Document Detail


Exogenous IFN-β has antiviral and anti-inflammatory properties in primary bronchial epithelial cells from asthmatic subjects exposed to rhinovirus.
MedLine Citation:
PMID:  21329968     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BACKGROUND: Rhinoviruses are the major cause of asthma exacerbations. Previous studies suggest that primary bronchial epithelial cells (PBECs) from asthmatic subjects are more susceptible to rhinovirus infection because of deficient IFN-β production. Although augmenting the innate immune response might provide a novel approach for treatment of virus-induced asthma exacerbations, the potential of IFN-β to modulate antiviral and proinflammatory responses in asthmatic epithelium is poorly characterized. OBJECTIVES: We sought to compare responses of PBECs from nonasthmatic and asthmatic subjects to exogenous IFN-β and test the inflammatory effects of IFN-β in response to rhinovirus infection. METHODS: PBECs were treated with IFN-β and infected with a low inoculum of human rhinovirus serotype 1B to simulate a natural viral infection. Expression of interferon-responsive genes and inflammatory responses were analyzed by using reverse transcription-quantitative real-time PCR, cytometric bead arrays, or both; viral titers were assessed by using the 50% tissue culture infection dose. RESULTS: Expression of IFN-β-stimulated antiviral genes was comparable in PBECs from nonasthmatic or asthmatic donors. Exogenous IFN-β significantly protected PBECs from asthmatic donors against rhinovirus infection by suppressing viral replication. Interferon-inducible protein 10 (IP-10), RANTES, and IL-6 release in response to rhinovirus infection was triggered only in PBECs from asthmatic donors. Although exogenous IFN-β alone stimulated some release of IP-10 (but not IL-6 or RANTES), it significantly reduced rhinovirus-induced IP-10, RANTES, and IL-6 expression when tested in combination with rhinovirus. CONCLUSIONS: PBECs from asthmatic donors have a normal antiviral response to exogenous IFN-β. The ability of IFN-β to suppress viral replication suggests that it might limit virus-induced exacerbations by shortening the duration of the inflammatory response.
Authors:
Julie A Cakebread; Yunhe Xu; Chris Grainge; Valia Kehagia; Peter H Howarth; Stephen T Holgate; Donna E Davies
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-2-15
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  -     ISSN:  1097-6825     ISO Abbreviation:  -     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-2-18     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
Affiliation:
Division of Infection, Inflammation and Immunity, University of Southampton School of Medicine, Southampton, United Kingdom and the National Institute for Health Research (NIHR) Respiratory Biomedical Research Unit, Southampton General Hospital.
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