Lee A, Chen M, Coltro N, O'Rourke J, Hazell S, Hu P, Li Y
School of Microbiology and Immunology, University of New South Wales, Sydney, Australia.
Zentralbl Bakteriol. 1993 Sep;280(1-2):38-50. doi: 10.1016/s0934-8840(11)80939-4.
Gastric atrophy is a precursor lesion in the development of gastric cancer. It has been proposed that atrophy is part of a natural progression of inflammatory changes that result from long term infection with the bacterium Helicobacter pylori. The aim of this study was to test this hypothesis using an animal model of human Helicobacter infection. Conventional mice were infected with either a cat isolate of Helicobacter felis or a human isolate of "Gastrospirillum hominis". All infected mice showed a slowly progressive chronic gastritis with increasing numbers of infiltrating mononuclear cells and polymorphonuclear leucocytes. After a year and a half, the inflammatory reaction was so severe that atrophic changes were seen in both the antral and fundic mucosa. Control animals initially showed no inflammatory changes however as the animals aged, the gastric mucosa of some animals became infected with a bacterium Helicobacter muridarum that normally inhabits the small and large bowel of the rodent. The presence of this bacterium was also associated with gastritis and atrophic changes. This is the first report of experimentally induced atrophic changes induced by a gastric bacterium and opens the way for important experiments that will help better understand the induction of gastric cancer.
胃萎缩是胃癌发生过程中的一种前驱病变。有人提出，萎缩是由幽门螺杆菌长期感染导致的炎症变化自然进展的一部分。本研究的目的是使用人类幽门螺杆菌感染的动物模型来验证这一假设。将传统小鼠分别感染猫源幽门螺杆菌分离株或人源“人胃螺杆菌”分离株。所有感染小鼠均表现出缓慢进展的慢性胃炎，浸润的单核细胞和多形核白细胞数量增加。一年半后，炎症反应非常严重，在胃窦和胃底黏膜均出现萎缩性改变。对照动物最初未表现出炎症变化，然而随着动物年龄增长，一些动物的胃黏膜感染了通常栖息于啮齿动物小肠和大肠的鼠幽门螺杆菌。这种细菌的存在也与胃炎和萎缩性改变有关。这是关于由胃细菌实验诱导萎缩性改变的首次报告，为有助于更好地理解胃癌诱导机制的重要实验开辟了道路。
