimuris) and Lactobacillus delbrueckii subsp. jakobsenii as keystone taxa positively correlated with acetate production.
CONCLUSION: Our findings elucidate temporal ecological principles governing AX metabolism by distinct swine gut microbial communities and identify key microbial players, offering a basis for developing microbiome-targeted nutritional strategies.
Additional Links: PMID-42413654
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42413654,
year = {2026},
author = {Wei, S and Zhang, H and Liu, Y and Chen, N and Li, S and Zhu, SJ and Zong, X and Wang, Y and Jin, M},
title = {Temporal response patterns of swine gut microbiota to arabinoxylan.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.07.021},
pmid = {42413654},
issn = {2090-1224},
abstract = {INTRODUCTION: Arabinoxylan (AX) is a major dietary fiber that is depolymerized and fermented by gut microbiota to produce short-chain fatty acids (SCFAs), thereby influencing host energy harvest and gut homeostasis. However, it remains unclear how baseline differences in the gut microbiota among individuals shape the temporal dynamics and metabolic outcomes of AX fermentation.
OBJECTIVES: This study aimed to investigate how preexisting variation in swine gut microbial ecosystems affects the utilization of AX.
METHODS: We employed an in vitro fermentation model inoculated with fecal microbiota from two genetically divergent pig breeds: Jinhua (JH, a native breed) and Duroc × Landrace × Yorkshire (DLY, a commercial crossbred). Microbial succession was characterized by 16S rRNA gene amplicon sequencing coupled with time-series clustering, co-occurrence network reconstruction, and co-abundance response groups (CARGs) analysis. We used PICRUSt2 to predict the functional potential of the microbial communities and assessed fermentation outputs by measuring pH, SCFA concentrations, and key enzyme activities.
RESULTS: JH and DLY maintained distinct baseline community structures and displayed pronounced, stage-dependent succession during AX fermentation, with most structural changes occurring within 24 h. The JH microbiota consistently exhibited higher α-diversity than DLY, driven by enrichment of fiber-degrading bacteria. Functional prediction identified the pentose and glucuronate interconversion pathways as key functional differences between the two microbial ecosystems. CARG analysis revealed a consortium of Limosilactobacillus species (L. mucosae, L. balticus, L. agrestimuris) and Lactobacillus delbrueckii subsp. jakobsenii as keystone taxa positively correlated with acetate production.
CONCLUSION: Our findings elucidate temporal ecological principles governing AX metabolism by distinct swine gut microbial communities and identify key microbial players, offering a basis for developing microbiome-targeted nutritional strategies.},
}
RevDate: 2026-07-07
Gut Microbiome-Modulating Therapeutics and Lipid Profile in Metabolic Syndrome: A Systematic Review and Meta-Analysis of Clinical Trials.
Clinical nutrition ESPEN pii:S2405-4577(26)00558-9 [Epub ahead of print].
OBJECTIVES: To evaluate the effects of gut microbiome-modulating interventions (probiotics, prebiotics, synbiotics, and fecal microbiota transplantation) on lipid profile parameters in adults with metabolic syndrome (MetS).
DESIGN AND DATA SOURCES: Systematic review and random-effects meta-analysis with univariate meta-regression of controlled clinical trials indexed in PubMed, Web of Science, and Scopus through June 2025.
ELIGIBILITY CRITERIA: Controlled clinical trials in adults with MetS diagnosed according to ATP III, IDF, or WHO criteria reporting at least one lipid outcome (total cholestrol (TC), low-density lipoprotein cholestrol (LDL-C), high desntiry lipoprotein cholestrol (HDL-C), or triglycerdies (TG)). Studies without control groups, insufficient data, or populations not meeting full MetS criteria were excluded.
DATA EXTRACTION AND SYNTHESIS: Two reviewers independently screened and extracted data. Risk of bias was assessed using the Cochrane RoB 2 tool. Random-effects meta-analysis (DerSimonian-Laird) generated pooled mean differences (MDs) with 95% confidence intervals (CIs). Heterogeneity was assessed using I[2] statistics. Meta-regression evaluated moderators including age, baseline BMI, intervention dose, duration, and geographic region.
