Evidence map›Paper›PMID 24910174›Full record

ArticleThe Journal of allergy and clinical immunology2014

Neonatal rhinovirus induces mucous metaplasia and airways hyperresponsiveness through IL-25 and type 2 innate lymphoid cells.

Jun Young Hong, J Kelley Bentley, Yutein Chung, Jing Lei, Jessica M Steenrod, Qiang Chen, Uma S Sajjan, Marc B Hershenson

Open access · greenAbstract read
PubMed Full text at PMC Publisher
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 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 171 citations in OpenAlex.

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  18. Diverging patterns in innate immunity against respiratory viruses during a lifetime: lessons from the young and the old.European respiratory review : an official journal of the European Respiratory Society · 2024
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53 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jun Young HongDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Mich.
J Kelley BentleyDepartment of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich.
Yutein ChungDepartment of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich.
Jing LeiDepartment of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich.
Jessica M SteenrodDepartment of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich.
Qiang ChenDepartment of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich.
Uma S SajjanDepartment of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich.
Marc B HershensonDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Mich; Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Mich. Electronic address: mhershen@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Rhinovirus and Airway Epithelial Cell ResponsesR01HL081420 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HERSHENSON, MARC B. · 2006 to 2014
$3.3M
NHLBI NIH HHS R01 HL081420
6 · The paper itself

Abstract

backgroundEarly-life human rhinovirus infection has been linked to asthma development in high-risk infants and children. Nevertheless, the role of rhinovirus infection in the initiation of asthma remains unclear.

objectiveWe hypothesized that, in contrast to infection of mature BALB/c mice, neonatal infection with rhinovirus promotes an IL-25-driven type 2 response, which causes persistent mucous metaplasia and airways hyperresponsiveness.

methodsSix-day-old and 8-week-old BALB/c mice were inoculated with sham HeLa cell lysate or rhinovirus. Airway responses from 1 to 28 days after infection were assessed by using quantitative PCR, ELISA, histology, immunofluorescence microscopy, flow cytometry, and methacholine responsiveness. Selected mice were treated with a neutralizing antibody to IL-25.

resultsCompared with mature mice, rhinovirus infection in neonatal mice increased lung IL-13 and IL-25 production, whereas IFN-γ, IL-12p40, and TNF-α expression was suppressed. In addition, the population of IL-13-secreting type 2 innate lymphoid cells (ILC2s) was expanded with rhinovirus infection in neonatal but not mature mice. ILC2s were the major cell type secreting IL-13 in neonates. Finally, anti-IL-25 neutralizing antibody attenuated ILC2 expansion, mucous hypersecretion, and airways responsiveness.

conclusionsThese findings suggest that early-life viral infection could contribute to asthma development by provoking age-dependent, IL-25-driven type 2 immune responses.

Indexed as

Age FactorsAnimalsAnimals, NewbornAntibodies, NeutralizingCell ProliferationChildGene Expression RegulationHumansInterferon-gammaInterleukin-12 Subunit p40Interleukin-13InterleukinsLungLymphocytesMiceMucusAntibodies, NeutralizingInterferon-gammaInterleukin-12 Subunit p40Interleukin-13InterleukinsMydgf protein, mouseTumor Necrosis Factor-alphaAsthmaIL-25mouseneonatalrhinovirustype 2 innate lymphoid cells

Identifiers

PMID24910174
PMCPMC4119851
OpenAlexW2048993960

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.