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Tag: Microbiome & Microbiology

  • Gut microbiome may affect colorectal cancer immunotherapy response

    Gut microbiome may affect colorectal cancer immunotherapy response

    What the study found

    The review says the gut microbiome appears to influence how colorectal cancer responds to immune checkpoint inhibitors, especially by affecting resistance in mismatch repair-proficient, microsatellite-stable disease. It also reports that microbiome-based interventions may help restore immune function and support antitumor responses.

    Why the authors say this matters

    The authors conclude that microbiome-based approaches may be a promising adjunct to colorectal cancer immunotherapy. They also say this area needs rigorous clinical trials and mechanistic validation before routine clinical use.

    What the researchers tested

    This was a narrative review, so the authors summarized preclinical and clinical studies rather than testing a new intervention themselves. They focused on the gut microbiome, immune checkpoint inhibitors, and microbiome-based interventions such as probiotics, fecal microbiota transplantation, dietary modulation, and traditional medicines.

    What worked and what didn't

    The review reports that dysbiosis, an imbalance in the gut microbiota, has been linked to treatment resistance, while certain microbial taxa have been associated with stronger antitumor immune responses. It also states that probiotics, fecal microbiota transplantation, diet-based changes, and traditional medicines have shown effects on immune cell populations and immunoregulatory metabolites in preclinical and clinical studies, but findings have been inconsistent.

    What to keep in mind

    The abstract notes inconsistent findings and safety concerns, including infection risks. Because this is a review, the summary is limited to the studies the authors included, and the abstract does not provide detailed trial results or full methodological limits.

    • Immune checkpoint inhibitors are reported to work mainly in mismatch repair-deficient colorectal cancer.
    • Responses in mismatch repair-proficient, microsatellite-stable colorectal cancer remain limited.
    • The gut microbiome is described as a factor in colorectal cancer development, progression, and treatment response.
    • Probiotics, fecal microbiota transplantation, dietary modulation, and traditional medicines are discussed as possible microbiome-based interventions.
    • The abstract notes inconsistent findings and safety concerns, including infection risks.

  • Authors call for more inclusive human microbiome research

    What the study found

    The authors argue that globalizing human microbiome research raises ethical concerns about European and North American dominance. They identify three main concerns: scientific bias toward those populations, limited meaningful community inclusion and ownership, and too little inclusion of diverse global researchers.

    Why the authors say this matters

    The authors suggest these concerns may reproduce a colonial bias and perpetuate inequities in global health research and outcomes. They conclude that more inclusive and participatory microbiome research could benefit global communities, individuals, and researchers, and help decolonize and improve health worldwide.

    What the researchers tested

    The article is a conceptual and ethical discussion rather than a report of an experiment. The authors divide the problem into three concerns and propose three recommendations centered on co-laboration, meaning joint labor among diverse partners across disciplines, cultures, and kinds of knowledge, and co-laborative science, a form of citizen science based on those synergies.

    What worked and what didn't

    The authors present co-laboration and co-laborative science as their proposed responses to the ethical concerns they describe. The abstract does not report empirical testing or measured outcomes, so it does not say what worked in practice or what did not.

    What to keep in mind

    The abstract provides recommendations and a programmatic list, but no study data, sample, or outcome measures are described. The claims and proposals are limited to the ethical issues and solutions stated in the abstract.

    • The authors say human microbiome research is becoming globalized but remains dominated by Europe and North America.
    • They identify three ethical concerns: population bias, weak community inclusion, and limited inclusion of diverse global researchers.
    • They propose co-laboration and co-laborative science as ways to support more inclusive research.
    • The abstract says these ideas are meant to guide ethical human microbiome research and a programmatic list for practice.

  • Maternal HIV infection was linked to altered gut microbes and metabolites

    What the study found

    The study found gut dysbiosis, meaning an imbalance in gut microbes, and distinct plasma metabolomic profiles in women with HIV and their infants compared with seronegative women. It also identified specific microbes and metabolites that differed by HIV status.

    Why the authors say this matters

    The authors conclude that these results suggest potential biological pathways through which HIV affects maternal and infant health. They also note that some of the differentially abundant taxa and metabolites were linked to adverse outcomes such as preterm birth, low birth weight, and inflammation.

    What the researchers tested

    The PRACHITi cohort study followed 244 pregnant women with and without HIV in Pune, India, along with their children through 1 year postpartum. The researchers analyzed longitudinal gut microbiota samples using 16S rRNA sequencing and examined plasma metabolomic profiles during pregnancy, postpartum, and infancy, with more frequent sampling in a sub-study.

