Evidence map›Paper›PMID 23806456›Full record

ArticleAnnals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology2013

Interaction between allergy and innate immunity: model for eosinophil regulation of epithelial cell interferon expression.

Sameer K Mathur, Paul S Fichtinger, John T Kelly, Wai-Ming Lee, James E Gern, Nizar N Jarjour

Open access · greenAbstract read
In one paragraph

Article in Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 43 citations in OpenAlex.

  1. Lower viral loads in subjects with rhinovirus-challenged allergy despite reduced innate immunity.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022
    Trial
  2. INEXAS: A Phase 2 Randomized Trial of On-demand Inhaled Interferon Beta-1a in Severe Asthmatics.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Trial
  3. Trial
  4. Article
  5. The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025
    Review
  6. Review
  7. Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024
    Review
  8. Subsets of Eosinophils in Asthma, a Challenge for Precise Treatment.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Review
  11. Eosinophils and Bacteria, the Beginning of a Story.International journal of molecular sciences · 2021
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. The Regulatory Function of Eosinophils.Microbiology spectrum · 2016
    Review
  19. Review
  20. The immunology of asthma.Nature immunology · 2015
    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 2 institutions in 1 country.

Sameer K MathurDivision of Allergy, Pulmonary and Critical Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53792, USA. sm4@medicine.wisc.edu
Paul S Fichtinger
John T Kelly
Wai-Ming Lee
James E Gern
Nizar N Jarjour
University of Wisconsin–Madison · USWilliam S. Middleton Memorial Veterans Hospital · US

Funding

Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
Thr Role of Pin1 in AirwayP01HL088594 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 2008 to 2017
$21.0M
Severe Asthma From Respiratory InfectionsR01HL069116 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI BUSSE, WILLIAM W. · 2001 to 2010
$7.6M
Wisconsin Allergy Research Training (WISCART) ProgramT32AI007635 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI James E. Gern, DANIEL J JACKSON · 2000 to 2026
$6.5M
NCATS NIH HHS UL1 TR000427NCRR NIH HHS UL1 RR025011NCRR NIH HHS UL1RR025011NHLBI NIH HHS HL088594NHLBI NIH HHS HL69116NHLBI NIH HHS P01 HL088594NHLBI NIH HHS R01 HL069116NIAID NIH HHS T32 AI007635
6 · The paper itself

Abstract

backgroundEosinophils in asthmatic airways are associated with risk of exacerbations. The most common cause of asthma exacerbations is viral respiratory infections, particularly human rhinovirus (HRV).

objectiveTo determine the mechanism by which eosinophils may influence virus-induced responses.

methodsWe used an in vitro coculture model of primary human eosinophils and the BEAS-2B epithelial cell line either stimulated with HRV1A infection or polyinosinic-polycytidylic acid (poly[I:C]). The messenger RNA (mRNA) expression of interferon (IFN) β1 and IFN-λ1 was assessed by quantitative reverse-transcriptase polymerase chain reaction and the protein level of IFN- λ1 by enzyme-linked immunosorbent assay.

resultsBoth poly(I:C) and HRV1A infection induced BEAS-2B expression of IFN-β1 and IFN-λ1 mRNA. Coculture of eosinophils resulted in suppression of poly(I:C)-stimulated IFN-β1 and IFN-λ1 mRNA expression (2.5-fold and 3.6-fold less, respectively). Separation of cells did not block eosinophil regulatory activity. Coculture of eosinophils with HRV1A-infected BEAS-2B cells also suppressed IFN-β1 and IFN-λ1 mRNA (5.7-fold and 5.0-fold less, respectively) and reduced IFN-λ1 protein secretion (1.6-fold decrease). This corresponded to a 34% increase in the quantity of HRV1A virus RNA on coculture with eosinophils. Recombinant transforming growth factor β suppressed IFN-λ1 from HRV1A-infected BEAS-2B cells. Coculture of eosinophils and BEAS-2B cells induced transforming growth factor β secretion, which may mediate suppression of HRV-induced interferon expression.

conclusionEosinophils suppressed HRV-induced expression of interferons from epithelial cells, resulting in increased quantity of HRV. This represents one mechanism for interaction between allergic inflammation and innate immunity.

Indexed as

AdolescentAdultAsthmaCell LineCoculture TechniquesEosinophilsEpithelial CellsFemaleHumansImmunity, InnateInterferon-betaInterferon LambdaInterferonsInterleukinsMaleMiddle AgedInterferon-betaInterferon Lambdainterferon-lambda, humanInterferonsInterleukinsPoly I-CRNA, Messenger

Identifiers

PMID23806456
PMCPMC3708694
OpenAlexW1990846818

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.