Anaerobic Pathogen ETBF Rewires Host Metabolism for Oxidative Growth in Inflamed Gut
Recent research published in the journal Cell reveals a novel mechanism by which Enterotoxigenic Bacteroides fragilis (ETBF), a traditionally anaerobic pathogen, adapts to survive and thrive within the inflamed human colon. The study demonstrates that ETBF utilizes its specific toxin, Bacteroides fragilis toxin (BFT), to fundamentally remodel host epithelial cell metabolism. By shifting these cells toward a fermentative metabolic state, the pathogen increases the local availability of lactate and oxygen. This process creates a localized oxidative niche in the colon, an environment typically hostile to anaerobes. Consequently, ETBF is able to deploy oxidative metabolism, allowing it to adapt effectively to inflammatory conditions. This discovery highlights a sophisticated strategy where the pathogen manipulates host biological processes to fuel its own growth. The findings provide critical insights into the complex interactions between gut microbiota and host physiology during inflammation, potentially opening new avenues for understanding and treating inflammatory bowel diseases and other gut-related disorders driven by such pathogens.
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Anaerobic Pathogen ETBF Rewires Host Metabolism for Oxidative Growth in Inflamed Gut
Recent research published in the journal Cell reveals a novel mechanism by which Enterotoxigenic Bacteroides fragilis (ETBF), a traditionally anaerobic pathogen, adapts to survive and thrive within the inflamed human colon. The study demonstrates that ETBF utilizes its specific toxin, Bacteroides fragilis toxin (BFT), to fundamentally remodel host epithelial cell metabolism. By shifting these cells toward a fermentative metabolic state, the pathogen increases the local availability of lactate and oxygen. This process creates a localized oxidative niche in the colon, an environment typically hostile to anaerobes. Consequently, ETBF is able to deploy oxidative metabolism, allowing it to adapt effectively to inflammatory conditions. This discovery highlights a sophisticated strategy where the pathogen manipulates host biological processes to fuel its own growth. The findings provide critical insights into the complex interactions between gut microbiota and host physiology during inflammation, potentially opening new avenues for understanding and treating inflammatory bowel diseases and other gut-related disorders driven by such pathogens.
Cell