    What worked and what didn't

    The study found differences in gut microbiota composition and plasma metabolites by HIV status across pregnancy, postpartum, and infancy. Specific taxa and metabolites were differentially abundant, and some were linked to adverse outcomes mentioned in the abstract.

    What to keep in mind

    The abstract describes secondary objectives from the PRACHITi study and does not provide detailed limitations in the available summary. The findings are based on one cohort in India and on associations reported in the abstract.

    • Women with HIV and their infants showed gut dysbiosis compared with seronegative women.
    • Plasma metabolomic profiles differed by HIV status across pregnancy, postpartum, and infancy.
    • Some taxa and metabolites were associated with preterm birth, low birth weight, and inflammation.
    • The cohort included 244 pregnant women followed with their children through 1 year postpartum.
    • Gut microbiota were assessed with 16S rRNA sequencing.

  • COMT inhibitors alter microbiome-linked L-DOPA metabolism

    What the study found

    The study found that catechol-O-methyltransferase inhibitors, or COMT inhibitors, used with levodopa for Parkinson's disease symptoms can act as antibiotics and alter gut microbiome-related levodopa metabolism. The effects depended on iron availability and varied across human fecal microbial communities.

    Why the authors say this matters

    The authors conclude that the gut microbiome may help mediate drug-drug interactions. The study suggests that microbial features could help predict individual responses to co-prescribed drugs.

    What the researchers tested

    The researchers examined the antibiotic properties of COMT inhibitor drugs in vitro, ex vivo, and in vivo. They also studied how these interactions changed microbiome-mediated levodopa metabolism in vitro and ex vivo, including tests in human fecal microbial communities.

    What worked and what didn't

    In vitro, extracellular iron could drive non-enzymatic inactivation of COMT inhibitors, which rescued COMT inhibitor-mediated bacterial iron starvation responses. At the same time, limiting intracellular iron could protect sensitive bacteria from COMT inhibitor antibiotic activity. When COMT inhibitors and levodopa were co-administered to human fecal microbial communities ex vivo, COMT inhibitor-dependent changes in levodopa metabolism were seen in an individual-specific manner.

    What to keep in mind

    The abstract does not give detailed effect sizes, sample sizes, or clinical outcome data. It also does not describe limitations beyond the scope of the experiments summarized here.

    • COMT inhibitors used with levodopa can alter gut microbiome composition.
    • Iron availability changes COMT inhibitor antibiotic activity in vitro.
    • Extracellular iron can inactivate COMT inhibitors non-enzymatically.
    • Intracellular iron limitation can protect sensitive bacteria from COMT inhibitor activity.
    • Co-administration with levodopa changed microbial levodopa metabolism in an individual-specific way ex vivo.

  • Antibiotic use was linked to long-lasting gut microbiome changes

    What the study found

    Oral antibiotic use was associated with changes in gut microbiome composition, including lower species diversity and altered abundance of some species. The associations were strongest for antibiotic use less than 1 year before fecal sampling, but they were also seen for use 1-4 years and 4-8 years earlier.

    Why the authors say this matters

    The authors conclude that antibiotics may have long-lasting consequences for the gut microbiome. They note this because disruptions in the gut microbiome have been implicated in cardiometabolic disorders and other health outcomes.

    What the researchers tested

    The researchers combined data from the Swedish Prescribed Drug Register with fecal metagenomes from 14,979 adults. They examined associations between oral antibiotic use over 8 years and gut microbiome features using multivariable confounder-adjusted regression models.

    What worked and what didn't

    Antibiotic use less than 1 year before sampling was associated with the greatest reduction in species diversity. Clindamycin, fluoroquinolones, and flucloxacillin accounted for most of the associations with individual species, while penicillin V, extended-spectrum penicillins, and nitrofurantoin were associated with only a few species. Similar results were found when comparing one antibiotic course 4-8 years before sampling with no antibiotic use in the past 8 years.

    What to keep in mind

    The abstract does not describe specific limitations beyond the observational nature of the analysis. The results show associations, not proof that antibiotics caused the microbiome changes.

    • Oral antibiotic use was linked to lower gut microbiome species diversity.
    • The strongest associations were seen when antibiotics were used less than 1 year before sampling.
    • Associations were also present for antibiotic use 1-4 years and 4-8 years earlier.
    • Clindamycin, fluoroquinolones, and flucloxacillin explained most species-level associations.
    • The study included 14,979 adults and combined prescription records with fecal metagenomes.

  • Gut metabolite linked to OXPHOS-related epithelial damage in EAE

    What the study found

    The study found that intestinal epithelial cells and the mucosal barrier were disrupted during experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. This disruption was linked to inhibition of mitochondrial oxidative phosphorylation (OXPHOS), the process cells use to make energy in mitochondria.

