Gastric mucosal recognition of Helicobacter pylori is independent of Toll-like receptor 4

J Infect Dis. 2003 Mar 1;187(5):829-36. doi: 10.1086/367896. Epub 2003 Feb 24.


Little is known about the interactions between Helicobacter pylori, which specializes in colonizing the mucin layer that covers the gastric mucosa, and primary gastric epithelial cells. The expression pattern of Toll-like receptors (TLRs) in primary gastric epithelial cells and cell lines was compared. Primary cells did not express TLR4, whereas all cell lines expressed a nonsignaling form of TLR4. Because other cells within the mucosa expressed TLR4, it was next investigated whether H. pylori can be recognized by TLR4--they cannot. Moreover, H. pylori infection of primary cells induced a regulated production of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha, whereas infection of cell lines only resulted in IL-8 production. The cytokine production in all cell types was strictly cag dependent. These findings indicate that, although the epithelium is important in directing the immune response against H. pylori infections, the response is independent of TLR4.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Biopsy
  • Cells, Cultured
  • Drosophila Proteins*
  • Epithelial Cells / immunology
  • Epithelial Cells / microbiology
  • Female
  • Gastric Mucosa / microbiology*
  • Helicobacter pylori / pathogenicity*
  • Humans
  • Male
  • Membrane Glycoproteins / metabolism*
  • Middle Aged
  • Pyloric Antrum / cytology
  • Pyloric Antrum / immunology
  • Pyloric Antrum / microbiology
  • Receptors, Cell Surface / metabolism*
  • Toll-Like Receptor 4
  • Toll-Like Receptors
  • Tumor Cells, Cultured


  • Drosophila Proteins
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Toll-Like Receptors