Inflammatory bowel disease (IBD) is a refractory disease characterized by chronic intestinal inflammation. Its typical pathological characteristics are the destruction of intestinal mucosal barrier and the imbalance of immune microenvironment. In severe cases, it can cause intestinal fibrosis and functional failure. Sulfation, a critical post-translational modification, plays an essential role in regulating intestinal homeostasis. Abnormal sulfation metabolism in the intestine of IBD patients can lead to the impairment of intestinal barrier function, immune system disorders and changes in the composition of microbiota. Consequently, targeting the sulfation pathway may be a novel therapeutic strategy for IBD. By supplementing exogenous sulfation substrates, regulating the activity of related key enzymes involved in sulfation or remodeling the microbiota, the level of intestinal sulfation can be effectively restored, thereby repairing the intestinal barrier function and inhibit the inflammatory response. This article systematically summarizes the pathogenic mechanisms of sulfation in IBD, providing a theoretical foundation for developing precision therapeutic strategies targeting the intestinal microenvironment.

Inflammatory bowel disease (IBD) is a refractory disease characterized by chronic intestinal inflammation. Its typical pathological characteristics are the destruction of intestinal mucosal barrier and the imbalance of immune microenvironment. In severe cases, it can cause intestinal fibrosis and functional failure. Sulfation, a critical post-translational modification, plays an essential role in regulating intestinal homeostasis. Abnormal sulfation metabolism in the intestine of IBD patients can lead to the impairment of intestinal barrier function, immune system disorders and changes in the composition of microbiota. Consequently, targeting the sulfation pathway may be a novel therapeutic strategy for IBD. By supplementing exogenous sulfation substrates, regulating the activity of related key enzymes involved in sulfation or remodeling the microbiota, the level of intestinal sulfation can be effectively restored, thereby repairing the intestinal barrier function and inhibit the inflammatory response. This article systematically summarizes the pathogenic mechanisms of sulfation in IBD, providing a theoretical foundation for developing precision therapeutic strategies targeting the intestinal microenvironment.