Rationale: The gut microbiota plays a significant role in the pathogenesis of
inflammatory bowel disease (IBD). However, the role of
Blastocystis infection and Blastocystis-altered gut microbiota in the development of inflammatory diseases and their underlying mechanisms are not well understood. Methods: We investigated the effect of Blastocystis ST4 and ST7
infection on the intestinal microbiota, metabolism, and host immune responses, and then explored the role of Blastocystis-altered gut microbiome in the development of
dextran sulfate sodium (DSS)-induced
colitis in mice. Results: 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. Conclusions: 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.