Nobutani Kentaro, Yoshida Masaru, Nishiumi Shin, Nishitani Yosuke, Takagawa Tetsuya, Tanaka Hiroshi, Yamamoto Koji, Mimura Takuya, Bensuleiman Yahaya, Ota Hiroyoshi, Takahashi Shinichi, Matsui Hidenori, Nakamura Masahiko, Azuma Takeshi
Department of Internal Medicine, Division of Gastroenterology, Kobe University Graduate School of Medicine, Hyogo, Japan.
FEMS Immunol Med Microbiol. 2010 Nov;60(2):156-64. doi: 10.1111/j.1574-695X.2010.00731.x. Epub 2010 Sep 16.
Helicobacter heilmannii induces gastric lymphoid follicles in mice. However, the pathogenic mechanisms behind the induction of gastric lymphoid follicles by H. heilmannii infection have not been elucidated. The aim of this study was to investigate the roles of Peyer's patches (PP) in H. heilmannii-induced immune responses and the development of gastric lymphoid follicles. C57BL/6J and PP deficient mice were infected with H. heilmannii, and in addition to histological and immunohistological examinations, the expression levels of cytokines and chemokines in gastric mucosa were investigated. Gastric lymphoid follicle formation and the infiltration of dendritic cells, B cells, and helper T cells were milder in the PP-deficient mice 1 month after infection, but they were similar in both types of mice after 3 months. The mRNA expression levels of tumor necrosis factor α and CC chemokine ligand 2 were significantly high in the H. heilmannii-infected groups, and CXC chemokine ligand 13 expression was significantly increased in the infected C57BL/6J wild-type mice 1 month after infection. These results suggest that PP are not essential for the formation and development of gastric lymphoid follicles induced by H. heilmannii infection, although they are involved in the speed of gastric lymphoid follicle formation.
海氏螺杆菌可诱导小鼠胃淋巴滤泡形成。然而，海氏螺杆菌感染诱导胃淋巴滤泡形成背后的致病机制尚未阐明。本研究的目的是探讨派尔集合淋巴结（PP）在海氏螺杆菌诱导的免疫反应及胃淋巴滤泡发育中的作用。将C57BL/6J小鼠和PP缺陷小鼠感染海氏螺杆菌，除进行组织学和免疫组织学检查外，还研究了胃黏膜中细胞因子和趋化因子的表达水平。感染后1个月，PP缺陷小鼠的胃淋巴滤泡形成以及树突状细胞、B细胞和辅助性T细胞的浸润程度较轻，但3个月后两种小鼠的情况相似。肿瘤坏死因子α和CC趋化因子配体2的mRNA表达水平在海氏螺杆菌感染组显著升高，感染后1个月，感染的C57BL/6J野生型小鼠中CXC趋化因子配体13的表达显著增加。这些结果表明，PP对于海氏螺杆菌感染诱导的胃淋巴滤泡的形成和发育并非必不可少，尽管它们参与了胃淋巴滤泡形成的速度。
