Matsushima Y, Kinoshita Y, Watanabe M, Hassan S, Fukui H, Maekawa T, Okada A, Kawanami C, Kishi K, Watanabe N, Nakao M, Chiba T
Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Digestion. 1999 Jan-Feb;60(1):34-40. doi: 10.1159/000007586.
Inoculation of Helicobacter felis into the murine stomach has been reported to induce chronic gastric inflammation and may be a model of Helicobacter pylori-induced chronic gastritis. In this study, to characterize H. felis-induced gastritis, the gastric production of interleukin-1beta (IL-1beta) and hepatocyte growth factor (HGF) was measured in mice.
Gastric mucosal lesions were induced in H. felis-infected BALB/c mice by water-immersion stress. The severity score of gastric erosions per stomach was measured as the sum of the length of erosions. Gene expression of IL-1beta and HGF were analyzed by Northern blot analysis and production of HGF was examined using the enzyme immunoassay method.
Water-immersion stress induced gastric mucosal lesions accompanied by increased expression of IL-1beta mRNA. H. felis infection evoked enhanced expression of IL-1beta and HGF genes. When H. felis-infected mice were stressed by water immersion, the mucosal lesions were more severe than those in non-infected mice. Moreover, IL-1beta gene expression as well as HGF production was further increased.
Although H. felis inoculation did not cause gastric mucosal erosions by itself, it augmented the stress-induced erosions.
据报道，将猫幽门螺杆菌接种到小鼠胃内可诱发慢性胃炎症，可能是幽门螺杆菌诱发慢性胃炎的一种模型。在本研究中，为了明确猫幽门螺杆菌诱发胃炎的特征，对小鼠胃内白细胞介素-1β（IL-1β）和肝细胞生长因子（HGF）的产生情况进行了测定。
通过水浸应激在感染猫幽门螺杆菌的BALB/c小鼠中诱发胃黏膜损伤。将每只胃的胃糜烂严重程度评分测定为糜烂长度之和。通过Northern印迹分析检测IL-1β和HGF的基因表达，并使用酶免疫测定法检测HGF的产生情况。
水浸应激诱发了胃黏膜损伤，同时伴有IL-1β mRNA表达增加。猫幽门螺杆菌感染引起IL-1β和HGF基因表达增强。当感染猫幽门螺杆菌的小鼠受到水浸应激时，其黏膜损伤比未感染小鼠更严重。此外，IL-1β基因表达以及HGF产生进一步增加。
虽然接种猫幽门螺杆菌本身不会引起胃黏膜糜烂，但它会加剧应激诱导的糜烂。
