About: Nasal cytokine responses to natural colds in asthmatic children

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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
has title	Nasal cytokine responses to natural colds in asthmatic children
Creator	Hershenson, Marc Nguyen, E Ren, X Burke, D Burke, M Burns, D Burns, M Carpenter, A Carpenter, I Goldsmith, A Goldsmith, X Henderson, A Henderson, T Hershenson, M Joiner, L Joiner, T Lewis, T Mchenry, A Mchenry, C Mentz, B Mentz, G Mohammad, E Mohammad, L Mukherjee, B Mukherjee, T Nguyen, M Ramirez, C Ramirez, I Ren, G Robins, T
Source	Medline; PMC
abstract	BACKGROUND: The mechanisms by which viruses induce asthma exacerbations are not well-understood. OBJECTIVE: We characterized fluctuations in nasal aspirate cytokines during naturally-occurring respiratory viral infections in children with asthma. METHODS: Sixteen children underwent home collections of nasal aspirates when they were without cold symptoms and again during self-reported respiratory illnesses. The presence of viral infection was ascertained by multiplex PCR. Cytokines were measured by multiplex immune assay. mRNA expression for selected markers of viral infection was measured by RT-PCR. A cumulative respiratory symptom score was calculated for each day of measurement. Generalized estimated equations were used to evaluate associations between viral infection and marker elevation, and between marker elevation and symptom score. RESULTS: The 16 patients completed a total of 37 weeks of assessment (15 “well” weeks; 22 self-assessed “sick” weeks). Viral infections were detected in three of the “well” weeks and 17 of the “sick” weeks (10 rhinovirus, 3 coronavirus, 2 influenza A, 2 influenza B, 2 respiratory syncytial virus, 1 parainfluenza). Compared to virus-negative well weeks, nasal aspirate IFN-γ, CXCL8/IL-8, CXCL10/IP-10, CCL5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MIP-1β, CCL7/MCP-3 and CCL20/MIP3α protein levels increased during virus-positive sick weeks. Only a subset of cytokines (IFN-γ, CXCL8, CCL2, CCL4, CCL5 and CCL20) correlated with self-reported respiratory tract symptoms. While many aspirates were dilute and showed no mRNA signal, viral infection significantly increased the number of samples that were positive for IFN-λ1, IFN-λ2/3, TLR3, RIG-I and IRF7 mRNA. CONCLUSIONS & CLINICAL RELEVANCE: We conclude that, in children with asthma, naturally-occurring viral infections apparently induce a robust innate immune response including expression of specific chemokines, IFNs and IFN-responsive genes.
has issue date	2012-11-26(xsd:dateTime)
bibo:doi	10.1111/cea.12005
bibo:pmid	23181789
has license	green-oa
sha1sum (hex)	be902d89e87bf2337dc2ff1df92a8c05cdfedb96
schema:url	https://doi.org/10.1111/cea.12005
resource representing a document's title	Nasal cytokine responses to natural colds in asthmatic children
has PubMed Central identifier	PMC4219353
has PubMed identifier	23181789
schema:publication	Clinical & Experimental Allergy
resource representing a document's body	covid:be902d89e87bf2337dc2ff1df92a8c05cdfedb96#body_text
is schema:about of	named entity 'NASAL' named entity 'COLDS' named entity 'CYTOKINE ' named entity 'CHILDREN' named entity 'NATURAL' named entity 'RESPONSES' named entity 'ASTHMATIC' named entity 'non-atopic' named entity 'CCL4' named entity 'CXCL8' named entity 'MDA-5' named entity 'CXCL10' named entity 'FeNO' named entity 'Qiagen' named entity 'asthma' named entity 'SAS' named entity 'daily activities' named entity 'nucleic acid' named entity 'IFN-a' named entity 'human parainfluenza viruses' named entity 'ribonucleases' named entity 'respiratory illness' named entity 'picornavirus' named entity 'FeNO' named entity 'viral infection' named entity 'detection limit' named entity 'lower airway' named entity 'CCL11' named entity 'epithelial cells' named entity 'mRNA' named entity 'Lenexa' named entity 'asthma' named entity 'CCL5' named entity 'inflammatory cells' named entity 'viral infections' named entity 'inflammatory cells' named entity 'biomarkers' named entity 'viruses' named entity 'asthma' named entity 'infection' named entity 'shortness of breath' named entity 'virus' named entity 'CCL11' named entity 'eosinophils' named entity 'respiratory tract' named entity 'CCL19' named entity 'IFN' named entity 'FeNO' named entity 'PCR' named entity 'gene expression' named entity 'immune cells' named entity 'IP-10'

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