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      Asthma exacerbation related to viral infections: An up to date summary

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          Abstract

          Asthma exacerbation can be a major life threatening event. Viruses have been pinned as the cause behind the vast majority of these exacerbations. The purpose of this short review is to explore the mechanisms behind these exacerbations, focusing mostly on viral infections as triggers. We will also be discussing the phenotypes prone to asthma exacerbation, the pathophysiology of viral induced asthma and ventilation patterns of asthmatic lungs. This manuscript will assist primary care physicians in delineating the proper pathophysiology of the disease as well as the management.

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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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            Rhinovirus-induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production.

            Simon D. Message, Vasile Laza-Stanca, Patrick Mallia … (2008)
            Acute exacerbations are the major cause of asthma morbidity, mortality, and health-care costs and are difficult to treat and prevent. The majority of asthma exacerbations are associated with rhinovirus (RV) infection, but evidence supporting a causal relationship is weak and mechanisms are poorly understood. We hypothesized that in asthmatic, but not normal, subjects RV infection would induce clinical, physiologic, and pathologic lower airway responses typical of an asthma exacerbation and that these changes would be related to virus replication and impaired T helper 1 (Th1)/IL-10 or augmented Th2 immune responses. We investigated physiologic, virologic, and immunopathologic responses to experimental RV infection in blood, induced sputum, and bronchial lavage in 10 asthmatic and 15 normal volunteers. RV infection induced significantly greater lower respiratory symptoms and lung function impairment and increases in bronchial hyperreactivity and eosinophilic lower airway inflammation in asthmatic compared with normal subjects. In asthmatic, but not normal, subjects virus load was significantly related to lower respiratory symptoms, bronchial hyperreactivity, and reductions in blood total and CD8(+) lymphocytes; lung function impairment was significantly related to neutrophilic and eosinophilic lower airway inflammation. The same virologic and clinical outcomes were strongly related to deficient IFN-gamma and IL-10 responses and to augmented IL-4, IL-5, and IL-13 responses. This study demonstrates increased RV-induced clinical illness severity in asthmatic compared with normal subjects, provides evidence of strong relationships between virus load, lower airway virus-induced inflammation and asthma exacerbation severity, and indicates augmented Th2 or impaired Th1 or IL-10 immunity are likely important mechanisms.
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              A critical role for eosinophils in allergic airways remodeling.

              Alison A. Humbles, Clare Lloyd, Sarah McMillan … (2004)
              Features of chronic asthma include airway hyperresponsiveness, inflammatory infiltrates, and structural changes in the airways, termed remodeling. The contribution of eosinophils, cells associated with asthma and allergy, remains to be established. We show that in mice with a total ablation of the eosinophil lineage, increases in airway hyperresponsiveness and mucus secretion were similar to those observed in wild-type mice, but eosinophil-deficient mice were significantly protected from peribronchiolar collagen deposition and increases in airway smooth muscle. These data suggest that eosinophils contribute substantially to airway remodeling but are not obligatory for allergen-induced lung dysfunction, and support an important role for eosinophil-targeted therapies in chronic asthma.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Family Med Prim Care
                Journal ID (iso-abbrev): J Family Med Prim Care
                Journal ID (publisher-id): JFMPC
                Title: Journal of Family Medicine and Primary Care
                Publisher: Wolters Kluwer - Medknow (India )
                ISSN (Print): 2249-4863
                ISSN (Electronic): 2278-7135
                Publication date Collection: September 2019
                Publication date (Electronic): 30 September 2019
                Volume: 8
                Issue: 9
                Pages: 2753-2759
                Affiliations
                [1 ] Department of Pediatrics, Section of Academic General Pediatrics, Sidra Medicine, Doha, Qatar
                [2 ] Department of Pediatrics, Hamad General Corporation, Doha, Qatar
                [3 ] Department of Clinical Pediatrics, Weill- Cornell Medicine, Doha, Qatar
                Author notes
                Address for correspondence: Dr. Mehdi Adeli, Department of Pediatrics, Sidra Medicine, Doha - 26999, Qatar. E-mail: madeli@ 123456sidra.org
                Article
                Publisher ID: JFMPC-8-2753
                DOI: 10.4103/jfmpc.jfmpc_86_19
                PMC ID: 6820381
                PubMed ID: 31681638
                SO-VID: c13501c6-0be1-4a77-8934-fb4743ceb98f
                Copyright © Copyright: © 2019 Journal of Family Medicine and Primary Care
                License:

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                Date received : 31 January 2019
                Date revision received : 01 February 2019
                Date accepted : 27 August 2019
                Related
                Competency-based medical education: How far, how much
                Categories
                Subject: Commentary

                Keywords: asthma,exacerbations,pulmonary function,virus-induced asthma
                Data availability:
                Keywords: asthma, exacerbations, pulmonary function, virus-induced asthma

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