Evidence map›Paper›PMID 17891168›Full record

ArticleBritish journal of pharmacology2007

Potentiation of NF-kappaB-dependent transcription and inflammatory mediator release by histamine in human airway epithelial cells.

N S Holden, W Gong, E M King, M Kaur, M A Giembycz, R Newton

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Histamine-mediated autocrine signaling in mesenteric perilymphatic mast cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  6. Effect of budesonide and azelastine on histamine signaling regulation in human nasal epithelial cells.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Receptor mediation and nociceptin inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009
    Article
  12. 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

6 authors at 1 institution in 1 country.

N S HoldenDepartment of Cell Biology and Anatomy, Respiratory Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.
W Gong
E M King
M Kaur
M A Giembycz
R Newton
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeIn asthma, histamine contributes to bronchoconstriction, vasodilatation and oedema, and is associated with the late phase response. The current study investigates possible inflammatory effects of histamine acting on nuclear factor kappaB (NF-kappaB)-dependent transcription and cytokine release. EXPERIMENTAL APPROACH: Using BEAS-2B bronchial epithelial cells, NF-kappaB-dependent transcription and both release and mRNA expression of IL-6 and IL-8 were examined by reporter assay, ELISA and quantitative RT-PCR. Histamine receptors were detected using qualitative RT-PCR and function examined using selective agonists and antagonists. KEY

resultsAddition of histamine to TNFalpha-stimulated BEAS-2B cells maximally potentiated NF-kappaB-dependent transcription 1.8 fold, whereas IL-6 and IL-8 protein release were enhanced 7.3- and 2.7-fold respectively. These responses were, in part, NF-kappaB-dependent and were associated with 2.6- and 1.7-fold enhancements of IL-6 and IL-8 mRNA expression. The H(1) receptor antagonist, mepyramine, caused a rightward shift in the concentration-response curves of TNFalpha-induced NF-kappaB-dependent transcription (pA(2)=9.91) and release of IL-6 (pA(2)=8.78) and IL-8 (pA(2)=8.99). Antagonists of histamine H(2), H(3) and H(4) receptors were without effect. Similarly, H(3) and H(4) receptor agonists did not affect TNFalpha-induced NF-kappaB-dependent transcription, or IL-6 and IL-8 release at concentrations below 10 microM. The anti-inflammatory glucocorticoid, dexamethasone, inhibited the histamine enhanced NF-kappaB-dependent transcription and IL-6 and IL-8 release. CONCLUSIONS AND IMPLICATIONS: Potentiation of NF-kappaB-dependent transcription and inflammatory cytokine release by histamine predominantly involves receptors of the H(1) receptor subtype. These data support an anti-inflammatory role for H(1) receptor antagonists by preventing the transcription and release of pro-inflammatory cytokines.

Indexed as

AdenoviridaeAnti-Inflammatory AgentsBlotting, WesternBronchiCell LineCells, CulturedDexamethasoneEpithelial CellsGene ExpressionGenetic VectorsHistamineHistamine AntagonistsHumansI-kappa B ProteinsInflammation MediatorsInterleukin-6Anti-Inflammatory AgentsDexamethasoneHistamineHistamine AntagonistsI-kappa B ProteinsInflammation MediatorsInterleukin-6Interleukin-8NF-kappa BReceptors, HistamineTumor Necrosis Factor-alpha

Identifiers

PMID17891168
PMCPMC2078227
OpenAlexW2129972458

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.