Helicobacter pylori infection in the cat: Evaluation of gastric colonization, inflammation and function

Background. Further elucidation of the consequences of Helicobacter pylori infection on gastric mucosal inflammation and gastric secretory function wo uld be facilitated by an animal model that is susceptible to infection with H, pylori, is broadly similar in gastric physiology and pathology to peopl e, and is amenable to repeated non-invasive evaluation. The goal of this st udy was to examine the interrelationship of bacterial colonization, mucosal inflammation and gastric secretory function in cats with naturally acquire d H. pylori infection. Materials and Methods. Twenty clinically healthy cats with naturally acquir ed H. pylori infection (cdgA(-), picB) and 19 Helicobacter-free cats were e valuated. Gastric colonization was determined by tissue urease activity, li ght microscopy, culture and PCR. The mucosal inflammatory response was eval uated by light microscopy, and by RT-PCR of the pro-inflammatory cytokines IL-1 alpha, IL-1 beta, IL-8 and TNF-alpha in gastric mucosa. Gastric secret ory function was assessed by measuring pentagastrin-stimulated acid secreti on, fasting plasma gastrin, and antral mucosal gastrin and somatostatin imm unoreactivity. Results. H. pylori colonized the pylorus, fundus and cardia in similar dens ity. Bacteria were observed free in the lumen of gastric glands and were al so tightly adherent to epithelial cells where they were associated with mic rovillus effacement. Mononuclear inflammation, lymphoid follicle hyperplasi a, atrophy and fibrosis were observed primarily in H. pylori-infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic inf iltrates, epithelial dysplasia, and upregulation of mucosal IL-1 beta and I L-8 were observed solely in infected cats. Fasting plasma gastrin concentra tions and pentagastrin stimulated acid output were similar in both infected and uninfected cats. There was no relationship of bacterial colonization d ensity or gastric inflammation to plasma gastrin concentrations or gastric acid output. Conclusions. The pattern of colonization and the mucosal inflammatory respo nse in cats with naturally acquired H, pylori are broadly similar to those in infected people, particularly children, and non human primates. The upre gulation of IL-8 in infected cats was independent of cagA and picB. Our fin dings argue against a direct acid-suppressing effect of H. pylori on the ga stric secretory-axis in chronically infected cats.