Asunto(s)
Colangiopancreatografia Retrógrada Endoscópica/efectos adversos , Remoción de Dispositivos/métodos , Cálculos Biliares/terapia , Litotricia/efectos adversos , Anciano , Colangiopancreatografia Retrógrada Endoscópica/métodos , Estudios de Cohortes , Falla de Equipo , Femenino , Estudios de Seguimiento , Cálculos Biliares/diagnóstico , Humanos , Litotricia/métodos , Masculino , Persona de Mediana Edad , Medición de RiesgoRESUMEN
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.