    Why the authors say this matters

    The authors conclude that their findings help explain a potential mechanism by which gut microbiota dysbiosis, an imbalance in gut microbes, observed in EAE mice compromises intestinal epithelial integrity and disrupts the mucosal barrier. They present this as relevant to understanding the underlying mechanisms of multiple sclerosis development.

    What the researchers tested

    The researchers used a multi-omics approach, combining proteomic analysis and metabolomic analysis, during EAE induction. They examined small intestinal epithelial cells and cecal contents from EAE mice to look for changes in OXPHOS-related proteins and metabolites.

    What worked and what didn't

    Proteomic analysis showed altered OXPHOS complexes, with a pronounced decrease in cytochrome c oxidase and ATP synthase subunits in small intestinal epithelial cells. Metabolomic analysis showed enrichment of phenyllactic acid, a phenolic acid typically produced by Lactobacillus murinus, in cecal contents, and the study reports that phenyllactic acid downregulated OXPHOS complexes and restrained maximal mitochondrial respiration.

    What to keep in mind

    The available summary does not describe limitations in detail. The findings are reported in experimental autoimmune encephalomyelitis mice, so the abstract does not state whether the same mechanism was directly shown in humans.

    • Intestinal epithelial cells and the mucosal barrier were disrupted during EAE induction.
    • The disruption was linked to inhibition of mitochondrial oxidative phosphorylation.
    • Cytochrome c oxidase and ATP synthase subunits were reduced in small intestinal epithelial cells.
    • Phenyllactic acid was enriched in cecal contents of EAE mice.
    • The study reports that phenyllactic acid downregulated OXPHOS complexes and limited maximal mitochondrial respiration.

  • Wild boar and domestic pig gut microbiomes differ by diet and lifestyle

    What the study found

    The study found that wild boar and domestic pig faecal microbiomes form two main community types linked to diet and lifestyle rather than host species alone. It also found many previously unknown microbial taxa in wild boars and identified species with substantial carbohydrate-degrading potential.

    Why the authors say this matters

    The authors conclude that the wild boar microbiome may be a source of microbes useful for improving fibre degradation in pigs. They also suggest that the curated catalogue of carbohydrate degraders could help guide probiotic supplementation during transitions to more fibrous feedstocks.

    What the researchers tested

    The researchers collected 89 faecal samples from wild boars in four countries and analysed them mainly with metagenomic sequencing, which reads all genetic material in a sample. They assembled metagenome-assembled genomes and compared the results with 125 previously published pig samples, most from domestic pigs.

    What worked and what didn't

    De novo assembly produced 3,288 high- and medium-quality metagenome-assembled genomes representing 968 species, including 538 that were previously unknown. The comparison revealed two community types: one dominated by free-ranging, foraging wild boars and one dominated by captive, fed domestic pigs; the first had lower alpha-diversity, while both types retained substantial carbohydrate utilization potential. The domestic-pig-associated community had a higher relative abundance of carbohydrate-active enzyme sub genes linked to a broader range of carbohydrate classes, while the wild-boar-associated community was enriched in species that were generally richer in these genes and classes.

    What to keep in mind

    The summary does not provide details on experimental validation beyond sequencing and comparative analysis. The findings are based on faecal samples from wild boars and previously published pig samples, so the abstract does not describe outcomes beyond this comparison.

    • The study identified 3,288 metagenome-assembled genomes from wild boar faecal samples.
    • Among 968 species represented, 538 were previously unknown.
    • Two microbiome community types were linked to free-ranging wild boars and captive domestic pigs.
    • The wild-boar-associated community showed lower alpha-diversity than the domestic-pig-associated community.
    • Both community types showed substantial carbohydrate utilization potential.
    • The authors curated 47 highly versatile carbohydrate-degrading species, including several novel species.

  • Gut microbiota metabolic reprogramming may contribute to metabolic disease

    What the study found

    The review argues that metabolic reprogramming in the gut microbiota, meaning changes in how microbes use and process nutrients, may occur before disease appears and may contribute to metabolic diseases in the host. It describes changes in lipid, glucose, amino acid, and uric acid metabolism as part of this process.

    Why the authors say this matters

    The authors conclude that this framework refines the basic understanding of metabolic disorders and highlights new possibilities for targeting the microbiome in the prevention and treatment of metabolic disorders. The study suggests that understanding microbial metabolic changes may help explain systemic metabolic disease.

    What the researchers tested

    This is a review article, not an experimental study. The authors introduce the concept of gut microbiota metabolic reprogramming and synthesize existing evidence to build a model linking gut microbiota imbalance, microbial metabolic changes, and host disease.

