ArticleThe Journal of biological chemistry2011
BabA-mediated adherence is a potentiator of the Helicobacter pylori type IV secretion system activity.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 4 of them syntheses that pooled it.
What it found
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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.
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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.
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Who cites it
110 citing papers in PubMed, 4 syntheses or guidelines pooled it, 197 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- Association between ABO gene polymorphism (rs505922) and cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- Association of Helicobacter pylori babA2 with peptic ulcer disease and gastric cancer.World journal of gastroenterology · 2013Pooled it
- ABO blood group system and gastric cancer: a case-control study and meta-analysis.International journal of molecular sciences · 2012Pooled it
- Internalization ofAnnals of medicine · 2026Review
- Review
- Bacterial Infections Role in Gynecological Cancers Development: Narrative Review.Cancer reports (Hoboken, N.J.) · 2026Review
- Correlation versus causation:mSphere · 2026Article
- Monoclonal stool antigen test for diagnosingFrontiers in cellular and infection microbiology · 2026Article
- Gut mucin fucosylation dictates the entry of botulinum toxin complexes.Nature communications · 2025Article
- Article
- Gut mucin fucosylation dictates the entry of botulinum toxin complexes.bioRxiv : the preprint server for biology · 2025Article
- Species-specific components of theInfection and immunity · 2025Article
- Relationship between Helicobacter Pylori infection and metabolic syndrome components in adults.Frontiers in endocrinology · 2025Article
- Immunoinformatic strategy for developing multi-epitope subunit vaccine against Helicobacter pylori.PloS one · 2025Article
- Dynamics of Bacteria-Mucus Interactions: Quantitative Assessment of MUC5AC and Helicobacter pylori Adhesion to the Gastric Tissue on the Model of Cavia porcellus.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Architectural dissection of adhesive bacterial cell surface appendages from a "molecular machines" viewpoint.Journal of bacteriology · 2024Review
- Review
- LOX-1 acts as an NNature communications · 2024Article
- Pivotal role ofFrontiers in medicine · 2024Review
50 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
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic infection of Helicobacter pylori in the stomach mucosa with translocation of the bacterial cytotoxin-associated gene A (CagA) effector protein via the cag-Type IV secretion system (TFSS) into host epithelial cells are major risk factors for gastritis, gastric ulcers, and cancer. The blood group antigen-binding adhesin BabA mediates the adherence of H. pylori to ABO/Lewis b (Le(b)) blood group antigens in the gastric pit region of the human stomach mucosa. Here, we show both in vitro and in vivo that BabA-mediated binding of H. pylori to Le(b) on the epithelial surface augments TFSS-dependent H. pylori pathogenicity by triggering the production of proinflammatory cytokines and precancer-related factors. We successfully generated Le(b)-positive cell lineages by transfecting Le(b)-negative cells with several glycosyltransferase genes. Using these established cell lines, we found increased mRNA levels of proinflammatory cytokines (CCL5 and IL-8) as well as precancer-related factors (CDX2 and MUC2) after the infection of Le(b)-positive cells with WT H. pylori but not with babA or TFSS deletion mutants. This increased mRNA expression was abrogated when Le(b)-negative cells were infected with WT H. pylori. Thus, H. pylori can exploit BabA-Le(b) binding to trigger TFSS-dependent host cell signaling to induce the transcription of genes that enhance inflammation, development of intestinal metaplasia, and associated precancerous transformations.
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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.