Genistein Inhibits Colonic Goblet Cell Loss and Colorectal Inflammation Induced by Salmonella Typhimurium Infection

Scope Salmonella is the main food‐borne pathogen, which can infect intestinal epithelial cells and causes colitis. Genistein has a variety of biological activities that alleviates colitis induced by sodium dextran sulfate in a variety of ways, but its protective effects on colitis caused by pathogenic bacteria are still unknown. Methods and Results This study explores the protective effect of genistein in reducing colitis caused by Salmonella infection. Salmonella causes colon inflammation through activating cyclooxygenase‐2/prostaglandin E2, and genistein inhibits colitis caused by Salmonella typhimurium infection. Salmonella infection increases colonic mucosal damage, proliferating cells, and goblet cell loss, while the administration of genistein solves these pathological changes. In addition, it is further proved that Salmonella causes severe colitis related to goblet cell loss and activates the host crypt stem cells to repair the damaged epithelium. Salmonella infection inhibites the host mammalian target of rapamycin, activates light chain 3 II pathways to induce autophagy to eliminate pathogenic bacteria. Genistein increases Lactobacillus in feces and reduces Salmonella colonization to inhibit colitis induces by Salmonella infection. Conclusion This study demonstrates genistein alleviated colitis and inhibites the goblet cell loss causes by Salmonella infection through regulating the gut bacteria and intestinal stem cell development. Genistein alleviates the colonic goblet cells loss and mucosal damage causes by Salmonella infection. Salmonella infection causes intestinal epithelial cells inflammation, autophagy and apoptosis, and activates the differentiation of host colonic stem cells to compensate for epithelial integrity. Genistein maintains intestinal homeostasis to reverse the negative effects of Salmonella by regulating intestinal bacteria.