Publication Date:
2019
Description:
〈p〉The interaction between gastric epithelium and immune response plays key roles in 〈i〉H. pylori〈/i〉–associated pathology. We demonstrated a procolonization and proinflammation role of MMP-10 in 〈i〉H. pylori〈/i〉 infection. MMP-10 is elevated in gastric mucosa and is produced by gastric epithelial cells synergistically induced by 〈i〉H. pylori〈/i〉 and IL-22 via the ERK pathway. Human gastric MMP-10 was correlated with 〈i〉H. pylori〈/i〉 colonization and the severity of gastritis, and mouse MMP-10 from non–BM-derived cells promoted bacteria colonization and inflammation. 〈i〉H. pylori〈/i〉 colonization and inflammation were attenuated in IL-22〈sup〉–/–〈/sup〉, MMP-10〈sup〉–/–〈/sup〉, and IL-22〈sup〉–/–〈/sup〉MMP-10〈sup〉–/–〈/sup〉 mice. MMP-10–associated inflammation is characterized by the influx of CD8〈sup〉+〈/sup〉 T cells, whose migration is induced via MMP-10–CXCL16 axis by gastric epithelial cells. Under the influence of MMP-10, Reg3a, E-cadherin, and zonula occludens–1 proteins decrease, resulting in impaired host defense and increased 〈i〉H. pylori〈/i〉 colonization. Our results suggest that MMP-10 facilitates 〈i〉H. pylori〈/i〉 persistence and promotes gastritis.〈/p〉
Electronic ISSN:
2375-2548
Topics:
Natural Sciences in General