Nod1 Responds to Peptidoglycan Delivered by the Helicobacter Pylori Cag Pathogenicity Island

Nat Immunol. 2004 Nov;5(11):1166-74. doi: 10.1038/ni1131. Epub 2004 Oct 17.

Abstract

Epithelial cells can respond to conserved bacterial products that are internalized after either bacterial invasion or liposome treatment of cells. We report here that the noninvasive Gram-negative pathogen Helicobacter pylori was recognized by epithelial cells via Nod1, an intracellular pathogen-recognition molecule with specificity for Gram-negative peptidoglycan. Nod1 detection of H. pylori depended on the delivery of peptidoglycan to host cells by a bacterial type IV secretion system, encoded by the H. pylori cag pathogenicity island. Consistent with involvement of Nod1 in host defense, Nod1-deficient mice were more susceptible to infection by cag pathogenicity island-positive H. pylori than were wild-type mice. We propose that sensing of H. pylori by Nod1 represents a model for host recognition of noninvasive pathogens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / immunology
  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Epithelial Cells / immunology*
  • Epithelial Cells / metabolism
  • Genomic Islands
  • Helicobacter pylori / immunology*
  • Humans
  • Immunity, Innate / immunology*
  • NF-kappa B / immunology
  • NF-kappa B / metabolism
  • Nod1 Signaling Adaptor Protein
  • Peptidoglycan / genetics
  • Peptidoglycan / immunology*

Substances

  • Adaptor Proteins, Signal Transducing
  • NF-kappa B
  • NOD1 protein, human
  • Nod1 Signaling Adaptor Protein
  • Peptidoglycan