Bovine lactoferricin ameliorates intestinal inflammation and mucosal barrier lesions in colitis through NF-κB/NLRP3 signaling pathways

Abstract

• LfcinB ameliorates intestinal tissue morphology and distribution disorder of tight junction proteins in an established model of acute colitis. • LfcinB improves the production and distribution of mucin in colon of rats. • LfcinB alters the immune status of acute UC rats and inhibits the activities of inflammatory mediators. • NF-κB/NLRP3 signaling pathway involved the protection role of LfcinB on intestinal inflammation and mucosal barrier. Bovine lactoferricin (LfcinB) has biological properties such as anti-inflammatory and immunological activity. This study aimed to investigate the protective effects of LfcinB on mucosal injury during the pathological process of ulcerative colitis in rats. The thirty-two rats were randomly assigned to four groups: control (C group), colitis model (DSS group; oral intake of 5.0% dextran sodium sulfate), colitis model with LfcinB (LBD group; 5 mg/kg for 7 days, starting while DSS treatment) and LfcinB (LfcinB group; 5 mg/kg for 7 days) group. Treatment with LfcinB reduced the disease activity index and diamine oxidase concentration in rats with colitis. Histology analysis revealed a better preservation of the epithelium as well as attenuated inflammatory infiltration of the colon epithelium in LfcinB-treated rats. LfcinB treatment also downregulated the colonic expression of IL-1β and restored the expression levels of zonula occludens-1, occludin and mucin 2, by suppressing DSS-induced increases in inflammation and myeloperoxidase concentration in the rats of LBD group. During this process, the decreased expression levels of ASC, Caspase-1, NLRP3, and NF-κB in the rats of LBD group were characterized by quantitative RT-PCR. These results suggest LfcinB ameliorates DSS-induced changes in intestinal inflammation and mucosal barrier in colitis rats, possibly through NF-κB/NLRP3 signaling pathway.