Inflammatory cytokine mRNA expression during early and persistent Helicobacter pylori infection in nonhuman primates

P R Harris1, L E Smythies, P D Smith

  • 1Departments of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

Insights

Helicobacter pylori infection significantly increases the expression of inflammatory cytokines, including interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, in primate gastric tissue. This indicates an innate immune response to H. pylori gastritis.

Area of Science:

  • Immunology
  • Gastroenterology
  • Microbiology

Background:

  • The role of mononuclear phagocytes in Helicobacter pylori infection is not well understood.
  • H. pylori is a common cause of gastritis and peptic ulcers.

Purpose of the Study:

  • To investigate the gene expression of key inflammatory cytokines (IL-1beta, IL-6, TNF-alpha) in nonhuman primates during H. pylori infection.
  • To correlate cytokine gene expression with the progression of H. pylori-induced gastritis.

Main Methods:

  • Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to measure mRNA levels of IL-1beta, IL-6, and TNF-alpha.
  • Gene expression was analyzed in gastric tissue samples from rhesus monkeys before and during H. pylori infection (early and chronic stages).
  • Gastritis severity was assessed using established scoring systems.

Main Results:

  • A significant increase in IL-1beta, IL-6, and TNF-alpha mRNA levels was observed in gastric tissue during early H. pylori infection compared to preinfection levels.
  • Elevated cytokine mRNA levels persisted in chronically infected animals.
  • Increased cytokine gene expression correlated with progressive gastritis scores.

Conclusions:

  • H. pylori infection stimulates the local gene expression of monocyte/macrophage-derived inflammatory cytokines in primate gastric tissue.
  • These findings demonstrate an innate immune response in the gastric mucosa during H. pylori infection.
  • Mononuclear phagocytes play a crucial role in orchestrating the host's inflammatory response to H. pylori.