Evidence map›Paper›PMID 21130381›Full record

ArticleAnnals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology2010

Development of atopy by severe paramyxoviral infection in a mouse model.

Dorothy S Cheung, Sarah J Ehlenbach, Tom Kitchens, Desire A Riley, Mitchell H Grayson

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03039101 (Double Blind Study of Leukotriene Antagonism in the Nasal Recruitment of CD49d Expressing Neutrophils in Atopic Subjects), which is not on this map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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.

NCT03039101 nacompletednot on this mapstarted 2017, after this paper: background citation

Double Blind Study of Leukotriene Antagonism in the Nasal Recruitment of CD49d Expressing Neutrophils in Atopic Subjects

TypeinterventionalSponsorMitchell GraysonRan2017 to 2018Enrolled25ConditionsNasal AllergyArmsNasal lavage, Nasal allergen challenge, Epicutaneous skin testing, Peripheral blood, Montelukast 10Mg Tablet
3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Atopic Neutrophils Prevent Postviral Airway Disease.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  5. Article
  6. Asthma and viral infections: An intricate relationship.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2019
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. The role of early life viral bronchiolitis in the inception of asthma.Current opinion in allergy and clinical immunology · 2013
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

5 authors at 2 institutions in 1 country.

Dorothy S CheungMedical College of Wisconsin, MACC Fund Research Center, Milwaukee, WI 53226, USA.
Sarah J Ehlenbach
Tom Kitchens
Desire A Riley
Mitchell H Grayson
Medical College of Wisconsin · USWashington University in St. Louis · US

Funding

Mechanisms of Atopic Disease Development in the LungR01HL087778 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GRAYSON, MITCHELL H · 2008 to 2018
$3.7M
NHLBI NIH HHS HL087778NHLBI NIH HHS R01 HL087778
6 · The paper itself

Abstract

backgroundAtopic diseases have been increasing in prevalence, yet the initial inciting events that lead to atopy are not understood. Paramyxoviral infections have been suggested to play a role; however, much of these data are correlative.

objectiveTo determine whether exposure to a nonviral antigen during a paramyxoviral infection is sufficient to drive IgE production against the bystander antigen and whether clinical disease against this antigen would result.

methodsWild-type C57BL6 mice or mice deficient in FcεRIα (FcεRIα(-/-)) or IgE (IgE(-/-)) were inoculated with Sendai virus (SeV) or UV-inactivated SeV (UV-SeV) and subsequently exposed to ovalbumin (OVA) intranasally. Mice were further challenged 3 times with intranasal OVA on days 20 to 22 after inoculation with SeV, and airway hyperreactivity and mucous cell metaplasia were determined.

resultsExposure to OVA during SeV infection led to significant OVA specific IgE production (median, 548 vs 0 ng/mL; P = .03; SeV vs UV-SeV). This induction of OVA specific IgE production depended on FcεRI because FcεRIα(-/-) mice produced significantly less IgE (112 ng/mL; P = .03; vs wild-type mice). Furthermore, in wild-type mice OVA exposure and challenge significantly enhanced SeV-induced airway hyperreactivity and mucous cell metaplasia, but this failed to occur in either FcεRIα(-/-) or IgE(-/-) mice.

conclusionA single exposure to a bystander allergen during a paramyxoviral infection is sufficient to drive allergen specific IgE production in a partial FcεRI-dependent mechanism. These data begin to provide mechanistic insight into how viral infections might drive development of atopic disease.

Indexed as

AllergensAnimalsDisease Models, AnimalHypersensitivity, ImmediateImmunoglobulin EMiceMice, Inbred C57BLMice, KnockoutOvalbuminReceptors, IgERespirovirus InfectionsSendai virusAllergensImmunoglobulin EOvalbuminReceptors, IgE

Identifiers

PMID21130381
PMCPMC3059126
OpenAlexW2035230720

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

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.