    What worked and what didn't

    The review presents a coherent model in which gut microbiota imbalance leads to metabolic reprogramming that affects host metabolic and immune homeostasis. It specifically identifies lipid, glucose, amino acid, and uric acid metabolism as involved pathways, but it does not report original experimental comparisons or quantitative effect sizes.

    What to keep in mind

    The abstract does not provide details of the review methods, criteria for selecting evidence, or limitations of the synthesis. It also does not present new experimental data, so the claims reflect a proposed framework based on previously reported evidence.

    • The review proposes that gut microbiota metabolic reprogramming may be an early pathogenic event in metabolic disease.
    • It links gut microbiota imbalance to changes in lipid, glucose, amino acid, and uric acid metabolism.
    • The authors say these microbial changes may influence host metabolic and immune homeostasis.
    • The paper is a review article and does not report original experiments.
    • The authors suggest the framework may support new microbiome-based prevention and treatment strategies.

  • Maternal microbiome changes are linked to pregnancy and infant health

    What the study found

    The review finds that the maternal microbiota, meaning the communities of microbes living in the body, is linked to pregnancy outcomes and early infant immune programming. It also describes how microbiota changes across pregnancy and early life are associated with pregnancy complications and later health risks.

    Why the authors say this matters

    The authors conclude that understanding how microbiota, hormones, and immunity interact provides a foundation for approaches intended to improve maternal and child health. They also note that this period may be important for shaping immune development and disease susceptibility.

    What the researchers tested

    This is a review article that synthesizes current findings on maternal–infant microbiome interactions. It covers evidence on microbial changes during gestation, possible microbial signals in the placenta and uterus, transfer of microbes during delivery and breastfeeding, and emerging microbiome-targeted therapies under investigation.

    What worked and what didn't

    The review states that microbial transfer through delivery, breastfeeding, and early environmental exposure is associated with seeding the neonatal gut with beneficial taxa such as Bifidobacterium and with immune tolerance mediated by factors including IgA, TGF-β, and human milk oligosaccharides. It also reports that cesarean delivery, antibiotic exposure, or maternal dysbiosis have been associated with higher risks of allergy, autoimmunity, obesity, and neurodevelopmental abnormalities later in life. Emerging therapies listed in the abstract include probiotics, prebiotics, fecal microbiota transplantation, next-generation microbial ecosystem therapeutics, and CRISPR-based approaches, but the abstract does not report their effectiveness.

    What to keep in mind

    The abstract says evidence for a true placental microbiome is still debated, and key gaps remain in understanding maternal immune–microbial signaling. It also notes that the long-term efficacy of microbiome-targeted therapies is not yet established.

    • Maternal microbiota is linked to pregnancy outcomes and early infant immune programming.
    • The review says the first 1,000 days are a critical window for gut microbiota establishment and immune development.
    • Cesarean delivery, antibiotic exposure, and maternal dysbiosis are associated with higher risks of later health problems.
    • Beneficial microbes such as Bifidobacterium may be transferred to infants through delivery, breastfeeding, and early-life exposures.
    • The abstract says evidence for a placental microbiome remains debated.

  • Nursery peer transmission shapes infant gut microbes

    What the study found

    The study found extensive baby-to-baby transmission of microbial strains in nursery groups during the first year of life. By the end of the first term, nursery-acquired strains made up a share of the infant gut microbiome comparable to strains from family.

    Why the authors say this matters

    The authors conclude that social interactions in infancy are crucial drivers of infant microbiome development. The findings indicate that transmission among babies, not only from mothers or families, helps shape the developing gut microbiome.

    What the researchers tested

    The researchers carried out a metagenomic survey, which uses DNA from mixed microbial communities to identify strains, in nursery settings. They sampled 134 people, including babies attending nursery during the first year, educators, and families, and collected 1,013 fecal samples across three facilities.

    What worked and what didn't

    They detected baby-to-baby microbiome transmission after only one month of nursery attendance, and the transmission network became more complex over the nursery year. Having siblings was associated with higher microbiome diversity and less strain acquisition from nursery peers, while antibiotic treatment was the condition most associated with increased influx of strains.

    What to keep in mind

    The abstract does not describe detailed limitations beyond the study’s nursery-based scope and first-year timeframe. The findings come from three facilities and should be read within that setting.

    • Extensive baby-to-baby strain transmission was detected in nursery groups.
    • Nursery-acquired strains reached a contribution comparable to family strains by the end of the first term.
    • Transmission continued to increase over the nursery year in a more intricate network.
    • Having siblings was linked to higher microbiome diversity and less strain acquisition from nursery peers.
    • Antibiotic treatment was the condition most associated with increased influx of strains.