BACKGROUND: There is still controversy about the relationship between Helicobacter pylori infection and autoimmune gastritis. The aim of this study was to clarify whether or not H. pylori infection interacts with the development of autoimmune gastritis. METHODS: Neonatally thymectomized BALB/c mice with autoimmune gastritis received orally administered H. pylori and were examined histologically and serologically. The T-helper (Th)1/Th2 immune balance in the microenvironment of the stomach was evaluated by reverse-transcriptase-polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma and interleukin (IL)-4. RESULTS: Uninfected mice showed disappearance of parietal cells, and upregulation of IFN-Gamma, but no germinal center formation. The infected neonatally thymectomized mice showed follicular gastritis, preserved parietal cells, decreased serum anti-parietal antibodies, and upregulation of IL-4 and IFN-gamma. CONCLUSIONS: H. pylori infection changes the microenvironment of the gastric mucosa by inducing a Th2 immune response in addition to a Th1 response, and regresses autoimmune gastritis in neonatally thymectomized BALB/c mice.
BACKGROUND: There is still controversy about the relationship between Helicobacter pyloriinfection and autoimmune gastritis. The aim of this study was to clarify whether or not H. pyloriinfection interacts with the development of autoimmune gastritis. METHODS: Neonatally thymectomized BALB/c mice with autoimmune gastritis received orally administered H. pylori and were examined histologically and serologically. The T-helper (Th)1/Th2 immune balance in the microenvironment of the stomach was evaluated by reverse-transcriptase-polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma and interleukin (IL)-4. RESULTS: Uninfected mice showed disappearance of parietal cells, and upregulation of IFN-Gamma, but no germinal center formation. The infected neonatally thymectomized mice showed follicular gastritis, preserved parietal cells, decreased serum anti-parietal antibodies, and upregulation of IL-4 and IFN-gamma. CONCLUSIONS:H. pyloriinfection changes the microenvironment of the gastric mucosa by inducing a Th2 immune response in addition to a Th1 response, and regresses autoimmune gastritis in neonatally thymectomized BALB/c mice.