Nagai Shigenori, Mimuro Hitomi, Yamada Taketo, Baba Yukiko, Moro Kazuyo, Nochi Tomonori, Kiyono Hiroshi, Suzuki Toshihiko, Sasakawa Chihiro, Koyasu Shigeo
Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Proc Natl Acad Sci U S A. 2007 May 22;104(21):8971-6. doi: 10.1073/pnas.0609014104. Epub 2007 May 14.
Helicobacter pylori is a Gram-negative spiral bacterium that causes gastritis and peptic ulcer and has been implicated in the pathogenesis of gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. Although Th1 immunity is involved in gastritis and the accumulation of H. pylori-specific CD4(+) T cells in the H. pylori-infected gastric mucosa in human patients, how T cells are primed with H. pylori antigens is unknown because no apparent lymphoid tissues are present in the stomach. We demonstrate here that Peyer's patches (PPs) in the small intestine play critical roles in H. pylori-induced gastritis; no gastritis is induced in H. pylori-infected mice lacking PPs. We also observed that the coccoid form of H. pylori is phagocytosed by dendritic cells in PPs. We propose that H. pylori converts to the coccoid form in the anaerobic small intestine and stimulates the host immune system through PPs.
幽门螺杆菌是一种革兰氏阴性螺旋菌,可引起胃炎和消化性溃疡,并与胃腺癌和黏膜相关淋巴组织淋巴瘤的发病机制有关。虽然Th1免疫参与了人类患者胃炎以及幽门螺杆菌感染的胃黏膜中幽门螺杆菌特异性CD4(+) T细胞的积累,但由于胃中不存在明显的淋巴组织,T细胞如何被幽门螺杆菌抗原致敏尚不清楚。我们在此证明,小肠中的派尔集合淋巴结(PPs)在幽门螺杆菌诱导的胃炎中起关键作用;缺乏PPs的幽门螺杆菌感染小鼠不会诱发胃炎。我们还观察到,幽门螺杆菌的球形体形式被PPs中的树突状细胞吞噬。我们提出,幽门螺杆菌在厌氧的小肠中转化为球形体形式,并通过PPs刺激宿主免疫系统。