Okazaki Kazuichi, Ohana Masaya, Oshima Chikashi, Uchida Kazushige, Nishi Toshiki, Iwano Masahiro, Fukui Toshiro, Kawasaki Kimio, Matsuura Minoru, Asada Masanori, Tamaki Hiroyuki, Hiai Hiroshi, Chiba Tsutomu
Department of Endoscopic Medicine and Gastroenterology, Kyoto University Hospital, Kyoto, Japan.
J Gastroenterol. 2003;38(12):1131-7. doi: 10.1007/s00535-003-1219-3.
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.
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.
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.
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.
幽门螺杆菌感染与自身免疫性胃炎之间的关系仍存在争议。本研究的目的是阐明幽门螺杆菌感染是否与自身免疫性胃炎的发展相互作用。
对患有自身免疫性胃炎的新生期胸腺切除的BALB/c小鼠口服给予幽门螺杆菌,并进行组织学和血清学检查。通过逆转录聚合酶链反应(RT-PCR)检测胃微环境中辅助性T细胞(Th)1/Th₂免疫平衡,检测干扰素(IFN)-γ和白细胞介素(IL)-4。
未感染的小鼠壁细胞消失,IFN-γ上调,但无生发中心形成。感染幽门螺杆菌的新生期胸腺切除小鼠表现为滤泡性胃炎,壁细胞保留,血清抗壁细胞抗体降低,IL-4和IFN-γ上调。
幽门螺杆菌感染除诱导Th1反应外,还通过诱导Th2免疫反应改变胃黏膜微环境,并使新生期胸腺切除的BALB/c小鼠的自身免疫性胃炎消退。