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

• 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)

MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

Keyword

Adolescent

Adult

Biopsy

Cells

Cultured

Drosophila Proteins

Epithelial Cells/immunology/microbiology

Female

Gastric Mucosa/ microbiology

Helicobacter pylori/ pathogenicity

Humans

Male

Membrane Glycoproteins/ metabolism

Middle Aged

Pyloric Antrum/cytology/immunology/microbiology

Receptors

Cell Surface/ metabolism

Toll-Like Receptor 4

Toll-Like Receptors

Tumor Cells

Cultured

Publication and Content Type

ref (subject category)

art (subject category)