The inflammatory response in CD1 mice shortly after infection with a CagA+/VacA+ Helicobacter pylori strain

Clin Exp Immunol. 1999 Mar;115(3):421-7. doi: 10.1046/j.1365-2249.1999.00789.x.

Abstract

To investigate the early events of Helicobacter pylori infection in a mouse model, CD1 mice were infected with a type I (CagA+/VacA+) H. pylori strain. Up to 4 weeks after infection the majority of gastric tissue biopsies were positive in culture. Immunohistochemical analysis showed that inflammatory changes started to occur after 3 weeks. Four weeks after infection a significant increase in T cells was observed in the cardia/corpus region of the stomachs of infected mice. These T cells were CD4+ and CD8+, and they were located in an area with increased expression of MHC class II antigens. In 50% of the infected mice also an increased number of mast cells was seen. Furthermore, aggregates of B and T cells were present in the submucosa. Characterization of cytokines by immunohistochemistry showed an increase in IL-5-secreting cells in the inflamed area of the infected stomach. No difference was observed between interferon-gamma (IFN-gamma)-, IL-4- and IL-10-secreting cells in control and infected mice. These results suggest that no polarized T-helper cell response was present at this early phase of infection. Infection with H. pylori also induced a serum response and especially IgG was increased after 4 weeks of infection. However, no particular increase in IgG1, IgG2a or IgG3 isotype was observed. Part of the serum antibodies was directed against lipopolysaccharide (LPS), but no evidence for anti-Lewis antibodies or antibodies against epitopes on the gastric mucosa was found.

MeSH terms

  • Animals
  • Antibodies, Bacterial / blood
  • Antigens, Bacterial*
  • Autoantibodies / blood
  • B-Lymphocytes / immunology
  • Bacterial Proteins / metabolism
  • Disease Models, Animal
  • Gastritis / etiology*
  • Gastritis / immunology
  • Gastritis / pathology
  • Helicobacter Infections / etiology*
  • Helicobacter Infections / immunology
  • Helicobacter Infections / pathology
  • Helicobacter pylori / classification
  • Helicobacter pylori / immunology
  • Helicobacter pylori / pathogenicity*
  • Histocompatibility Antigens Class II / metabolism
  • Immunoglobulin G / blood
  • Immunohistochemistry
  • Inflammation / etiology*
  • Inflammation / immunology
  • Inflammation / pathology
  • Lipopolysaccharides / immunology
  • Male
  • Mast Cells / pathology
  • Mice
  • T-Lymphocytes, Helper-Inducer / immunology
  • Time Factors

Substances

  • Antibodies, Bacterial
  • Antigens, Bacterial
  • Autoantibodies
  • Bacterial Proteins
  • Histocompatibility Antigens Class II
  • Immunoglobulin G
  • Lipopolysaccharides
  • VacA protein, Helicobacter pylori
  • cagA protein, Helicobacter pylori