Simpson K W, Strauss-Ayali D, Straubinger R K, Scanziani E, McDonough P L, Straubinger A F, Chang Y F, Esteves M I, Fox J G, Domeneghini C, Arebi N, Calam J
College of Veterinary Medicine, Cornell University, Ithaca NY 14853, USA.
Helicobacter. 2001 Mar;6(1):1-14. doi: 10.1046/j.1523-5378.2001.00010.x.
Further elucidation of the consequences of Helicobacter pylori infection on gastric mucosal inflammation and gastric secretory function would be facilitated by an animal model that is susceptible to infection with H. pylori, is broadly similar in gastric physiology and pathology to people, and is amenable to repeated non-invasive evaluation. The goal of this study was to examine the interrelationship of bacterial colonization, mucosal inflammation and gastric secretory function in cats with naturally acquired H. pylori infection.
Twenty clinically healthy cats with naturally acquired H. pylori infection (cagA-, picB) and 19 Helicobacter-free cats were evaluated. Gastric colonization was determined by tissue urease activity, light microscopy, culture and PCR. The mucosal inflammatory response was evaluated by light microscopy, and by RT-PCR of the pro-inflammatory cytokines IL-1alpha, IL-1beta, IL-8 and TNF-alpha in gastric mucosa. Gastric secretory function was assessed by measuring pentagastrin-stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity.
H. pylori colonized the pylorus, fundus and cardia in similar density. Bacteria were observed free in the lumen of gastric glands and were also tightly adherent to epithelial cells where they were associated with microvillus effacement. Mononuclear inflammation, lymphoid follicle hyperplasia, atrophy and fibrosis were observed primarily in H. pylori-infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up-regulation of mucosal IL-1beta and IL-8 were observed solely in infected cats. Fasting plasma gastrin concentrations and pentagastrin-stimulated acid output were similar in both infected and uninfected cats. There was no relationship of bacterial colonization density or gastric inflammation to plasma gastrin concentrations or gastric acid output.
The pattern of colonization and the mucosal inflammatory response in cats with naturally acquired H. pylori are broadly similar to those in infected people, particularly children, and non-human primates. The upregulation of IL-8 in infected cats was independent of cagA and picB. Our findings argue against a direct acid-suppressing effect of H. pylori on the gastric secretory-axis in chronically infected cats.
一种易感染幽门螺杆菌、胃生理和病理与人广泛相似且适合进行反复无创评估的动物模型，将有助于进一步阐明幽门螺杆菌感染对胃黏膜炎症和胃分泌功能的影响。本研究的目的是检查自然感染幽门螺杆菌的猫中细菌定植、黏膜炎症和胃分泌功能之间的相互关系。
对20只自然感染幽门螺杆菌（cagA-、picB）的临床健康猫和19只无幽门螺杆菌的猫进行评估。通过组织尿素酶活性、光学显微镜、培养和聚合酶链反应确定胃定植情况。通过光学显微镜以及对胃黏膜中促炎细胞因子白细胞介素-1α、白细胞介素-1β、白细胞介素-8和肿瘤坏死因子-α进行逆转录聚合酶链反应来评估黏膜炎症反应。通过测量五肽胃泌素刺激的胃酸分泌、空腹血浆胃泌素以及胃窦黏膜胃泌素和生长抑素免疫反应性来评估胃分泌功能。
幽门螺杆菌在幽门、胃底和贲门的定植密度相似。在胃腺管腔中观察到游离的细菌，并且它们还紧密附着于上皮细胞，在此处它们与微绒毛消失有关。单核炎症、淋巴滤泡增生、萎缩和纤维化主要在幽门螺杆菌感染的猫中观察到，幽门受影响最严重。仅在感染的猫中观察到嗜中性和嗜酸性浸润、上皮发育异常以及黏膜白细胞介素-1β和白细胞介素-8的上调。感染和未感染的猫空腹血浆胃泌素浓度和五肽胃泌素刺激的酸分泌相似。细菌定植密度或胃炎与血浆胃泌素浓度或胃酸分泌之间没有关系。
自然感染幽门螺杆菌的猫的定植模式和黏膜炎症反应与感染的人，特别是儿童以及非人灵长类动物广泛相似。感染猫中白细胞介素-8的上调独立于cagA和picB。我们的研究结果反对幽门螺杆菌对慢性感染猫的胃分泌轴有直接的抑酸作用。
