Evidence map›Paper›PMID 28008678›Full record

ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2017

Mast cells are permissive for rhinovirus replication: potential implications for asthma exacerbations.

C Akoto, D E Davies, E J Swindle

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  16. Mast Cell Responses to Viruses and Pathogen Products.International journal of molecular sciences · 2019
    Review
  17. Rhinovirus Attributes that Contribute to Asthma Development.Immunology and allergy clinics of North America · 2019
    Review
  18. Review
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  20. Mast cells are permissive for rhinovirus replication: potential implications for asthma exacerbations.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017
    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

3 authors at 2 institutions in 1 country.

C AkotoClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, University Hospital Southampton, Southampton, UK.
D E DaviesClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, University Hospital Southampton, Southampton, UK.
E J SwindleClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, University Hospital Southampton, Southampton, UK.
NIHR Southampton Respiratory Biomedical Research Unit · GBSouthampton General Hospital · GB

Funding

Medical Research Council G0800766Medical Research Council G0900453Wellcome Trust
6 · The paper itself

Abstract

backgroundHuman rhinoviruses (HRVs) are a major trigger of asthma exacerbations, with the bronchial epithelium being the major site of HRV infection and replication. Mast cells (MCs) play a key role in asthma where their numbers are increased in the bronchial epithelium with increasing disease severity.

objectiveIn view of the emerging role of MCs in innate immunity and increased localization to the asthmatic bronchial epithelium, we investigated whether HRV infection of MCs generated innate immune responses which were protective against infection.

methodsThe LAD2 MC line or primary human cord blood-derived MCs (CBMCs) were infected with HRV or UV-irradiated HRV at increasing multiplicities of infection (MOI) without or with IFN-β or IFN-λ. After 24 h, innate immune responses were assessed by RT-qPCR and IFN protein release by ELISA. Viral replication was determined by RT-qPCR and virion release by TCID

resultsHRV infection of LAD2 MCs induced expression of IFN-β, IFN-λ and IFN-stimulated genes. However, LAD2 MCs were permissive for HRV replication and release of infectious HRV particles. Similar findings were observed with CBMCs. Neutralization of the type I IFN receptor had minimal effects on viral shedding, suggesting that endogenous type I IFN signalling offered limited protection against HRV. However, augmentation of these responses by exogenous IFN-β, but not IFN-λ, protected MCs against HRV infection. CONCLUSION AND CLINICAL RELEVANCE: MCs are permissive for the replication and release of HRV, which is prevented by exogenous IFN-β treatment. Taken together, these findings suggest a novel mechanism whereby MCs may contribute to HRV-induced asthma exacerbations.

Indexed as

Virus ReplicationAsthmaCell LineCommon ColdDisease ProgressionHost-Pathogen InteractionsHumansImmunity, InnateInterferon-betaMast CellsRhinovirusSeverity of Illness IndexVirus ReleaseInterferon-betaasthmainnate immunityinterferonmast cellsvirus

Identifiers

PMID28008678
PMCPMC5396281
OpenAlexW2561978452

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.