Elevated interleukin-32 expression is associated with Helicobacter pylori-related gastritis

PLoS One. 2014 Mar 14;9(3):e88270. doi: 10.1371/journal.pone.0088270. eCollection 2014.

Abstract

Background: Interleukin-32 (IL-32) is a recently discovered proinflammatory cytokine involved in inflammatory diseases. We investigated the expression of IL-32 and its regulation mechanism in the inflammatory response of patients with Helicobacter pylori (H. pylori) infection.

Design and methods: IL-32 mRNA and protein expression in gastric tissues was detected by quantitative real-time PCR and immunohistochemistry. The regulation of IL-32 in human gastric epithelia cell line AGS was investigated by different cytokine stimulation and different H. pylori strain infection.

Results: Gastric IL-32 mRNA and protein expression were elevated in patients with H. pylori infection and positively correlated with gastritis. In H. pylori-infected patients, the mRNA level of IL-32 was also correlated with that of proinflammatory cytokines IL-1β and TNF-α. In vitro IL-1β and TNF-α could upregulate IL-32 mRNA and protein level in AGS cells, which was dependent on NF-κB signal pathway. The regulation of IL-32 expression in response to H. pylori-infection could be weakened by using neutralizing antibodies to block IL-1β and TNF-α. Moreover, H. pylori-infected AGS cells also induced IL-32 mRNA and protein expression, which was dependent on CagA.

Conclusions: IL-32 level is elevated in patients with H. pylori infection and its expression is regulated by proinflammatory stimuli, suggesting that IL-32 may play a role in the pathogenesis of H. pylori-related gastritis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cell Line
  • Female
  • Gastritis / etiology*
  • Gastritis / metabolism*
  • Gastritis / microbiology
  • Helicobacter Infections / complications*
  • Helicobacter Infections / metabolism*
  • Helicobacter pylori / pathogenicity*
  • Humans
  • Immunohistochemistry
  • In Vitro Techniques
  • Interleukin-1beta / metabolism
  • Interleukins / genetics
  • Interleukins / metabolism*
  • Male
  • Middle Aged
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • IL32 protein, human
  • Interleukin-1beta
  • Interleukins
  • Tumor Necrosis Factor-alpha

Grants and funding

This work was supported by grants from the Medical Science Youth Training Project of Chinese People’s Liberation Army (13QNP108) and National Basic Research Program of China (973 Program, No. 2009CB522606). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.