Evidence map›Paper›PMID 26509876›Full record

ArticleMucosal immunology2016

Mucosal production of uric acid by airway epithelial cells contributes to particulate matter-induced allergic sensitization.

M J Gold, P R Hiebert, H Y Park, D Stefanowicz, A Le, M R Starkey, A Deane, A C Brown, G Liu, J C Horvat and 9 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  11. Understanding the pathogenesis of occupational coal and silica dust-associated lung disease.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  12. Inhibition of ABCC1 Decreases cAMP Egress and Promotes Human Airway Smooth Muscle Cell Relaxation.American journal of respiratory cell and molecular biology · 2022
    Article
  13. Review
  14. Potentiation of long-acting βRespiratory research · 2021
    Article
  15. Review
  16. Article
  17. Asthma-COPD overlap: current understanding and the utility of experimental models.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  18. Article
  19. Review
  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

19 authors at 4 institutions in 3 countries.

M J GoldBiomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
P R HiebertJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
H Y ParkDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
D StefanowiczJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
A LeJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
M R StarkeyPriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
A DeanePriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
A C BrownPriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
G LiuPriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
J C HorvatPriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
Z A IbrahimDiscipline of Pharmacy, Graduate School of Health, The University of Technology Sydney, Sydney, Australia.
M B SukkarDiscipline of Pharmacy, Graduate School of Health, The University of Technology Sydney, Sydney, Australia.
P M HansbroPriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
C CarlstenJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
S VanEedenJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
D D SinJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
K M McNagnyBiomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
D A KnightPriority Research Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Callaghan, Australia.
J A HirotaJames Hogg Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
University of British Columbia · CAUniversity of Technology Sydney · AUSungkyunkwan University · KRVancouver Coastal Health Research Institute · CA

Funding

CIHR
6 · The paper itself

Abstract

Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. PM induces innate immune responses and contributes to allergic sensitization, although the mechanisms governing this process remain unclear. Lung mucosal uric acid has also been linked to allergic sensitization. The links among PM exposure, uric acid, and allergic sensitization remain unexplored. We therefore investigated the mechanisms behind PM-induced allergic sensitization in the context of lung mucosal uric acid. PM10 and house dust mite exposure selectively induced lung mucosal uric acid production and secretion in vivo, which did not occur with other challenges (lipopolysaccharide, virus, bacteria, or inflammatory/fibrotic stimuli). PM10-induced uric acid mediates allergic sensitization and augments antigen-specific T-cell proliferation, which is inhibited by uricase. We then demonstrate that human airway epithelial cells secrete uric acid basally and after stimulation through a previously unidentified mucosal secretion system. Our work discovers a previously unknown mechanism of air pollution-induced, uric acid-mediated, allergic sensitization that may be important in the pathogenesis of asthma.

Indexed as

AnimalsAntigens, DermatophagoidesCell ProliferationCells, CulturedEnvironmental ExposureFemaleHumansHypersensitivityImmunity, MucosalImmunizationLungMiceMice, Inbred C57BLMice, KnockoutParticulate MatterPyroglyphidaeAntigens, DermatophagoidesParticulate MatterTlr4 protein, mouseToll-Like Receptor 4Uric Acid

Identifiers

PMID26509876
OpenAlexW2344828733

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.