Helicobacter pylori-induced macrophage apoptosis requires activation of ornithine decarboxylase by c-Myc

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Yulan Cheng1, Rupesh Chaturvedi, Mohammad Asim

  • 1Department of Medicine, Division of Gastroenterology, and Greenebaum Cancer Center, University of Maryland School of Medicine, 22 South Greene Street, Baltimore, MD 21201, USA.

The Journal of Biological Chemistry
|April 22, 2005
PubMed

Insights

Helicobacter pylori infection triggers macrophage apoptosis via polyamines, mediated by c-Myc and ornithine decarboxylase (ODC) activation. Inhibiting c-Myc or ODC reduces this cell death, impacting gastric inflammation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gastroenterology

Background:

  • Helicobacter pylori infection causes chronic gastric inflammation due to ineffective immune responses.
  • Polyamines, synthesized via ornithine decarboxylase (ODC), mediate macrophage apoptosis.
  • The transcription factor c-Myc is linked to ODC induction.

Purpose of the Study:

  • To investigate if H. pylori stimulates ODC transcription in macrophages via c-Myc.
  • To determine if these events regulate macrophage apoptosis.
  • To elucidate the role of c-Myc and ODC in H. pylori-induced gastric inflammation.

Main Methods:

  • Macrophage stimulation with H. pylori.
  • Measurement of ODC promoter activity, mRNA, protein, and enzyme activity.
  • Analysis of c-Myc expression, nuclear translocation, and DNA binding.
  • Inhibition studies using c-Myc inhibitors and dominant-negative constructs.
  • Assessment of apoptosis via ODC small interfering RNA (siRNA).

Main Results:

  • H. pylori significantly increased ODC promoter activity, mRNA, protein, and enzyme activity.
  • c-Myc expression and nuclear translocation were induced early after H. pylori stimulation.
  • Inhibition of c-Myc binding or expression attenuated H. pylori-induced ODC activity and apoptosis.
  • ODC siRNA similarly inhibited ODC activity and apoptosis, mirroring c-Myc inhibition effects.

Conclusions:

  • c-Myc is a key mediator of H. pylori-induced ODC activation in macrophages.
  • The c-Myc/ODC pathway contributes to macrophage apoptosis during H. pylori infection.
  • This mechanism plays a role in the gastric mucosal inflammatory response to H. pylori.

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