Establishment ofHelicobacter pyloriinfection model in Mongolian gerbils

Abstract

AIM:To establish a stable and reliable model of Helicobacter pylori infection model in Mongolian gerbils and to observe pathological changes in gastric mucosa in infected animals. METHODS:Mongolian gerbils were randomly divided into 18 groups; 6 groups were infected with H pylori clinical strain Y06 (n=6, groups Y), 6 groups were infected with H pylori strain NCTC11637 (n=6, groups N), and 6 uninfected groups as negative controls (n=4, groups C). H pylori suspensions at the concentrations of 2×10 8 and 2×10 9 CFU/mL of strain NCTC11637 and strain Y06 were prepared. The animals in three groups N and in three groups Y were orally challenged once with 0.5 mL of the low concentration of the bacterial suspension. The animals in another three groups N and in another three groups Y were orally challenged with 0.5 mL of the high concentration of the bacterial suspension for 3 times at the intervals of 24 h, respectively. For the negative controls, the animals in six groups C were orally given w i th t he s am e v ol u m e o f Br u c el l a b r o t h a t t h e corresponding inoculating time. The animals were killed after 2nd, 4 th and 6 th week after the last challenge and the gastric mucosal specimens were taken for urease test, bacterial isolation, pathological and immunohistochemical examinations. RESULTS:Positive isolation rates of H pylori in the animals of groups Y at the 2nd, 4 th and 6 th week after one challenge were 0%, 16.7% and 66.7%, while in the animals of groups N were 0%, 0% and 16.7%, respectively. Positive isolation rates of H pylori in the animals of groups Y at the 2nd, 4 th and 6 th week after three challenges were 66.7%, 100% and 100%, while in the animals of groups N were 66.7%, 66.7% and 100%, respectively. In animals with positive isolation of H pylori, the bacterium was found to colonized on the surface of gastric mucosal cells and in the gastric pits, and the gastric mucosal lamina propria was infiltrated with inflammatory cells.

Phosphorylation of phosphatase and tensin homolog induced by Helicobacter pylori promotes cell invasion by activation of focal adhesion kinase

“…The use of various animal species and bacterial strains results in a large variability in the reported results ( 40 ). Mongolian gerbils are a unique model due to their low incidence of naturally occurring gastritis and bacterial disease, and have, therefore, commonly been used for studying infection with a standard strain of H. pylori (ATCC43504) ( 41 ). The results of the current study demonstrate that, concordant with previous results from patients ( 28 ), 6–12 months of infection in these gerbils did not significantly alter PTEN expression levels.…”

Animal Models and Helicobacter pylori Infection

“…H. pylori infection in the gastric mucosa of Mongolian gerbils exhibits a significant level of gastric inflammation after multiple inoculations with a high concentration of bacterial challenge, contributing to increased infection rates [ 73 ]. In one study, Mongolian gerbils developed moderate atrophy after 12 months of infection with H. pylori 26695, whereas no metaplasia was observed until 12 months, and light metaplasia was observed after 18 months [ 74 ].…”

Interaction between intestinal flora and gastric cancer in tumor microenvironment

“…It is well established that H. pylori infection is a major risk factor for intestinal GC, with the International Agency for Research on Cancer classifying it as a class I carcinogen as early as 1994 ( 30 ). Animal infection models have shown that H. pylori can induce GC in Mongolian gerbils, closely resembling the Correa model of intestinal GC ( 31 , 32 ). Infection with H. pylori leads to chronic inflammation of the gastric mucosa, destruction of oxytocin cells, an increase in stomach pH, and an imbalance in the gastric microbiota, resulting in decreased H. pylori levels and colonization by non- H. pylori bacteria.…”