ArticleScientific reports2018
Evaluating the origin and virulence of a Helicobacter pylori cagA-positive strain isolated from a non-human primate.
Article in Scientific reports, 2018. 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, 16 citations in OpenAlex.
- Microbiome influence in gastric cancer progression and therapeutic strategies.Frontiers in medicine · 2025Review
- Developing a potent vaccine againstExpert reviews in molecular medicine · 2024Review
- Role of MARK2 in the nervous system and cancer.Cancer gene therapy · 2024Review
- Analysis of Genetic Relatedness between Gastric and OralInternational journal of molecular sciences · 2023Article
- Bioengineered Co-culture of organoids to recapitulate host-microbe interactions.Materials today. Bio · 2022Review
- Animal Models andJournal of clinical medicine · 2022Review
- Organoids as host models for infection biology - a review of methods.Experimental & molecular medicine · 2021Review
- Review
- Detection ofPathogens (Basel, Switzerland) · 2020Article
- Application of 16S rRNA gene sequencing inPeerJ · 2020Article
- Molecular anatomy and pathogenic actions of Helicobacter pylori CagA that underpin gastric carcinogenesis.Cellular & molecular immunology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Helicobacter pylori cagA-positive strains are critically involved in the development of gastric cancer. Upon delivery into gastric epithelial cells via type IV secretion, the cagA-encoded CagA interacts with and thereby perturbs the pro-oncogenic phosphatase SHP2 and the polarity-regulating kinase PAR1b via the tyrosine-phosphorylated EPIYA-C/D segment and the CM sequence, respectively. Importantly, sequences spanning these binding regions exhibit variations among CagA proteins, which influence the pathobiological/oncogenic potential of individual CagA. Here we isolated an H. pylori strain (Hp_TH2099) naturally infecting the stomach of a housed macaque, indicating a zoonotic feature of H. pylori infection. Whole genome sequence analysis revealed that Hp_TH2099 belongs to the hpAsia2 cluster and possesses ABC-type Western CagA, which contains hitherto unreported variations in both EPIYA-C and CM sequences. The CM variations almost totally abolished PAR1b binding. Whereas pTyr + 5 variation in the EPIYA-C segment potentiated SHP2-binding affinity, pTyr-2 variation dampened CagA tyrosine phosphorylation and thus impeded CagA-SHP2 complex formation. As opposed to the H. pylori standard strain, infection of mouse ES cell-derived gastric organoids with Hp_TH2099 failed to elicit CagA-dependent epithelial destruction. Thus, the macaque-isolated H. pylori showed low virulence due to attenuated CagA activity through multiple substitutions in the sequences involved in binding with SHP2 and PAR1b.
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Registered trials
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