The microbiota provides protection from invading pathogens through a process known as colonization resistance, which comprises various inhibitory mechanisms that can be either direct or indirect, or host-mediated. However, how prior infections influence colonization resistance and the underlying mechanisms are not well explored. Now, Stacy et al. provide evidence that prior infections enhance colonization resistance through a process whereby the host, prompted by transient infection, deploys the sulfonic acid taurine as a nutrient to train the gut microbiota and provide resistance to subsequent infections.
Next, the authors examined metagenomes of wildR and post-ΔyopM mice and found an enrichment in sulfur metabolism, the main source of which was Deltaproteobacteria metagenomes. Deltaproteobacteria use sulfur-containing compounds such as taurine and sulfate for anaerobic respiration. Metagenomic analyses of wildR and post-ΔyopM microbiota suggested that taurine contributed to expansion of Deltaproteobacteria. In agreement with this, the most significantly increased metabolite in cecal contents of post-ΔyopM mice was taurine, a primary source of which is bile acids produced in the liver. Taurine-conjugated bile acids as well as primary and secondary bile acids were also significantly increased. The authors found that infection of post-ΔyopM mice led to long-term increased immunity within the liver and enlargement of the gallbladder (which stores bile acids). These results suggest that transient infection has long-term effects on host bile acid metabolism, leading to an increase in gut taurine levels, which potentially promotes the expansion of taurine-utilizing Deltaproteobacteria. Remarkably, enrichment of the deltaproteobacterium Bilophila wadsworthia in the gut of mice conventionalized with complex SPF microbiota was sufficient to enhance resistance to K. pneumoniae, suggesting that taurine-utilizing Deltaproteobacteria contribute to colonization resistance.
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