Biology subjects

Webster, G. M.

Publications and source records attributed to Webster, G. M..

2 recordsLinked to original sources

bioRxiv2026

Lactococcus lactis subsp. cremoris Reprograms the Gut-Liver Axis and Protects Against Liver Injury

Metabolic diseases are increasingly linked to dysregulation of the gut-liver axis, highlighting the therapeutic potential of probiotics. Lactococcus lactis subsp. cremoris (LLC) protects against experimental hepatic steatosis, but the mechanisms underlying its benefits remain poorly understood. Here, we integrated untargeted metabolomics, gnotobiotic mouse models, targeted bile acid profiling, and liver injury paradigms to systematically define LLC-mediated metabolic reprogramming. LLC extensively remodeled serum and hepatic metabolomes in Western diet-fed mice, enriching pathways associated with lipid metabolism, xenobiotic biotransformation, and redox homeostasis. LLC attenuated ethanol-induced steatosis and acetaminophen-induced liver injury, accompanied by activation of Nrf2-dependent antioxidant programs and FXR signaling. LLC monocolonization was sufficient to reprogram the hepatic metabolome, revealing direct host metabolic effects. Reduced intestinal bile acid conjugation emerged as a prominent LLC-associated phenotype. Together, these findings identify LLC as a probiotic that reprograms the gut-liver metabolic axis to enhance metabolic resilience and hepatoprotection.

microbiology↗

bioRxiv2026

Anti-psychotic therapeutics modify gut microbial metabolism and modulate susceptibility to gastrointestinal infection in mice

Antipsychotic medications are widely prescribed and associated with increased infection risk, but underlying mechanisms remain unclear. We examined if antipsychotic-induced microbiome and metabolome alterations impair colonization resistance. Using a murine model, we evaluated haloperidol, olanzapine, risperidone, and quetiapine through longitudinal microbiome profiling, untargeted metabolomic fingerprinting, behavioral testing, and enteric infection challenge. Antipsychotic exposure induced persistent behavioral changes and increased susceptibility to Citrobacter rodentium, with quetiapine and olanzapine producing the greatest weight loss. Microbiome sequencing revealed treatment-specific shifts in beta diversity without consistent alpha diversity changes, while untargeted metabolomic analysis demonstrated robust, drug-specific metabolic reprogramming, particularly in lipid and sterol pathways. Although microbial compositional changes did not fully account for functional outcomes, their integration with metabolomics data revealed disrupted bacterial taxa-metabolite networks and loss of homeostatic metabolic modules. These results provide a potential mechanistic link between the disruptive effects of antipsychotics on the microbiome and impaired colonization resistance.

microbiology↗