TITLE

Roles of virD4 and cagG genes in the cag pathogenicity island of Helicobacter pylori using a Mongolian gerbil model

AUTHOR(S)
Soito, H; Yamaoka, Y; Ishizone, S; Maruta, F; Sugiyama, A; Graham, D Y; Yamauchi, K; Olo, H; Miyagawa, S
PUB. DATE
May 2005
SOURCE
Gut;May2005, Vol. 54 Issue 5, p584
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background and Aims: The roles of the virD4 and the cagG genes in the cog pathogen icily island of Helicobacter pylon for gastroduodenal pathogenesis are unclear and their roles in vivo have not been examined. Methods: Seven week old male Mongolian gerbils were inoculated with the wild type H pylon TN2GF4, its isogenic virD4, or cagG mutants. Animals were sacrificed at 4, 12, and 24 weeks after inoculation. Gastric inflammation and H pylori density were evaluated by histology, inflammatory response (as measured by interleukin (IL)-1 β mRNA levels), proliferative activity (as assessed by 5'-bromo- E 2'deoxyuridine labelling indices), and host systemic reaction (as measured by anti-H pylon IgG antibody). Results: Degree of gastric inflammation, proliferative activity, and mucosal IL-1 β mRNA levels remained low throughout the first 12 weeks in gerbils infected with the virD4 mutants. Degree of gastric inflammation and proliferative activity increased at 24 weeks with the virD4 mutants reaching levels comparative with p those seen at four weeks with the wild-type strains. Mucosal IL-1 β mRNA levels were also increased at 24 weeks with the vinD4 mutants and levels at 24 weeks were similar between the wild-type and virD4 mutants. In contrast, gerbils infected with the cogG mutants had reduced ability to colonise gerbils, and no or little gastric inflammation or proliferative activity was observed. Conclusions: loss of the vinD4 gene temporally retarded but did not abrogate gastric inflammation. Loss of the cagG gene abolished gastric inflammation partially via reduced ability to colonise gerbils. Unknown factors related to the type IV secretion system other than CagA may influence gastric inflammation.
ACCESSION #
16886327

 

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