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Nasal cytokine responses to natural colds in asthmatic children
Author(s) -
Lewis T. C.,
Henderson T. A.,
Carpenter A. R.,
Ramirez I. A.,
McHenry C. L.,
Goldsmith A. M.,
Ren X.,
Mentz G. B.,
Mukherjee B.,
Robins T. G.,
Joiner T. A.,
Mohammad L. S.,
Nguyen E. R.,
Burns M. A.,
Burke D. T.,
Hershenson M. B.
Publication year - 2012
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/cea.12005
Subject(s) - rhinovirus , medicine , eotaxin , immunology , respiratory system , asthma , common cold , chemokine , respiratory tract , cytokine , respiratory tract infections , virus , proinflammatory cytokine , influenza a virus , immune system , inflammation
Summary 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 using multiplex immune assay. mRNA expression for selected markers of viral infection was measured using 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 3 of the ‘well’ weeks and 17 of the ‘sick’ weeks (10 rhinovirus, three coronavirus, two influenza A , two influenza B , two respiratory syncytial virus, one parainfluenza). Compared to virus‐negative well weeks, nasal aspirate IFN ‐γ, CXCL 8/ IL ‐8, CXCL 10/ IP ‐10, CCL 5/ RANTES , CCL 11/eotaxin‐1, CCL 2/ MCP ‐1, CCL 4/ MIP ‐1β, CCL 7/ MCP ‐3, and CCL 20/ MIP 3α protein levels increased during virus‐positive sick weeks. Only a subset of cytokines ( IFN ‐γ, CXCL 8, CCL 2, CCL 4, CCL 5, and CCL 20) 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, TLR 3, RIG ‐I, and IRF 7 mRNA . Conclusions and 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, IFN s, and IFN ‐responsive genes.