ArticlePLoS pathogens2006
SabA is the H. pylori hemagglutinin and is polymorphic in binding to sialylated glycans.
Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 182 citations in OpenAlex.
- Therapeutic suppression ofFrontiers in microbiology · 2026Article
- New concepts of chitosan-based mucosal formulations for supporting control of the gastric pathogenFrontiers in microbiology · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Saucerneol D Suppresses the Growth ofCurrent issues in molecular biology · 2025Article
- Review
- Probing the expression and adhesion of glycans involved in Helicobacter pylori infection.Scientific reports · 2024Article
- ABO, Lewis blood group systems and secretory status with H.pylori infection in yemeni dyspeptic patients: a cross- sectional study.BMC infectious diseases · 2023Article
- Bacterial chemotaxis in human diseases.Trends in microbiology · 2023Review
- Lactate causes downregulation of Helicobacter pylori adhesin genes sabA and labA while dampening the production of proinflammatory cytokines.Scientific reports · 2022Article
- Bacterial colonization and TH17 immunity are shaped by intestinal sialylation in neonatal mice.Glycobiology · 2022Article
- AI-2 Induces Urease Expression Through Downregulation of Orphan Response Regulator HP1021 inFrontiers in medicine · 2022Article
- The biophysics of bacterial infections: Adhesion events in the light of force spectroscopy.Cell surface (Amsterdam, Netherlands) · 2021Article
- Hesperetin Inhibits Expression of Virulence Factors and Growth ofInternational journal of molecular sciences · 2021Article
- The Role of a Dipeptide Transporter in the Virulence of Human Pathogen,Frontiers in microbiology · 2021Article
- Assessing the Role of Pharyngeal Cell Surface Glycans in Group AAntibiotics (Basel, Switzerland) · 2020Article
- Virulence of Helicobacter pylori outer membrane proteins: an updated review.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Review
- Article
- Upregulation of MUC5AC production and deposition of LEWIS determinants by HELICOBACTER PYLORI facilitate gastric tissue colonization and the maintenance of infection.Journal of biomedical science · 2019Article
- Both diet and Helicobacter pylori infection contribute to atherosclerosis in pre- and postmenopausal cynomolgus monkeys.PloS one · 2019Article
- Helicobacter pylori SabA binding gangliosides of human stomach.Virulence · 2018Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 4 countries.
Funding
Abstract
Adherence of Helicobacter pylori to inflamed gastric mucosa is dependent on the sialic acid-binding adhesin (SabA) and cognate sialylated/fucosylated glycans on the host cell surface. By in situ hybridization, H. pylori bacteria were observed in close association with erythrocytes in capillaries and post-capillary venules of the lamina propria of gastric mucosa in both infected humans and Rhesus monkeys. In vivo adherence of H. pylori to erythrocytes may require molecular mechanisms similar to the sialic acid-dependent in vitro agglutination of erythrocytes (i.e., sialic acid-dependent hemagglutination). In this context, the SabA adhesin was identified as the sialic acid-dependent hemagglutinin based on sialidase-sensitive hemagglutination, binding assays with sialylated glycoconjugates, and analysis of a series of isogenic sabA deletion mutants. The topographic presentation of binding sites for SabA on the erythrocyte membrane was mapped to gangliosides with extended core chains. However, receptor mapping revealed that the NeuAcalpha2-3Gal-disaccharide constitutes the minimal sialylated binding epitope required for SabA binding. Furthermore, clinical isolates demonstrated polymorphism in sialyl binding and complementation analysis of sabA mutants demonstrated that polymorphism in sialyl binding is an inherent property of the SabA protein itself. Gastric inflammation is associated with periodic changes in the composition of mucosal sialylation patterns. We suggest that dynamic adaptation in sialyl-binding properties during persistent infection specializes H. pylori both for individual variation in mucosal glycosylation and tropism for local areas of inflamed and/or dysplastic tissue.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.