Colonization with two different subtypes in DSS-induced colitis mice is associated with strikingly different microbiome and pathological features.

The gut microbiota plays a significant role in the pathogenesis of inflammatory bowel disease (IBD). However, the role of infection and -altered gut microbiota in the development of inflammatory diseases and their underlying mechanisms are not well understood. We investigated the effect of ST4 and ST7 infection on the intestinal microbiota, metabolism, and host immune responses, and then explored the role of -altered gut microbiome in the development of dextran sulfate sodium (DSS)-induced colitis in mice. This study showed that prior colonization with ST4 conferred protection from DSS-induced colitis through elevating the abundance of beneficial bacteria, short-chain fatty acid (SCFA) production and the proportion of Foxp3 and IL-10-producing CD4 T cells. Conversely, prior ST7 infection exacerbated the severity of colitis by increasing the proportion of pathogenic bacteria and inducing pro-inflammatory IL-17A and TNF-α-producing CD4 T cells. Furthermore, transplantation of ST4- and ST7-altered microbiota resulted in similar phenotypes. Our data showed that ST4 and ST7 infection exert strikingly differential effects on the gut microbiota, and these could influence the susceptibility to colitis. ST4 colonization prevented DSS-induced colitis in mice and may be considered as a novel therapeutic strategy against immunological diseases in the future, while ST7 infection is a potential risk factor for the development of experimentally induced colitis that warrants attention.