Commensal bacteria play a fundamental role in maintaining gut immune homeostasis.

The intestinal microbiome, which is a key factor in the maintenance of host gut homeostasis, enhances intestinal mucosal barrier function and immune tolerance (Rooks and Garrett, 2016; Skelly et al., 2019). However, the specific immunomodulatory functions of microbiota-derived metabolites in mucosal inflammatory responses remain largely unknown. The effects of microbial metabolites may vary across different immune cell types and host homeostasis (Hu et al., 2023; Zhao et al., 2023). Hence, it is fundamental to understand how specific intestinal microbes and their metabolic small molecules cause or mitigate gut-related diseases like inflammatory bowel disease (IBD). It has been uncovered that during the pathogenesis of IBD, excessive T helper 1 cell (Th1)/Th17 activation and impaired function of colonic regulatory T cells (Tregs) occur (Subramanian, 2020). Given that colonic Tregs play an important role in inhibiting IBD via secreting immunosuppressive cytokines, the molecular mechanisms linking certain intestinal microbes and their metabolites to Treg-mediated immune tolerance are yet to be fully understood.