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Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages

Dah-Yuu Lu1, Chin-Hsin Tang, Chia-Hsian Chang

  • 1Graduate Institute of Neural and Cognitive Sciences, China Medical University, Taichung, Taiwan.

Innate Immunity
|September 20, 2011
PubMed

Insights

Helicobacter pylori evades immune responses by inhibiting nitric oxide (NO) production in macrophages. This suppression of inducible nitric oxide synthase (iNOS) allows the bacteria to survive and persist in the stomach.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Helicobacter pylori infection is linked to chronic inflammation via pro-inflammatory cytokines and nitric oxide (NO) production.
  • Macrophages produce NO in response to bacterial lipopolysaccharide (LPS), activating inducible nitric oxide synthase (iNOS).
  • H. pylori's mechanism for evading these immune responses is not fully understood.

Purpose of the Study:

  • To investigate how H. pylori evades the host's innate immune response.
  • To elucidate the mechanism by which H. pylori inhibits macrophage NO production.

Main Methods:

  • Utilized a murine model of macrophage infection.
  • Assessed LPS-induced iNOS expression and NO production in macrophages.
  • Analyzed iNOS mRNA and protein levels.
  • Examined the role of the mitogen-activated protein kinase (MAPK) pathway and NF-κB translocation.

Main Results:

  • H. pylori significantly inhibited LPS-induced iNOS expression and NO production in macrophages.
  • This inhibition led to increased H. pylori survival, an effect absent in iNOS-deficient macrophages.
  • H. pylori suppressed iNOS at both transcriptional and post-transcriptional levels, requiring live bacteria.
  • The bacteria downregulated the MAPK pathway and inhibited NF-κB nuclear translocation.

Conclusions:

  • H. pylori employs a novel mechanism to evade innate immunity by suppressing macrophage NO production.
  • This immune evasion strategy involves downregulating the MAPK pathway and NF-κB signaling.
  • These findings reveal how H. pylori establishes persistent infections in the stomach.

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