The researchers examined the interrelationship of bacterial colonization, mucosal inflammation, and gastric secretory function in cats with naturally acquired Helicobacter pylori infection.
They reported their findings in the March issue of Helicobacter.
20 clinically healthy cats with naturally acquired H. pylori infection (cagA-, picB), and 19 Helicobacter-free cats were evaluated.
|Mucosal IL-1b and IL-8 upregulated in H. pylori-infected cats.
Tissue urease activity, light microscopy, cultures, and PCR were used to determine gastric colonization.
The mucosal inflammatory response was evaluated by light microscopy, and by RT-PCR of the pro-inflammatory cytokines IL-1a, IL-1b, IL-8, and TNF-a in gastric mucosa.
Measuring pentagastrin-stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity assessed gastric secretory function.
The researchers found that 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-1b and IL-8 were observed solely in infected cats.
Fasting plasma gastrin concentrations and pentagastrin-stimulated acid output were found to be similar in both infected and uninfected cats.
In addition, there was no relationship of bacterial colonization density or gastric inflammation to plasma gastrin concentrations or gastric acid output.
Kenneth W. Simpson, of the College of Veterinary Medicine, Cornell University, Ithaca, New York, said on behalf of the group, "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," he concluded.