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Toll-like receptor 4 regulates gastric pit cell responses to Helicobacter pylori infection

T Kawahara1, Y Kuwano, S Teshima-Kondo

  • 1Department of Nutritional Physiology, University of Tokushima School of Medicine, Kuramoto-cho, Tokushima 770-8503, Japan.

The Journal of Medical Investigation : JMI
|November 7, 2001
PubMed

Insights

Gastric pit cells utilize Toll-like receptor 4 (TLR4) to detect Helicobacter pylori lipopolysaccharide (LPS), initiating inflammatory responses. This TLR4 activation is crucial for the gastric response to H. pylori infection.

Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Gastric pit cells express components of the phagocyte NADPH oxidase system, including mitogen oxidase 1 (Mox1).
  • Helicobacter pylori (Hp) lipopolysaccharide (LPS) is known to up-regulate Mox1 oxidase activity.

Purpose of the Study:

  • To investigate the expression of Toll-like receptors (TLRs) in guinea pig gastric pit cells.
  • To determine the role of TLRs in the gastric pit cell response to Hp infection.

Main Methods:

  • Primary cultures of guinea pig gastric pit cells were used.
  • Expression of TLR mRNA (TLR2, TLR4, TLR9) was assessed.
  • TLR protein levels were analyzed using immunoblotting and immunofluorescence.
  • Mox1 oxidase activity was measured.
  • Nuclear factor-kappa B activation and inflammatory gene expression (cyclooxygenase II, tumor necrosis factor alpha) were evaluated.

Main Results:

  • Gastric pit cells expressed TLR4 mRNA and protein, predominantly on the plasma membrane.
  • TLR2 and TLR9 transcripts and TLR2 protein were not detected.
  • Hp LPS, but not peptidoglycan or Hp DNA, activated nuclear factor-kappa B.
  • Hp LPS induced the expression of cyclooxygenase II and tumor necrosis factor alpha transcripts.
  • Neither peptidoglycan nor Hp DNA with CpG motifs affected Mox1 oxidase activity.

Conclusions:

  • Gastric pit cells express functional TLR4, which recognizes Hp LPS.
  • TLR4 activation by Hp LPS triggers inflammatory signaling pathways in gastric pit cells.
  • TLR4 plays a significant role in initiating gastric inflammatory responses to H. pylori infection.

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