Evidence map›Paper›PMID 18666312›Full record

ReviewWorld journal of gastroenterology2008

Roles of Helicobacter pylori BabA in gastroduodenal pathogenesis.

Yoshio Yamaoka

Open access · hybridAbstract readEditorialReview
In one paragraph

Review in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Integrative profiling ofMicrobial genomics · 2026
    Article
  3. Review
  4. Review
  5. Helicobacter pylori Infection in Colombia: Phylogeny, Resistome, and Virulome.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025
    Article
  6. Article
  7. Article
  8. FromWorld journal of clinical oncology · 2022
    Review
  9. Comparative Structural Dynamics of Isoforms ofFrontiers in molecular biosciences · 2022
    Article
  10. Frontiers in immunology · 2022
    Review
  11. Review
  12. Toxins · 2021
    Review
  13. Article
  14. Article
  15. Cells · 2020
    Review
  16. Article
  17. Article
  18. Prevalence of theThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2020
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 2 countries.

Yoshio Yamaoka
Baylor College of Medicine · US

Funding

REGULATION OF CXC CHEMOKINE EXPRESSION BY H. PYLORIR01DK062813 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI YAMAOKA, YOSHIO · 2004 to 2013
$3.0M
NIDDK NIH HHS R01 DK062813NIDDK NIH HHS R01 DK62813
6 · The paper itself

Abstract

Interactions between BabA and Lewis b (Le(b)) related antigens are the best characterized adhesin-receptor interactions in Helicobacter pylori (H pylori). Several mechanisms for the regulation of BabA expression are predicted, including at both transcriptional and translational levels. The formation of chimeric proteins (babA/B or babB/A chimeras) seems to play an especially important role in translational regulation. Chimeric BabB/A protein had the potential to bind Le(b); however, protein production was subject to phase variation through slipped strand mispairing. The babA gene was cloned initially from strain CCUG17875, which contains a silent babA1 gene and an expressed babA2 gene. The sequence of these two genes differs only by the presence of a 10 bp deletion in the signal peptide sequence of babA1 that eliminates its translational initiation codon. However, the babA1 type deletion was found only in strain CCUG17875. A few studies evaluated BabA status by immunoblot and confirmed that BabA-positive status in Western strains was closely associated with severe clinical outcomes. BabA-positive status also was associated with the presence of other virulence factors (e.g. cagA-positive status and vacA s1 genotype). A small class of strains produced low levels of the BabA protein and lacked Le(b) binding activity. These were more likely to be associated with increased mucosal inflammation and severe clinical outcomes than BabA-positive strains that exhibited Le(b) binding activity. The underlying mechanism is unclear, and further studies will be necessary to investigate how the complex BabA-receptor network is functionally coordinated during the interaction of H pylori with the gastric mucosa.

Indexed as

Adhesins, BacterialDuodenal DiseasesDuodenumGastric MucosaGenome, BacterialGenotypeHelicobacter InfectionsHelicobacter pyloriHumansLewis Blood Group AntigensModels, GeneticMutationStomachTranscription, GeneticTreatment OutcomeAdhesins, BacterialBabA protein, Helicobacter pyloriLewis Blood Group Antigens

Identifiers

PMID18666312
PMCPMC2731175
OpenAlexW2108717988

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.