Apoptosis of gastric lymphocytes in Helicobacter pylori-infected rhesus macaques.
In vitro studies suggest that H. pylori induces apoptosis in gastric epithelial cells and perhaps in gastric lymphocytes as well. However, the early effects of H. pylori infection on lymphocyte apoptosis have not been examined in experimental animal models, nor have studies been performed using markers specific for T cells and T-cell subsets. Gastric T-cell apoptosis and Fas ligand expression were examined by flow cytometry after experimental infection of rhesus macaques with H. pylori. Infection induced transient apoptosis of gastric CD4+ and CD8+ T-cells, which began as soon as three days after inoculation and declined to baseline within eight weeks. Fas ligand expression showed a similar transient induction, suggesting that it mediates gastric T-cell apoptosis. We propose that transient, Fas-mediated apoptosis in gastric lymphocytes is a compensatory response to the initial T-cell inflammatory response after acute H. pylori infection.
Dandekar
Satya
S
Department of Medical Microbiology and Immunology, University of California, Davis, California 95616, USA.
Reay
Elizabeth
E
Taylor
Jennifer M
JM
Solnick
Jay V
JV
D000818:Animals; D017209:Apoptosis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D008253:Macaca mulatta; D008297:Male; D013270:Stomach / Q000473:pathology; D013601:T-Lymphocytes / Q000473:pathology*; D019014:fas Receptor / Q000378:metabolism
D007074:Immunoglobulin G; D019014:fas Receptor