ArticleInfection and immunity2004
Functional analysis of the cag pathogenicity island in Helicobacter pylori isolates from patients with gastritis, peptic ulcer, and gastric cancer.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 129 citations in OpenAlex.
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- CagL polymorphisms between East Asian and Western Helicobacter pylori are associated with different abilities to induce IL-8 secretion.Journal of microbiology (Seoul, Korea) · 2021Article
- Cortactin Is Required for Efficient FAK, Src and Abl Tyrosine Kinase Activation and Phosphorylation ofInternational journal of molecular sciences · 2021Article
- Role of Serum Pepsinogen II andGut and liver · 2020Article
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- Type IV secretion ofGut pathogens · 2020Article
- T4SS-dependent TLR5 activation by Helicobacter pylori infection.Nature communications · 2019Article
- Tailor-Made Detection of Individual Phosphorylated and Non-Phosphorylated EPIYA-Motifs ofCancers · 2019Article
- Establishment of serine protease htrA mutants in Helicobacter pylori is associated with secA mutations.Scientific reports · 2019Article
- Flagellin glycosylation with pseudaminic acid in Campylobacter and Helicobacter: prospects for development of novel therapeutics.Cellular and molecular life sciences : CMLS · 2018Review
- Detection of human papillomavirus DNA in gastric carcinoma specimens in a high-risk region of Iran.Biomedical reports · 2016Article
- Characterisation of worldwide Helicobacter pylori strains reveals genetic conservation and essentiality of serine protease HtrA.Molecular microbiology · 2016Article
- Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis.World journal of gastroenterology · 2015Review
- The distribution of jhp0940, jhp0945, jhp0947, jhp0949 and jhp0951 genes of Helicobacter pylori in China.BMC gastroenterology · 2015Article
- Article
- Infection with CagA-positive Helicobacter pylori strain containing three EPIYA C phosphorylation sites is associated with more severe gastric lesions in experimentally infected Mongolian gerbils (Meriones unguiculatus).European journal of histochemistry : EJH · 2015Article
- Coiled coil rich proteins (Ccrp) influence molecular pathogenicity of Helicobacter pylori.PloS one · 2015Article
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is the causative agent of a variety of gastric diseases, but the clinical relevance of bacterial virulence factors is still controversial. Virulent strains carrying the cag pathogenicity island (cagPAI) are thought to be key players in disease development. Here, we have compared cagPAI-dependent in vitro responses in H. pylori isolates obtained from 75 patients with gastritis, peptic ulcer, and gastric cancer (n = 25 in each group). AGS gastric epithelial cells were infected with each strain and assayed for (i) CagA expression, (ii) translocation and tyrosine phosphorylation of CagA, (iii) c-Src inactivation, (iv) cortactin dephosphorylation, (v) induction of actin cytoskeletal rearrangements associated with cell elongation, (vi) induction of cellular motility, and (vii) secretion of interleukin-8. Interestingly, we found high but similar prevalences of all of these cagPAI-dependent host cell responses (ranging from 56 to 80%) among the various groups of patients. This study revealed CagA proteins with unique features, CagA subspecies of various sizes, and new functional properties for the phenotypic outcomes. We further showed that induction of AGS cell motility and elongation are two independent processes. Our data corroborate epidemiological studies, which indicate a significant association of cagPAI presence and functionality with histopathological findings in gastritis, peptic ulcer, and gastric cancer patients, thus emphasizing the importance of the cagPAI for the pathogenicity of H. pylori. Nevertheless, we found no significant association of the specific H. pylori-induced responses with any particular patient group. This may indicate that the determination of disease development is highly complex and involves multiple bacterial and/or host factors.
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