Gut microbiota and intestinal immunity interaction in ulcerative colitis and its application in treatment

Abstract

Ulcerative colitis (UC) is a chronic, non-specific inflammatory bowel disease characterized by inflammation and injury of the colonic mucosa, exhibiting an increasing global incidence. Although research into UC pathogenesis is ongoing, the precise mechanisms remain to be fully elucidated. Studies indicate that UC development results from a complex interplay of factors, including genetic predisposition, environmental exposures, gut microbial dysbiosis, and immune dysregulation. Specifically, UC pathogenesis involves aberrant immune responses triggered by interactions between the host and gut microbiota. A complex, dynamic relationship exists between the microbial community and the host immune system throughout UC pathogenesis. Accumulating evidence suggests that changes in microbiota composition significantly impact gut immunity. This review will examine the intricate balance between the gut microbiota and mucosal immunity in UC progression and discuss potential therapeutic applications, providing a reference for further clinical treatment of this patient population.

Keywords: fecal microbiota transplantation; gut microbiota; herb medicine; inflammatory diseases; intestinal immunity.

Figure 1

Interaction between gut microbiota and intestinal mucosal immunity. The interaction between gut microbiota and the intestinal mucosal system is the basis for achieving homeostasis of immune function and balance of intestinal ecology. The interaction between the gut microbiota and the host immune system commences at birth, with the microbiota influencing the development of the immune system, which, in turn, modulates the composition of the microbiota. This bidirectional relationship propagates through a network of signaling pathways that extend beyond the immune system. Through the interaction with various intestinal cells, gut microbiota and its metabolites initiate signal transduction pathways, regulate body responses, drive the maturation of intestinal immunity, and then maintain immune balance. AMP, antimicrobial peptide; BA, bile acid; IL, interleukin; ILC3, Type 3 innate lymphoid cells; SCFAs, short-chain fatty acids; SIgA, secretory immunoglobulin A; FOS, fructooligosaccharides. Tregs, regulatory T cells.