Lack of gastritis and of an adaptive immune response in interferon regulatory factor-1-deficient mice infected with Helicobacter pylori

Eur J Immunol. 2001 Feb;31(2):396-402. doi: 10.1002/1521-4141(200102)31:2<396::aid-immu396>3.0.co;2-y.

Abstract

To study the role of T cell responses in Helicobacter pylori gastritis, C57BL/6 wild-type and interferon regulatory factor-1-deficient (IRF-1(-/-)) mice were infected with the mouse-adapted H. pylori Sydney strain. Mice lacking the transcription factor IRF-1 are defective in Th1 development and are therefore biased to mount a Th2-type response. After 4 months of infection, C57BL/6 mice developed severe gastritis and atrophy and mounted a Th1-type response towards H. pylori. The Th1 response was abrogated in IRF-1(-/-) mice. This defective Th1 response was associated with the total lack of gastritis and atrophy in IRF-1(-/-) mice despite severe colonization with H. pylori. In addition, IRF-1(-/-) mice did also not develop a Th2 reaction, since they failed to generate H. pylori-specific antibodies and to produce IL-4 in response to H. pylori antigens in vitro. Thus, the transcription factor IRF-1 is necessary for the development of gastritis and atrophy in H. pylori-infected wild-type mice, suggesting a role of Th1 cells in the pathogenesis of H. pylori-associated diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Bacterial / blood
  • DNA-Binding Proteins / physiology*
  • Female
  • Gastritis / etiology*
  • Gastritis / microbiology
  • Helicobacter Infections / immunology*
  • Helicobacter pylori / immunology*
  • Immunoglobulin G / blood
  • Interferon Regulatory Factor-1
  • Mice
  • Mice, Inbred C57BL
  • Phosphoproteins / physiology*
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*

Substances

  • Antibodies, Bacterial
  • DNA-Binding Proteins
  • Immunoglobulin G
  • Interferon Regulatory Factor-1
  • Irf1 protein, mouse
  • Phosphoproteins