IL-10, TNF-α and IFN-γ levels in serum and stomach mucosa of Helicobacter pylori-infected patients

Iran J Allergy Asthma Immunol. 2011 Dec;10(4):267-71.

Abstract

H. pylori is a human pathogen that colonizes the epithelium of the stomach. The host immune response may influence the disease process, where cytokines play important roles in the development of disease. In this study, the concentrations of selected cytokines in the gastric antrum and stomach body mucosa and also in the serum were evaluated. Eighty patients according to their rapid urease test were divided into two groups: H. pylori positive (n=39) and H. pylori-negative (n=41). The concentrations of cytokines in biopsies and serum were determined by ELISA method. The mean TNF-α and IFN-γ levels in the infected group were significantly higher than that of uninfected patients. In contrast, IL-10 level in most patients was undetectable. The mean antral of stomach TNF-α and IFN-γ levels were significantly higher than that of the stomach body. IFN-γ serum level showed positive correlation with antrum and stomach body levels, whereas no correlation was found in TNF-α in different samples. Higher levels of TNF-α and IFN-γ in antral indicate that the colonization of bacteria in the antrum may be higher than stomach body (culture results from two sites support this statement). Increased serum level of IFN-γ indicates the activation of circulating-T cells against infection. Induced H. pylori-related TNF-α is concentrated is gastric mucosa and this pathogen does not cause any significant change in the serum level of this cytokine. Therefore H. pylori by inducing certain inflammatory cytokines but not IL-10 may contribute the process of disease development.

MeSH terms

  • Adult
  • Aged
  • Female
  • Gastric Mucosa / immunology*
  • Helicobacter Infections / immunology*
  • Helicobacter pylori*
  • Humans
  • Interferon-gamma / analysis*
  • Interleukin-10 / analysis*
  • Lymphocyte Activation
  • Male
  • Middle Aged
  • Tumor Necrosis Factor-alpha / analysis*

Substances

  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Interferon-gamma