Food safety has considerably improved worldwide, yet infections with food-borne human enteric pathogens, such as Listeria spp. and Salmonella spp., still cause numerous hospitalizations and fatalities. Thus, the need to shed more light on the mechanisms of enteropathogenesis is apparent. Since dietary alterations, including fiber deficiency, might impact the colonization resistance by the gut microbiota, studying diet-microbiota-pathogen axis holds promise in further understanding the pathogenesis mechanisms. Using a gnotobiotic mouse model containing a 14-member synthetic human gut microbiota (14SM), we have previously shown that dietary fiber deprivation promotes proliferation of mucin-degrading bacteria leading to a microbiota-mediated erosion of the colonic mucus barrier, which results in an increased susceptibility towards the rodent enteric pathogen Citrobacter rodentium. Here, we sought to understand how low-fiber diet affects susceptibility to Listeria monocytogenes and Salmonella typhimurium infections in our 14SM gnotobiotic mouse model, in BALB/c and C57BL/6N backgrounds, respectively. Intriguingly and in contrast to our results with C. rodentium, we observe that depriving mice of dietary fiber protected them from infections with the pathogens compared to mice fed a standard chow. The microbiota delayed the overall pathogenicity as compared to the onset of disease observed in germ-free control mice; nevertheless, we observe the same effect of diet in germ-free mice, suggesting that the susceptibility is microbiota independent. Our study points out an important observation that dietary fiber plays a crucial role on either the host susceptibility, the virulence of these pathogens, or both, which would be judicious to design and interpret future studies.
Effects of antiinflammatory agents on chronic Salmonella typhimurium infection in a mouse model.
