Nishikawa Kaori, Nakamura Masahiko, Takahashi Shinichi, Matsui Hidenori, Murayama Somay Yamagata, Matsumoto Tsukasa, Yamada Haruki, Tsuchimoto Kanji
3 Department of Internal Medicine, Kyorin University, Mitaka, Tokyo, Japan.
FEMS Immunol Med Microbiol. 2007 Jul;50(2):268-72. doi: 10.1111/j.1574-695X.2007.00252.x. Epub 2007 May 4.
Helicobacter heilmannii has been reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, but its precise pathophysiological mechanism remains to be clarified. We recently established a model of gastric B-cell MALT lymphoma in C57BL/6 mice by means of peroral infection of H. heilmannii primarily obtained from cynomolgus monkeys. Using this model, macroscopic, immunohistochemical, and electron microscopic observations of MALT lymphomas were carried out in order to examine the development of apoptosis and angiogenesis. Enhancement of the microvascular network and an increase in vascular endothelial growth factor-A were detected in the central region of the MALT lymphoma tissue in the infected mouse stomach, while vascular endothelial growth factor-C was detected at the margins of the MALT lymphomas. In addition, many H. heilmannii-invaded parietal cells showed caspase-3 immunoreactivity in the fundic mucosal tissue surrounding the MALT lymphoma. In conclusion, in H. heilmannii-induced MALT lymphoma, enhanced immunoreactivity of vascular endothelial growth factor-A and factor-C was observed in areas encircled by increased parietal cell apoptosis, which indicates the pathophysiological relevance of both angiogenesis and apoptosis in MALT lymphoma formation.
据报道，海尔曼螺杆菌可导致胃低度黏膜相关淋巴组织型（MALT）淋巴瘤，但其确切的病理生理机制仍有待阐明。我们最近通过经口感染主要从食蟹猴获得的海尔曼螺杆菌，在C57BL/6小鼠中建立了胃B细胞MALT淋巴瘤模型。利用该模型，对MALT淋巴瘤进行了宏观、免疫组织化学和电子显微镜观察，以研究细胞凋亡和血管生成的发展情况。在感染小鼠胃中MALT淋巴瘤组织的中央区域检测到微血管网络增强和血管内皮生长因子-A增加，而在MALT淋巴瘤边缘检测到血管内皮生长因子-C。此外，在MALT淋巴瘤周围的胃黏膜组织中，许多被海尔曼螺杆菌侵袭的壁细胞显示出半胱天冬酶-3免疫反应性。总之，在海尔曼螺杆菌诱导的MALT淋巴瘤中，在壁细胞凋亡增加所包围的区域观察到血管内皮生长因子-A和因子-C的免疫反应性增强，这表明血管生成和细胞凋亡在MALT淋巴瘤形成中具有病理生理相关性。
