Alleviates DSS-Induced Ulcerative Colitis in Mice by Repairing the Intestinal Barrier and Regulating Gut Microbiota and Its Metabolism.

Abstract

BACKGROUND: Inflammatory bowel disease (IBD) is a gut-based idiopathic disease characterized by chronic and relapsing inflammatory progression and intricate pathophysiology. It is now known that the key etiologies of IBD include immune dysregulation, imbalances in the gut microbiota, and metabolic disruptions. Probiotics are now the potential treatment for IBD, due to their ability to regulate the host immune system and microbiota of the gut. METHODS: The current study analytically tested the preventive benefit ofBL-01 on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) and also expounded on its molecular pathogenesis. RESULTS: Our results demonstrate that supplementation with BL-01 effectively mitigates DSS-induced weight loss, an elevated disease activity index (DAI), and colonic tissue injury in mice. Concomitantly, BL-01 rectifies dysregulated inflammatory cytokine profiles, attenuates oxidative stress, and restores the expression of colonic tight junction proteins as well as the number of goblet cells. Furthermore, BL-01 modulates the gut microbiota diversity by increasing the abundance of beneficial bacterial genera such asand decreasing the abundance of pathogenic genera such as. Notably, BL-01 restores DSS-induced microbial metabolic dysregulation, modulates key metabolic pathways including arachidonic acid metabolism and steroid hormone biosynthesis, and regulates associated metabolites to ameliorate UC. Finally,BL-01 mitigates oxidative stress, reverses gut dysbiosis and metabolic disorders, and has a protective effect on UC. CONCLUSIONS: The findings give new information on the development of probiotic-based therapeutics in the prevention and treatment of IBD.