Evidence map›Paper›PMID 16030249›Full record

ArticleMolecular biology of the cell2005

Regulation of interleukin-6 promoter activation in gastric epithelial cells infected with Helicobacter pylori.

Hong Lu, Jeng Yih Wu, Takahiko Kudo, Tomoyuki Ohno, David Y Graham, Yoshio Yamaoka

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Frontiers in cellular and infection microbiology · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. Role of Helicobacter pylori infection in pathogenesis of gastric carcinoma.World journal of gastrointestinal pathophysiology · 2016
    Review
  12. Nonalcoholic fatty liver disease induced by noncanonical Wnt and its rescue by Wnt3a.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Effect of Helicobacter pylori on gastric epithelial cells.World journal of gastroenterology · 2014
    Review
  18. Helicobacter pylori virulence and cancer pathogenesis.Future oncology (London, England) · 2014
    Review
  19. Article
  20. Virulence Factors of Helicobacter pylori: A Review.Clinical medicine insights. Gastroenterology · 2014
    Review
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

6 authors at 2 institutions in 2 countries.

Hong LuDepartment of Medicine, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, TX 77030, USA.
Jeng Yih Wu
Takahiko Kudo
Tomoyuki Ohno
David Y Graham
Yoshio Yamaoka
Michael E. DeBakey VA Medical Center · USKyoto Prefectural University of Medicine · JP

Funding

Tissue Analysis & Molecular Imaging CoreP30DK056338 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI FASIHA KANWAL · 2001 to 2026
$28.3M
REGULATION OF CXC CHEMOKINE EXPRESSION BY H. PYLORIR01DK062813 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI YAMAOKA, YOSHIO · 2004 to 2013
$3.0M
NIDDK NIH HHS DK56338NIDDK NIH HHS P30 DK056338NIDDK NIH HHS R01 DK062813NIDDK NIH HHS R01 DK62813
6 · The paper itself

Abstract

The regulation of Helicobacter pylori induced interleukin (IL)-6 in the gastric epithelium remains unclear. Primary gastric epithelial cells and MKN28 cells were cocultured with H. pylori and its isogenic cag pathogenicity island (PAI) mutant and/or oipA mutants. H. pylori infection-induced IL-6 mRNA expression and IL-6 protein production, which was further enhanced by the cag PAI and OipA. Luciferase reporter gene assays and electrophoretic mobility shift assays showed that full IL-6 transcription required binding sites for nuclear factor-kappaB (NF-kappaB), cAMP response element (CRE), CCAAT/enhancer binding protein (C/EBP), and activator protein (AP)-1. The cag PAI and OipA were involved in binding to NF-kappaB, AP-1, CRE, and C/EBP sites. The cag PAI activated the extracellular signal-regulated kinase (ERK) and Jun N-terminal kinase (JNK) pathways; OipA activated the p38 pathway. Transfection of dominant negative G-protein confirmed roles for Raf, Rac1, and RhoA in IL-6 induction. Overall, the cag PAI-related IL-6 signal transduction pathway involved the Ras/Raf/MEK1/2/ERK/AP-1/CRE pathway and the JNK/AP-1/CRE pathway; the OipA-related pathway is p38/AP-1/CRE and both the cag PAI and OipA appear to be involved in the RhoA/Rac1/NF-kappaB pathway. Combination of different pathways by the cag PAI and OipA will lead to the maximum IL-6 induction.

Indexed as

CCAAT-Enhancer-Binding ProteinsCells, CulturedEpithelial CellsExtracellular Signal-Regulated MAP KinasesGastric MucosaGene Expression RegulationGTP-Binding ProteinsHelicobacter InfectionsHelicobacter pyloriHumansInterleukin-6JNK Mitogen-Activated Protein KinasesMutationNF-kappa Bp38 Mitogen-Activated Protein KinasesPromoter Regions, GeneticCCAAT-Enhancer-Binding ProteinsExtracellular Signal-Regulated MAP KinasesGTP-Binding ProteinsInterleukin-6JNK Mitogen-Activated Protein KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesTranscription Factor AP-1

Identifiers

PMID16030249
PMCPMC1237095
OpenAlexW2143449877

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.