Evidence map›Paper›PMID 24486071›Full record

ArticleThe Journal of allergy and clinical immunology2014

Prostaglandin E2 resistance in granulocytes from patients with aspirin-exacerbated respiratory disease.

Tanya M Laidlaw, Anya J Cutler, Molly S Kidder, Tao Liu, Juan Carlos Cardet, Heng Chhay, Chunli Feng, Joshua A Boyce

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.2field-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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Utility of low-dose oral aspirin challenges for diagnosis of aspirin-exacerbated respiratory disease.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2016
    Trial
  2. Trial
  3. Mast Cells in Aspirin-Exacerbated Respiratory Disease.Current allergy and asthma reports · 2024
    Review
  4. Review
  5. Activation of the PGEFrontiers in immunology · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Biomarkers for predicting response to aspirin therapy in aspirin-exacerbated respiratory disease.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Article
  11. Review
  12. Lipid-mediated innate lymphoid cell recruitment and activation in aspirin-exacerbated respiratory disease.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Pathogenesis of NSAID-induced reactions in aspirin-exacerbated respiratory disease.World journal of otorhinolaryngology - head and neck surgery · 2018
    Review
  17. Article
  18. Review
  19. Eosinophil production of prostaglandin DThe Journal of allergy and clinical immunology · 2016
    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

8 authors at 2 institutions in 1 country.

Tanya M LaidlawDepartment of Medicine, Harvard Medical School, Boston, Mass; Division of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Anya J CutlerDivision of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Molly S KidderDivision of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Tao LiuDivision of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Juan Carlos CardetDepartment of Medicine, Harvard Medical School, Boston, Mass; Division of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Heng ChhayDivision of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Chunli FengDivision of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass.
Joshua A BoyceDepartment of Medicine, Harvard Medical School, Boston, Mass; Division of Rheumatology, Immunology, and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Brigham and Women's Hospital, Boston, Mass; Department of Pediatrics, Harvard Medical School, Boston, Mass. Electronic address: jboyce@rics.bwh.harvard.edu.
Brigham and Women's Hospital · USHarvard University · US

Funding

Therapeutic Control of Aspirin-Exacerbated Respiratory DiseaseU19AI095219 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Maria Gutierrez-Arcelus · 2011 to 2026
$29.1M
Role of PGE2 in Human Mast Cell BiologyP01HL036110 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI KATZ, HOWARD R · 1985 to 2009
$20.1M
The Wake Forest Center for Botanical Lipids and Inflammatory Disease PreventionP50AT002782 · NCCIH · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHILTON, FLOYD H · 2005 to 2014
$15.3M
IMMUNOLOGIC BASIS OF RESISTANCE AND HYPERSENSITIVITYT32AI007306 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Nora Amanda Barrett, Joshua A Boyce · 1985 to 2026
$12.2M
Regulation of Pulmonary Prostaglandins by Leukotriene E4R01AI078908 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2009 to 2025
$8.8M
CysLT and P2Y Receptors in Lung InflammationR37AI052353 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2013 to 2022
$5.2M
Eicosanoid Networks in Aspirin Exacerbated Respiratory DiseaseR01HL117945 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2013 to 2016
$1.5M
The inflammatory role of the platelet in aspirin-exacerbated respiratory disease.K23HL111113 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LAIDLAW, TANYA MARIA · 2012 to 2016
$721k
Lipidomic and Transcriptome Signatures in Aspirin-Exacerbated Respiratory DiseaseR21AI082369 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2009 to 2010
$487k
NCCIH NIH HHS AT002782NCCIH NIH HHS P50 AT002782NHLBI NIH HHS HL36110NHLBI NIH HHS K23 HL111113NHLBI NIH HHS P01 HL036110NHLBI NIH HHS R01 HL117945NIAID NIH HHS AI078908NIAID NIH HHS AI082369NIAID NIH HHS AI095219NIAID NIH HHS R01 AI078908NIAID NIH HHS R21 AI082369NIAID NIH HHS R37 AI052353NIAID NIH HHS T32 AI007306NIAID NIH HHS U19 AI095219
6 · The paper itself

Abstract

backgroundAspirin-exacerbated respiratory disease (AERD) is an inflammatory condition of the respiratory tract and is characterized by overproduction of leukotrienes (LT) and large numbers of circulating granulocyte-platelet complexes. LT production can be suppressed by prostaglandin E(2) (PGE(2)) and the cyclic AMP-dependent protein kinase A (PKA).

objectiveTo determine if PGE(2)-dependent control of LT production by granulocytes is dysregulated in AERD.

methodsGranulocytes from well-characterized patients with and without AERD were activated ex vivo and subjected to a range of functional and biochemical analyses.

resultsGranulocytes from subjects with AERD generated more LTB4 and cysteinyl LTs than did granulocytes from controls with aspirin-tolerant asthma and controls without asthma. When compared with controls, granulocytes from subjects with AERD had comparable levels of EP(2) protein expression and PGE(2)-mediated cAMP accumulation, yet were resistant to PGE(2)-mediated suppression of LT generation. Percentages of platelet-adherent neutrophils correlated positively with LTB4 generation and inversely with responsiveness to PGE(2)-mediated suppression of LTB(4). The PKA inhibitor H89 potentiated LTB4 generation by control granulocytes but was inactive in granulocytes from individuals with AERD and had no effect on platelet P-selectin induction. Both tonic PKA activity and levels of PKA catalytic gamma subunit protein were significantly lower in granulocytes from individuals with AERD relative to those from controls.

conclusionsImpaired granulocyte PKA function in AERD may lead to dysregulated control of 5-lipoxygenase activity by PGE(2), whereas adherent platelets lead to increased production of LTs, which contributes to the features of persistent respiratory tract inflammation and LT overproduction.

Indexed as

AdultAgedAspirinBlood PlateletsCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneFemaleGranulocytesHumansLeukotriene B4LeukotrienesMaleMiddle AgedNeutrophilsReceptors, Prostaglandin E, EP2 SubtypeAspirinCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneLeukotriene B4LeukotrienesReceptors, Prostaglandin E, EP2 SubtypeAERDaspirin-exacerbated respiratory diseaseaspirin triadasthmacyclic AMPleukotrienenonsteroidal anti-inflammatory drugprostaglandin E(2)protein kinase ASamter's triad

Identifiers

PMID24486071
PMCPMC4040319
OpenAlexW2002181055

What OpenQuestion holds

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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.