About: Virus-triggered exacerbation in allergic asthmatic children: neutrophilic airway inflammation and alteration of virus sensors characterize a subgroup of patients

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About: Virus-triggered exacerbation in allergic asthmatic children: neutrophilic airway inflammation and alteration of virus sensors characterize a subgroup of patients Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Virus-triggered exacerbation in allergic asthmatic children: neutrophilic airway inflammation and alteration of virus sensors characterize a subgroup of patients
Creator	Hober, Didier Boileau, Sophie Decleyre-Badiu, Irina Deschildre, Antoine Dewilde, Anny Drumez, Elodie Engelmann, Ilka Gosset, Philippe Langlois, Carole Lejeune, Stéphanie Mordacq, Clémence Néve, Véronique Pichavant, Muriel Pouessel, Guillaume Romero-Cubero, David Thumerelle, Caroline
source	Medline; PMC
abstract	BACKGROUND: Viruses are important triggers of asthma exacerbations. They are also detected outside of exacerbation. Alteration of anti-viral response in asthmatic patients has been shown although the mechanisms responsible for this defect remain unclear. The objective of this study was to compare in virus-infected and not-infected allergic asthmatic children, aged 6 to 16 years, admitted to hospital for a severe exacerbation, the innate immune response and especially the expression of pattern recognition receptor (PRR) and their function. METHODS: Virus identification was performed both during the exacerbation and at steady state (eight weeks later). Data assessed at both periods included clinical features, anti-viral response and inflammation (in sputum and plasma), and PRR expression/function in blood mononuclear cells. RESULTS: Viruses were identified in 46 out of 72 children (median age 8.9 years) during exacerbation, and among them, in 17 at steady state. IFN-β, IFN-γ and IL-29 levels in sputum and plasma were similar between infected and not infected patients at both times, as well as the expression of TLR3, RIG-I and MDA5 in blood monocytes and dendritic cells. Airway inflammation in infected patients was characterized by significantly higher IL-5 concentration and eosinophil count. Compared to patients only infected at exacerbation, the re-infected children significantly exhibited lower levels of IFN-γ in plasma and sputum at exacerbation associated with modifications in PRR expression and function in blood mononuclear cells. These re-infected patients also presented an airway neutrophilic inflammation at steady state. CONCLUSION: Our results reports in asthmatic children that impaired anti-viral response during virus-induced exacerbation is more pronounced in a subgroup of patients prone to re-infection by virus. This subgroup is characterized by altered PRR function and a different pattern of airway inflammation. TRIAL REGISTRATION: This multicenter prospective study was approved by the regional investigational review board (ref: 08/07). ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12931-017-0672-0) contains supplementary material, which is available to authorized users.
has issue date	2017-11-14(xsd:dateTime)
bibo:doi	10.1186/s12931-017-0672-0
bibo:pmid	29137638
has license	cc-by
sha1sum (hex)	5bc8dd515058e0fe94c6fc4a2c3cb85572030fec
schema:url	https://doi.org/10.1186/s12931-017-0672-0
resource representing a document's title	Virus-triggered exacerbation in allergic asthmatic children: neutrophilic airway inflammation and alteration of virus sensors characterize a subgroup of patients
has PubMed Central identifier	PMC5686805
has PubMed identifier	29137638
schema:publication	Respir Res
resource representing a document's body	covid:5bc8dd515058e0fe94c6fc4a2c3cb85572030fec#body_text
is schema:about of	named entity 'PRR' named entity 'inflammation' named entity 'HOSPITAL' named entity 'SUBGROUP' named entity 'VIRUS' named entity 'ALTERATION' named entity 'FUNCTION' named entity 'TRIGGERS' named entity 'IMPORTANT' named entity 'ANTI-VIRAL RESPONSE' named entity 'ASTHMATIC' named entity 'SENSORS' named entity 'DETECTED' named entity 'YEARS' named entity 'ALTERATION' named entity 'UNCLEAR' named entity 'DEFECT' named entity 'OBJECTIVE' named entity 'INNATE IMMUNE RESPONSE' named entity 'EXACERBATION' named entity 'OUTSIDE' named entity 'VIRUS' named entity 'PATIENTS' named entity 'ASTHMA EXACERBATIONS' named entity 'ALLERGIC' named entity 'INFECTED' named entity 'AGED' named entity 'MECHANISMS' named entity 'NEUTROPHILIC AIRWAY INFLAMMATION' named entity 'THEIR' named entity 'EXPRESSION' named entity 'SEVERE' named entity 'ASTHMATIC' named entity 'ALLERGIC' named entity 'PATIENTS' named entity 'CHILDREN' named entity 'CHILDREN' named entity 'STUDY' named entity 'BACKGROUND' named entity 'PATTERN RECOGNITION RECEPTOR' named entity 'TO COMPARE' named entity 'RESPONSIBLE' named entity 'TRIGGERED' named entity 'EXACERBATION' named entity 'VIRUSES' covid:arg/5bc8dd515058e0fe94c6fc4a2c3cb85572030fec named entity 'aged' named entity 'Viruses' named entity 'Alteration' named entity 'allergic' named entity 'innate immune response' named entity 'anti-viral' named entity 'innate immune response' named entity 'airway' named entity 'allergic' named entity 'Virus' named entity 'Korea' named entity 'IFN-γ' named entity 'sputum' named entity 'PRR' named entity 'hRV' named entity 'steady state' named entity 'sputum' named entity 'steady state' named entity 'squamous cells' named entity 'antiviral'

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