Expression of proinflammatory and Th1 but not Th2 cytokines is enhanced in gastric mucosa of Helicobacter pylori infected children

Dig Liver Dis. 2001 Jan-Feb;33(1):14-20. doi: 10.1016/s1590-8658(01)80130-4.

Abstract

Background: Helicobacter pylori-induced gastric inflammation is thought to be largely regulated by cytokines.

Patients and methods: The expression of interferon-gamma, interleukin-12, interleukin-4, interleukin-10, interleukin-8, and interleukin-17 mRNA was examined on gastric mucosal samples from 24 children by semiquantitative reverse transcription polymerase chain reaction and southern blotting. Biopsy-based tests, serology, and urea 13C breath test were used to assess Helicobacter pylori status. Gastric biopsies were also evaluated for bacterial density, chronic inflammation, and acute inflammatory activity.

Results: Interferon-gamma, interleukin-12, interleukin-8 and interleukin-17 expression was higher in Helicobacter pylori-infected (n=13) than uninfected (n=11) children. Conversely, interleukin-4 and interleukin-10 expression did not differ between Helicobacter pylori-infected and uninfected children. In Helicobacter pylori-infected children, interferon-gamma, interleukin-12, interleukin-8 and interleukin-17 expression correlated with bacterial density, and Interferon-gamma and interleukin-12 expression with chronic inflammation score.

Conclusions: The findings of this study indicate that, in children, Helicobacter pylori-induced inflammatory response would favour production of proinflammatory cytokines and development of cell-mediated immunity, namely Th1 response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Child
  • Child, Preschool
  • Colony Count, Microbial
  • Cytokines / metabolism*
  • Female
  • Gastritis / diagnosis
  • Gastritis / immunology*
  • Helicobacter Infections / diagnosis
  • Helicobacter Infections / immunology*
  • Helicobacter pylori / immunology*
  • Humans
  • Immunity, Mucosal / immunology*
  • Infant
  • Inflammation Mediators / metabolism
  • Male
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*

Substances

  • Cytokines
  • Inflammation Mediators