Activation of type I IFN signaling by NOD1 mediates mucosal host defense against Helicobacter pylori infection.

Tomohiro Watanabe, Naoki Asano, Atsushi Kitani, Ivan J. Fuss, Tsutomu Chiba, Warren Strober

Research output: Contribution to journalReview articlepeer-review

20 Citations (Scopus)

Abstract

Infection of gastric epithelial cells with Helicobacter pylori (H. pylori) induces a complex array of host protective immune responses. The best known are the adaptive T helper type 1 and type 17 responses that are induced in the gastric lamina propria by antigen-presenting cells via presentation of H. pylori antigens to CD4(+) T cells. Recently, it has become apparent that innate immune responses are also induced by H.pylori infection, both in epithelial cells and in underlying antigen-presenting cells. One important component of these innate responses involves the activity of NOD1, an intra-cellular sensor of peptides derived from the peptidoglycan component of the bacterial cell wall. In this review, we discuss our recent work showing that the signaling pathway utilized by NOD1 results in the generation of type I interferon and that this cytokine mediates both chemokine and cytokine responses that regulate the severity of gastric H. pylori infection.

Original languageEnglish
Pages (from-to)61-65
Number of pages5
JournalGut microbes
Volume2
Issue number1
DOIs
Publication statusPublished - 2011

ASJC Scopus subject areas

  • Microbiology
  • Gastroenterology
  • Microbiology (medical)
  • Infectious Diseases

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