title: Virulence factors of Helicobacter pylori responsible for gastric diseases in Mongolian gerbil.
abstract: Helicobacter pylori infection induces various gastroduodenal diseases. We examined the role of two genes, vacA and cagE, in the gastric pathogenesis induced by H. pylori using a long-term (62 wk) animal model. Reportedly, both genes are associated with the virulence of H. pylori: vacA encodes vacuolating cytotoxin, and cagE, with other genes in the cag pathogenicity islands, encodes a type IV secretion system. Mongolian gerbils were challenged in this study by a wild-type TN2 strain and its isogenic mutants of cagE or vacA. The wild-type and vacA mutants induced severe gastritis, whereas cagE mutants induced far milder changes. Gastric ulcer was induced at the highest rate (22/23) by the wild-type TN2, followed by the vacA mutant (19/28). No ulcer was found in the gerbils infected with the cagE mutant (0/27) or in controls (0/27). Intestinal metaplasia was also found in the gerbils infected with the wild-type (14/23) or vacA mutant (15/28). Gastric cancer developed in one gerbil with wild-type infection and in one with vacA mutant infection. In conclusion, the knocking out of the cagE gene deprived wild-type H. pylori of the pathogenicity for gastritis and gastric ulcer, suggesting that the secretion system encoded by cag pathogenicity island genes plays an essential role.
authors: Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan. OGURA-2IM@h.u-tokyo.ac.jp
authors: K
authors: K
authors: Ogura
authors: S
authors: S
authors: Maeda
authors: M
authors: M
authors: Nakao
authors: T
authors: T
authors: Watanabe
authors: M
authors: M
authors: Tada
authors: T
authors: T
authors: Kyutoku
authors: H
authors: H
authors: Yoshida
authors: Y
authors: Y
authors: Shiratori
authors: M
authors: M
authors: Omata
mesh_terms: D000230:Adenocarcinoma / Q000382:microbiology / Q000473:pathology; D000818:Animals; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D001427:Bacterial Toxins / Q000235:genetics; D003603:Cytotoxins / Q000235:genetics / Q000502:physiology*; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D016680:Genome, Bacterial; D005849:Gerbillinae; D016480:Helicobacter pylori / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity*; D008297:Male; D016296:Mutagenesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013272:Stomach Diseases / Q000382:microbiology* / Q000473:pathology; D013274:Stomach Neoplasms / Q000382:microbiology / Q000473:pathology; D013276:Stomach Ulcer / Q000382:microbiology / Q000473:pathology; D013997:Time Factors; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D003603:Cytotoxins; C103937:PicB protein, Helicobacter pylori; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori