ArticleMedical microbiology and immunology2006
Helicobacter pylori SabA adhesin evokes a strong inflammatory response in human neutrophils which is down-regulated by the neutrophil-activating protein.
Article in Medical microbiology and immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 37 citations in OpenAlex.
- Preparation of Corn Peptides with Anti-Adhesive Activity and Its Functionality to Alleviate Gastric Injury Induced byNutrients · 2023Article
- Lactate causes downregulation of Helicobacter pylori adhesin genes sabA and labA while dampening the production of proinflammatory cytokines.Scientific reports · 2022Article
- Review
- Serum Antibodies against Helicobacter pylori Neutrophil Activating Protein in Carriers of IL-4 C-590T Genetic Polymorphism Amplify the Risk of Gastritis and Gastric Cancer.Iranian biomedical journal · 2017Article
- Helicobacter pylori infection: An overview of bacterial virulence factors and pathogenesis.Biomedical journal · 2016Review
- Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.Gut microbes · 2016Review
- A repetitive DNA element regulates expression of the Helicobacter pylori sialic acid binding adhesin by a rheostat-like mechanism.PLoS pathogens · 2014Article
- H. pylori infection, inflammation and gastric cancer.Journal of gastrointestinal cancer · 2014Review
- Helicobacter pylori neutrophil-activating protein: from molecular pathogenesis to clinical applications.World journal of gastroenterology · 2014Review
- Virulence Factors of Helicobacter pylori: A Review.Clinical medicine insights. Gastroenterology · 2014Review
- Increasing evidence of the role of Helicobacter pylori SabA in the pathogenesis of gastroduodenal disease.Journal of infection in developing countries · 2008Review
- SabA is the H. pylori hemagglutinin and is polymorphic in binding to sialylated glycans.PLoS pathogens · 2006Article
- Helicobacter pylori virulence genotypes and their relationship with precursor lesions of gastric malignancy and histological parameters in infected patients in Colombia.Revista peruana de medicina experimental y salud publicaArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human pathogen Helicobacter pylori expresses two dominant adhesins; the Lewis b blood group antigen binding adhesin, BabA, and the sialic acid-binding adhesin, SabA. These adhesins recognize specific carbohydrate moieties of the gastric epithelium, i.e. the Lewis b antigen, Le(b), and the sialyl-Lewis x antigen, sLe(x), respectively, which promote infection and inflammatory processes in the gastroduodenal tract. To assess the contribution of each of BabA, SabA and the neutrophil activating protein (HP-NAP) in a local inflammation, we investigated the traits of H. pylori mutants in their capacity to interact with and stimulate human neutrophils. We thence found that the SabA adhesin was not only the key inducer of oxidative metabolism (Unemo et al. J Biol Chem 280:15390-15397, 2005), but also essential in phagocytosis induction, as evaluated by flow cytometry, fluorescence microscopy and luminol-enhanced chemiluminescence. The napA deletion resulted in enhanced generation of reactive oxygen species and impaired adherence to the host cells. In conclusion, the SabA adhesin stimulates human neutrophils through selectin-mimicry. Interestingly, HP-NAP modulates the oxidative burst, which could tune the impact of the H. pylori infection for establishment of balanced and chronic inflammation of the gastric mucosa.
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