Interferon response and respiratory virus control are preserved in bronchial epithelial cells in asthma - 05/12/14
Abstract |
Background |
Some investigators find a deficiency in IFN production from airway epithelial cells infected with human rhinovirus in asthma, but whether this abnormality occurs with other respiratory viruses is uncertain.
Objective |
To assess the effect of influenza A virus (IAV) and respiratory syncytial virus (RSV) infection on IFN production and viral level in human bronchial epithelial cells (hBECs) from subjects with and without asthma.
Methods |
Primary-culture hBECs from subjects with mild to severe asthma (n = 11) and controls without asthma (hBECs; n = 7) were infected with live or ultraviolet-inactivated IAV (WS/33 strain), RSV (Long strain), or RSV (A/2001/2-20 strain) with multiplicity of infection 0.01 to 1. Levels of virus along with IFN-β and IFN-λ and IFN-stimulated gene expression (tracked by 2′-5′-oligoadenylate synthetase 1 and myxovirus (influenza virus) resistance 1 mRNA) were determined up to 72 hours postinoculation.
Results |
After IAV infection, viral levels were increased 2-fold in hBECs from asthmatic subjects compared with nonasthmatic control subjects (P < .05) and this increase occurred in concert with increased IFN-λ1 levels and no significant difference in IFNB1, 2′-5′-oligoadenylate synthetase 1, or myxovirus (influenza virus) resistance 1mRNA levels. After RSV infections, viral levels were not significantly increased in hBECs from asthmatic versus nonasthmatic subjects and the only significant difference between groups was a decrease in IFN-λ levels (P < .05) that correlated with a decrease in viral titer. All these differences were found only at isolated time points and were not sustained throughout the 72-hour infection period.
Conclusions |
The results indicate that IAV and RSV control and IFN response to these viruses in airway epithelial cells is remarkably similar between subjects with and without asthma.
Le texte complet de cet article est disponible en PDF.Key words : Asthma, IFN, influenza A virus, respiratory syncytial virus, primary-culture airway epithelial cells
Abbreviations used : BEGM, hBEC, HRV, hTEC, IAV, ISG, MOI, MX1, OAS1, RSV, UV
Plan
| This work was supported by the National Institutes of Health (National Institute of Allergy and Infectious Diseases Asthma and Allergic Diseases Cooperative Research Center grant no. U19-AI070489 to M.J.H., grant no. U19-AI095227 to R.S.P., grant no. U10-HL109257 to M.C.), Clinical and Translational Science Award (CTSA) grant no. UL1 TR000448, and Roche Postdoctoral Fellowship awards (to D.A.P. and H.J.K.). |
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| Disclosure of potential conflict of interest: D. A. Patel has received research support from the National Institutes of Health and Hoffmann-La Roche. D. E. Byers has received research support from the National Institutes of Health and has received payments for lectures from Washington University CME. M. L. Moore has received research support from the National Institutes of Health; has a board membership with Alios Biopharma; has consultant arrangements with Alios Biopharma and RSV Corporation; has received payment for lectures from Merck; receives royalties from Alios, Biota, Crucell, GenVec, Janssen Pharmaceuticals, Merck, Novartis, Regeneron, Roche, Sanofi Paster, and Vertex; and is founder of Meissa Vaccines. R. S. Peebles, A. Shifren, and S. L. Brody have received research support from the National Institutes of Health. M. Castro has received research support from the National Institutes of Health, Boston Scientific, Amgen, Ception/Cephalon/Teva, Genentech, MedImmune, Merck, Novartis, GlaxoSmithKline, Sanofi-Aventis, Vectura, NextBio, and KalaBios; has consultant arrangements with Asthmatx/Boston Scientific, IPS/Holaira, Genentech, and Neostem; has received speakers fees from Merck, GlaxoSmithKline, Genentech, Boston Scientific, Boehringer-Ingelheim, and TEVA; has received royalties from Elsevier; and has stock in Sparo, Inc. K. Sumino has received research support from the National Institutes of Health, the American Lung Association, the Veterans' Administration, and the Patient-Centered Outcomes Research Institute and has received payment for lectures from Tokyo Bay Hospital. M. J. Holtzman has received research support from the National Institutes of Health, Hoffmann-La Roche, and Forest Labs; has a board membership with AstraZeneca; and has received payments for lectures from Merck and Genentech. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 134 - N° 6
P. 1402 - décembre 2014 Retour au numéro
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