The inflammatory response in CD1 mice shortly after infection with a CagA+/VacA+ Helicobacter pylori strain.
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.
van Doorn
N E
NE
Department of Medical Microbiology, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands.
van Rees
E P
EP
Namavar
F
F
Ghiara
P
P
Vandenbroucke-Grauls
C M
CM
de Graaff
J
J
D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial; D001323:Autoantibodies / Q000097:blood; D001402:B-Lymphocytes / Q000276:immunology; D001426:Bacterial Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D005756:Gastritis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D016481:Helicobacter Infections / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D016480:Helicobacter pylori / Q000145:classification / Q000276:immunology / Q000472:pathogenicity*; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D007074:Immunoglobulin G / Q000097:blood; D007150:Immunohistochemistry; D007249:Inflammation / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D008407:Mast Cells / Q000473:pathology; D051379:Mice; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D013997:Time Factors
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001323:Autoantibodies; D001426:Bacterial Proteins; D000949:Histocompatibility Antigens Class II; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori