Helicobacter pylori–induced matrix metallopeptidase-10 promotes gastric bacterial colonization and gastritis Academic Article uri icon


  • The interaction between gastric epithelium and immune response plays key roles in H. pylori–associated pathology. We demonstrated a procolonization and proinflammation role of MMP-10 in H. pylori infection. MMP-10 is elevated in gastric mucosa and is produced by gastric epithelial cells synergistically induced by H. pylori and IL-22 via the ERK pathway. Human gastric MMP-10 was correlated with H. pylori colonization and the severity of gastritis, and mouse MMP-10 from non–BM-derived cells promoted bacteria colonization and inflammation. H. pylori colonization and inflammation were attenuated in IL-22−/−, MMP-10−/−, and IL-22−/−MMP-10−/− mice. MMP-10–associated inflammation is characterized by the influx of CD8+ 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 H. pylori colonization. Our results suggest that MMP-10 facilitates H. pylori persistence and promotes gastritis.


  • Lv, Yi-pin
  • Cheng, Ping
  • Zhang, Jin-yu
  • Mao, Fang-yuan
  • Teng, Yong-sheng
  • Liu, Yu-gang
  • Kong, Hui
  • Wu, Xiao-long
  • Hao, Chuan-jie
  • Han, Bin
  • Ma, Qiang
  • Yang, Shi-ming
  • Chen, Weisan
  • Peng, Liu-sheng
  • Wang, Ting-ting
  • Zou, Quan-ming
  • Zhuang, Yuan

publication date

  • April 2019