RESULTS: Nineteen studies comprising 21 trial comparisons and 897 participants were included. Microbiome-modulating interventions were associated with reductions in TC (MD -8.97 mg/dL; 95% CI -12.55 to -5.38) and TG (MD -11.33 mg/dL; 95% CI -19.25 to -3.40), while HDL-C showed no significant change. LDL-C was also reduced in the primary pooled analysis (MD -5.05 mg/dL; 95% CI -9.57 to -0.53); however, this finding should be interpreted cautiously because of substantial between-study heterogeneity (I[2] = 73.8%) and loss of statistical significance in sensitivity analyses. Greater lipid reductions were generally observed in trials using higher probiotic doses and longer intervention durations, although moderator effects were not consistent across all lipid outcomes.
CONCLUSIONS: Microbiome-modulating interventions are associated with modest improvements in selected lipid parameters in adults with metabolic syndrome, particularly TC and TG. Evidence for LDL-C reduction is less robust because of substantial heterogeneity and sensitivity to analytical assumptions. Larger, well-standardized clinical trials are required to confirm lipid-specific effects, identify responsive populations, and determine the clinical relevance of these interventions.
Additional Links: PMID-42413732
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42413732,
year = {2026},
author = {Paul, P and Kaul, R and Ayyan, M and Lakshmanan, AP and Chaari, A},
title = {Gut Microbiome-Modulating Therapeutics and Lipid Profile in Metabolic Syndrome: A Systematic Review and Meta-Analysis of Clinical Trials.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {103461},
doi = {10.1016/j.clnesp.2026.103461},
pmid = {42413732},
issn = {2405-4577},
abstract = {OBJECTIVES: To evaluate the effects of gut microbiome-modulating interventions (probiotics, prebiotics, synbiotics, and fecal microbiota transplantation) on lipid profile parameters in adults with metabolic syndrome (MetS).
DESIGN AND DATA SOURCES: Systematic review and random-effects meta-analysis with univariate meta-regression of controlled clinical trials indexed in PubMed, Web of Science, and Scopus through June 2025.
ELIGIBILITY CRITERIA: Controlled clinical trials in adults with MetS diagnosed according to ATP III, IDF, or WHO criteria reporting at least one lipid outcome (total cholestrol (TC), low-density lipoprotein cholestrol (LDL-C), high desntiry lipoprotein cholestrol (HDL-C), or triglycerdies (TG)). Studies without control groups, insufficient data, or populations not meeting full MetS criteria were excluded.
DATA EXTRACTION AND SYNTHESIS: Two reviewers independently screened and extracted data. Risk of bias was assessed using the Cochrane RoB 2 tool. Random-effects meta-analysis (DerSimonian-Laird) generated pooled mean differences (MDs) with 95% confidence intervals (CIs). Heterogeneity was assessed using I[2] statistics. Meta-regression evaluated moderators including age, baseline BMI, intervention dose, duration, and geographic region.
RESULTS: Nineteen studies comprising 21 trial comparisons and 897 participants were included. Microbiome-modulating interventions were associated with reductions in TC (MD -8.97 mg/dL; 95% CI -12.55 to -5.38) and TG (MD -11.33 mg/dL; 95% CI -19.25 to -3.40), while HDL-C showed no significant change. LDL-C was also reduced in the primary pooled analysis (MD -5.05 mg/dL; 95% CI -9.57 to -0.53); however, this finding should be interpreted cautiously because of substantial between-study heterogeneity (I[2] = 73.8%) and loss of statistical significance in sensitivity analyses. Greater lipid reductions were generally observed in trials using higher probiotic doses and longer intervention durations, although moderator effects were not consistent across all lipid outcomes.
CONCLUSIONS: Microbiome-modulating interventions are associated with modest improvements in selected lipid parameters in adults with metabolic syndrome, particularly TC and TG. Evidence for LDL-C reduction is less robust because of substantial heterogeneity and sensitivity to analytical assumptions. Larger, well-standardized clinical trials are required to confirm lipid-specific effects, identify responsive populations, and determine the clinical relevance of these interventions.},
}
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Fossils of miniature humans (hobbits) discovered in Indonesia
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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.