ArticleScientific reports2016
Moonlighting of Helicobacter pylori catalase protects against complement-mediated killing by utilising the host molecule vitronectin.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Targeting catalase in cancer.Redox biology · 2024Review
- Recruitment of Vitronectin by Bacterial Pathogens: A Comprehensive Overview.Microorganisms · 2024Review
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Helicobacter pylori in the post-antibiotics era: from virulence factors to new drug targets and therapeutic agents.Archives of microbiology · 2023Review
- Helicobacter pylori initiates successful gastric colonization by utilizing L-lactate to promote complement resistance.Nature communications · 2023Article
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- FromWorld journal of clinical oncology · 2022Review
- Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022Review
- Genomic differentiation within East AsianMicrobial genomics · 2022Article
- A Multi-Omics Study on the Effect of Helicobacter Pylori-Related Genes in the Tumor Immunity on Stomach Adenocarcinoma.Frontiers in cellular and infection microbiology · 2022Article
- Review
- Adaptations and evolution of a heritable leaf nodule symbiosis between Dioscorea sansibarensis and Orrella dioscoreae.The ISME journal · 2019Article
- Article
- Host pathogen interactions inWorld journal of gastroenterology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is an important human pathogen and a common cause of peptic ulcers and gastric cancer. Despite H. pylori provoking strong innate and adaptive immune responses, the bacterium is able to successfully establish long-term infections. Vitronectin (Vn), a component of both the extracellular matrix and plasma, is involved in many physiological processes, including regulation of the complement system. The aim of this study was to define a receptor in H. pylori that binds Vn and determine the significance of the interaction for virulence. Surprisingly, by using proteomics, we found that the hydrogen peroxide-neutralizing enzyme catalase KatA is a major Vn-binding protein. Deletion of the katA gene in three different strains resulted in impaired binding of Vn. Recombinant KatA was generated and shown to bind with high affinity to a region between heparin-binding domain 2 and 3 of Vn that differs from previously characterised bacterial binding sites on the molecule. In terms of function, KatA protected H. pylori from complement-mediated killing in a Vn-dependent manner. Taken together, the virulence factor KatA is a Vn-binding protein that moonlights on the surface of H. pylori to promote bacterial evasion of host innate immunity.
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