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      The role of viruses in acute exacerbations of asthma

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          Abstract

          Viral respiratory infections are the most common cause of an acute asthma exacerbation in both children and adults and represent a significant global health burden. An increasing body of evidence supports the hypothesis that these infections cause a greater degree of morbidity in asthmatic subjects than in the healthy population, emphasizing a discrepancy in the antiviral response of asthmatics. In this review we discuss why such a discrepancy might exist, examining the role of the bronchial epithelium as well as the main inflammatory cells, mediators, and molecular pathways that are involved in the immune response. In addition, the potential impact of virus-induced asthma exacerbations on airway remodelling is reviewed and we explore which therapeutic options might be of benefit in preventing the deterioration of asthma control seen following viral infection.

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          Community study of role of viral infections in exacerbations of asthma in 9-11 year old children.

          S Johnston, P Pattemore, G. Sanderson … (1995)
          To study the association between upper and lower respiratory viral infections and acute exacerbations of asthma in schoolchildren in the community. Community based 13 month longitudinal study using diary card respiratory symptom and peak expiratory flow monitoring to allow early sampling for viruses. 108 Children aged 9-11 years who had reported wheeze or cough, or both, in a questionnaire. Southampton and surrounding community. Upper and lower respiratory viral infections detected by polymerase chain reaction or conventional methods, reported exacerbations of asthma, computer identified episodes of respiratory tract symptoms or peak flow reductions. Viruses were detected in 80% of reported episodes of reduced peak expiratory flow, 80% of reported episodes of wheeze, and in 85% of reported episodes of upper respiratory symptoms, cough, wheeze, and a fall in peak expiratory flow. The median duration of reported falls in peak expiratory flow was 14 days, and the median maximum fall in peak expiratory flow was 81 l/min. The most commonly identified virus type was rhinovirus. This study supports the hypothesis that upper respiratory viral infections are associated with 80-85% of asthma exacerbations in school age children.
          Article 0 comments Cited 427 times – based on 0 reviews     Review now
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            Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus

            Peter Wark, Sebastian L. Johnston, Fabio Bucchieri … (2005)
            Rhinoviruses are the major trigger of acute asthma exacerbations and asthmatic subjects are more susceptible to these infections. To investigate the underlying mechanisms of this increased susceptibility, we examined virus replication and innate responses to rhinovirus (RV)-16 infection of primary bronchial epithelial cells from asthmatic and healthy control subjects. Viral RNA expression and late virus release into supernatant was increased 50- and 7-fold, respectively in asthmatic cells compared with healthy controls. Virus infection induced late cell lysis in asthmatic cells but not in normal cells. Examination of the early cellular response to infection revealed impairment of virus induced caspase 3/7 activity and of apoptotic responses in the asthmatic cultures. Inhibition of apoptosis in normal cultures resulted in enhanced viral yield, comparable to that seen in infected asthmatic cultures. Examination of early innate immune responses revealed profound impairment of virus-induced interferon-β mRNA expression in asthmatic cultures and they produced >2.5 times less interferon-β protein. In infected asthmatic cells, exogenous interferon-β induced apoptosis and reduced virus replication, demonstrating a causal link between deficient interferon-β, impaired apoptosis and increased virus replication. These data suggest a novel use for type I interferons in the treatment or prevention of virus-induced asthma exacerbations.
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              Pattern recognition receptors TLR4 and CD14 mediate response to respiratory syncytial virus.

              E. Kurt-Jones, L. Popova, L Kwinn … (2000)
              The innate immune system contributes to the earliest phase of the host defense against foreign organisms and has both soluble and cellular pattern recognition receptors for microbial products. Two important members of this receptor group, CD14 and the Toll-like receptor (TLR) pattern recognition receptors, are essential for the innate immune response to components of Gram-negative and Gram-positive bacteria, mycobacteria, spirochetes and yeast. We now find that these receptors function in an antiviral response as well. The innate immune response to the fusion protein of an important respiratory pathogen of humans, respiratory syncytial virus (RSV), was mediated by TLR4 and CD14. RSV persisted longer in the lungs of infected TLR4-deficient mice compared to normal mice. Thus, a common receptor activation pathway can initiate innate immune responses to both bacterial and viral pathogens.
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                Author and article information

                Contributors
                David J. Jackson
                Journal
                Journal ID (nlm-ta): J Allergy Clin Immunol
                Journal ID (iso-abbrev): J. Allergy Clin. Immunol
                Title: The Journal of Allergy and Clinical Immunology
                Publisher: American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc.
                ISSN (Print): 0091-6749
                ISSN (Electronic): 1097-6825
                Publication date PMC-release: 31 May 2010
                Publication date (Print): June 2010
                Publication date (Electronic): 31 May 2010
                Volume: 125
                Issue: 6
                Pages: 1178-1187
                Affiliations
                Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom
                Author notes
                [∗ ]Reprint requests: David J. Jackson, MD, Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom. d.jackson@ 123456imperial.ac.uk
                Article
                Publisher ID: S0091-6749(10)00689-5
                DOI: 10.1016/j.jaci.2010.04.021
                PMC ID: 7172767
                PubMed ID: 20513517
                SO-VID: 868080bd-0983-4fb2-96c9-f612bd86a8b8
                Copyright © Copyright © 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 14 April 2010
                Date accepted : 21 April 2010
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: asthma,acute exacerbation,virus,bal, bronchoalveolar lavage,bec, bronchial epithelial cell,fgf, fibroblast growth factor,hrv, human rhinovirus,icam-1, intercellular adhesion molecule 1,ip-10, interferon-inducible protein 10,irf, interferon regulatory factor,nf-κb, nuclear factor kappa b,prr, pattern-recognition receptor,socs1, suppressor of cytokine signaling 1,tlr, toll-like receptor,vegf, vascular endothelial growth factor
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: asthma, acute exacerbation, virus, bal, bronchoalveolar lavage, bec, bronchial epithelial cell, fgf, fibroblast growth factor, hrv, human rhinovirus, icam-1, intercellular adhesion molecule 1, ip-10, interferon-inducible protein 10, irf, interferon regulatory factor, nf-κb, nuclear factor kappa b, prr, pattern-recognition receptor, socs1, suppressor of cytokine signaling 1, tlr, toll-like receptor, vegf, vascular endothelial growth factor

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