Helicobacter pylori-induced Th17 responses modulate Th1 cell responses, benefit bacterial growth, and contribute to pathology in mice.


Journal Article

CD4(+) T cell responses are critical for the pathogenesis of Helicobacter pylori infection. The present study evaluated the role of the Th17 subset in H. pylori infection. H. pylori infection induced significant expression of IL-17 and IFN-gamma in mouse gastric tissue. IL-23 and IL-12 were increased in the gastric tissue and in H. pylori-stimulated macrophages. Cell responses were examined by intracellular staining for IFN-gamma, IL-4, and IL-17. Mice infected with H. pylori developed a mixed Th17/Th1 response; Th17 responses preceded Th1 responses. Treatment of mice with an anti-IL-17 Ab but not a control Ab significantly reduced the H. pylori burden and inflammation in the stomach. H. pylori colonization and gastric inflammation were also lower in IL-17(-/-) mice. Furthermore, administration of recombinant adenovirus encoding mouse IL-17 increased both H. pylori load and inflammation. Further analysis showed that the Th1 cell responses to H. pylori were downregulated when IL-17 is deficient. These results together suggest that H. pylori infection induces a mixed Th17/Th1 cell response and the Th17/IL-17 pathway modulates Th1 cell responses and contributes to pathology.

Full Text

Cited Authors

  • Shi, Y; Liu, X-F; Zhuang, Y; Zhang, J-Y; Liu, T; Yin, Z; Wu, C; Mao, X-H; Jia, K-R; Wang, F-J; Guo, H; Flavell, RA; Zhao, Z; Liu, K-Y; Xiao, B; Guo, Y; Zhang, W-J; Zhou, W-Y; Guo, G; Zou, Q-M

Published Date

  • May 2010

Published In

Volume / Issue

  • 184 / 9

Start / End Page

  • 5121 - 5129

PubMed ID

  • 20351183

Pubmed Central ID

  • 20351183

Electronic International Standard Serial Number (EISSN)

  • 1550-6606

International Standard Serial Number (ISSN)

  • 0022-1767

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.0901115


  • eng