ArticleGut2005
Roles of virD4 and cagG genes in the cag pathogenicity island of Helicobacter pylori using a Mongolian gerbil model.
Article in Gut, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Transient Intraperitoneal Residence ofPathogens (Basel, Switzerland) · 2026Article
- Roles of the components of theFuture microbiology · 2024Review
- Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Animal Models andJournal of clinical medicine · 2022Review
- Genomic population structure ofVirulence · 2021Article
- Article
- The Mongolian Gerbil: A Robust Model of Helicobacter pylori-Induced Gastric Inflammation and Cancer.Methods in molecular biology (Clifton, N.J.) · 2016Article
- What exists beyond cagA and vacA? Helicobacter pylori genes in gastric diseases.World journal of gastroenterology · 2015Review
- Clinical relevance of cagPAI intactness in Helicobacter pylori isolates from Vietnam.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010Article
- NF-kappaB activation during acute Helicobacter pylori infection in mice.Infection and immunity · 2008Article
- Pattern of transcription factor activation in Helicobacter pylori-infected Mongolian gerbils.Gastroenterology · 2007Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsThe roles of the virD4 and the cagG genes in the cag pathogenicity island of Helicobacter pylori for gastroduodenal pathogenesis are unclear and their roles in vivo have not been examined.
methodsSeven week old male Mongolian gerbils were inoculated with the wild type H pylori 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)-1beta mRNA levels), proliferative activity (as assessed by 5'-bromo-2'deoxyuridine labelling indices), and host systemic reaction (as measured by anti-H pylori IgG antibody).
resultsDegree of gastric inflammation, proliferative activity, and mucosal IL-1beta 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 those seen at four weeks with the wild-type strains. Mucosal IL-1beta mRNA levels were also increased at 24 weeks with the virD4 mutants and levels at 24 weeks were similar between the wild-type and virD4 mutants. In contrast, gerbils infected with the cagG mutants had reduced ability to colonise gerbils, and no or little gastric inflammation or proliferative activity was observed.
conclusionsLoss of the virD4 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.
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