PMID:11104802

Citation	Ogura, K, Maeda, S, Nakao, M, Watanabe, T, Tada, M, Kyutoku, T, Yoshida, H, Shiratori, Y and Omata, M (2000) Virulence factors of Helicobacter pylori responsible for gastric diseases in Mongolian gerbil. J. Exp. Med. 192:1601-10
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.
Links	PubMed PMC2193104
Keywords	Adenocarcinoma/microbiology; Adenocarcinoma/pathology; Animals; Antigens, Bacterial; Bacterial Proteins/genetics; Bacterial Proteins/physiology; Bacterial Toxins/genetics; Cytotoxins/genetics; Cytotoxins/physiology; Disease Models, Animal; Gastric Mucosa/microbiology; Gastric Mucosa/pathology; Gastritis/microbiology; Gastritis/pathology; Genome, Bacterial; Gerbillinae; Helicobacter pylori/genetics; Helicobacter pylori/growth & development; Helicobacter pylori/pathogenicity; Male; Mutagenesis; Reverse Transcriptase Polymerase Chain Reaction; Stomach Diseases/microbiology; Stomach Diseases/pathology; Stomach Neoplasms/microbiology; Stomach Neoplasms/pathology; Stomach Ulcer/microbiology; Stomach Ulcer/pathology; Time Factors; Virulence
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
HELPX:Q9R2Y4		GO:0009405: pathogenesis	ECO:0000315:		P		Table 4 shows gerbils infected with TN2ΔvacA mutants developed significantly fewer ulcers than gerbils infected with wild type H. pylori.	complete CACAO 9849

References

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