ArticleInfection and immunity2012
In vivo expression of Helicobacter pylori virulence genes in patients with gastritis, ulcer, and gastric cancer.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
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- Transient recombinant expression of highly immunogenicBiotechnology reports (Amsterdam, Netherlands) · 2022Article
- Contribution of Heptose Metabolites and theFrontiers in immunology · 2021Article
- Phenotypic and Genotypic Antibiotic Resistance Patterns inFrontiers in cellular and infection microbiology · 2020Article
- Host Determinants of Expression of the Helicobacter pylori BabA Adhesin.Scientific reports · 2017Article
- Helicobacter pylori vacA transcription is genetically-determined and stratifies the level of human gastric inflammation and atrophy.Journal of clinical pathology · 2016Article
- Expression of cagA, virB/D Complex and/or vacA Genes in Helicobacter pylori Strains Originating from Patients with Gastric Diseases.PloS one · 2016Article
- Cortactin Mediates Apoptosis of Gastric Epithelial Cells Induced by VacA Protein of Helicobacter pylori.Digestive diseases and sciences · 2016Article
- Gastric cancer research in Mexico: a public health priority.World journal of gastroenterology · 2014Review
- Association of the virulence factors of Helicobacter pylori and gastric mucosal interleukin-17/23 mRNA expression in dyspeptic patients.EXCLI journal · 2013Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
The best-studied Helicobacter pylori virulence factor associated with development of peptic ulcer disease or gastric cancer (GC) rather than asymptomatic nonatrophic gastritis (NAG) is the cag pathogenicity island (cagPAI), which encodes a type IV secretion system (T4SS) that injects the CagA oncoprotein into host epithelial cells. Here we used real-time reverse transcription-PCR (RT-PCR) to measure the in vivo expression of genes on the cagPAI and of other virulence genes in patients with NAG, duodenal ulcer (DU), or GC. In vivo expression of H. pylori virulence genes was greater overall in gastric biopsy specimens of patients with GC than in those of patients with NAG or DU. However, since in vitro expression of cagA was not greater in H. pylori strains from patients with GC than in those from patients with NAG or DU, increased expression in GC in vivo is likely a result of environmental conditions in the gastric mucosa, though it may in turn cause more severe pathology. Increased expression of virulence genes in GC may represent a stress response to elevated pH or other environmental conditions in the stomach of patients with GC, which may be less hospitable to H. pylori colonization than the acidic environment in patients with NAG or DU.
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