Evidence map›Paper›PMID 22579987›Full record

ReviewPulmonary pharmacology & therapeutics2012

Airway epithelial regulation of allergic sensitization in asthma.

Matthew E Poynter

Abstract readReview
In one paragraph

Review in Pulmonary pharmacology & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Regulatory tone and mucosal immunity in asthma.International immunopharmacology · 2014
    Review
  13. Article
  14. Inflammasome Activity in Non-Microbial Lung Inflammation.Journal of environmental immunology and toxicology · 2014
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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 1 country.

Matthew E PoynterDepartment of Medicine and Vermont Lung Center, University of Vermont, Given E410A, 89 Beaumont Avenue, Burlington, VT 05405, USA. Matthew.Poynter@uvm.edu
University of Vermont · US

Funding

WEIGHT LOSS & ASTHMAP20RR015557 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI IRVIN, CHARLES G · 2000 to 2009
$21.4M
VERMONT IMMUNOBIOLOIGY/ INFECTIOUS DISEASES CENTERP20RR021905 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI HILL, JACK · 2006 to 2011
$14.5M
Vermont Immunobioloigy/ Infectious Diseases CenterP20GM103496 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2012 to 2015
$8.7M
Nitrogen Dioxide in the Sensitization to Allergic Airway DiseaseR01HL089177 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI POYNTER, MATTHEW E · 2007 to 2011
$2.2M
Serum Amyloid A3 in Allergic Asthma: An Endogenous Mediator of Disease SeverityR01HL107291 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI POYNTER, MATTHEW E · 2012 to 2015
$1.5M
NCRR NIH HHS P20 RR015557NCRR NIH HHS P20 RR 021905NCRR NIH HHS P20 RR021905NCRR NIH HHS P20 RR15557NHLBI NIH HHS R01 HL089177NHLBI NIH HHS R01 HL107291NIGMS NIH HHS P20 GM103496
6 · The paper itself

Abstract

While many of the contributing cell types and mediators of allergic asthma are known, less well understood are the factors that influence the development of allergic responses that lead to the development of allergic asthma. As the first airway cell type to respond to inhaled factors, the epithelium orchestrates downstream interactions between dendritic cells (DCs) and CD4⁺ T cells that quantitatively and qualitatively dictate the degree and type of the allergic asthma phenotype, making the epithelium of critical importance for the genesis of allergies that later manifest in allergic asthma. Amongst the molecular processes of critical importance in airway epithelium is the transcription factor, nuclear factor-kappaB (NF-κB). This review will focus primarily on the genesis of pulmonary allergies and the participation of airway epithelial NF-κB activation therein, using examples from our own work on nitrogen dioxide (NO₂) exposure and genetic modulation of airway epithelial NF-κB activation. In addition, the mechanisms through which Serum Amyloid A (SAA), an NF-κB-regulated, epithelial-derived mediator, influences allergic sensitization and asthma severity will be presented. Knowledge of the molecular and cellular processes regulating allergic sensitization in the airways has the potential to provide powerful insight into the pathogenesis of allergy, as well as targets for the prevention and treatment of asthma.

Indexed as

AnimalsAsthmaCD4-Positive T-LymphocytesDendritic CellsEpithelial CellsHumansHypersensitivityNF-kappa BNitrogen DioxideSerum Amyloid A ProteinSeverity of Illness IndexNF-kappa BNitrogen DioxideSerum Amyloid A Protein

Identifiers

PMID22579987
PMCPMC3425713
OpenAlexW1985236271

What OpenQuestion holds

Textmetadata
LicenceTDM
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.