Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus
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 b...
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| Published in | The Journal of experimental medicine Vol. 201; no. 6; pp. 937 - 947 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
The Rockefeller University Press
21.03.2005
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| Subjects | |
| Online Access | Get full text |
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| Abstract | 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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| AbstractList | 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. 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-beta mRNA expression in asthmatic cultures and they produced >2.5 times less interferon-beta protein. In infected asthmatic cells, exogenous interferon-beta induced apoptosis and reduced virus replication, demonstrating a causal link between deficient interferon-beta, 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. 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-beta mRNA expression in asthmatic cultures and they produced >2.5 times less interferon-beta protein. In infected asthmatic cells, exogenous interferon-beta induced apoptosis and reduced virus replication, demonstrating a causal link between deficient interferon-beta, 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.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-beta mRNA expression in asthmatic cultures and they produced >2.5 times less interferon-beta protein. In infected asthmatic cells, exogenous interferon-beta induced apoptosis and reduced virus replication, demonstrating a causal link between deficient interferon-beta, 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. |
| Author | Wark, Peter A.B. Laza-Stanca, Vasile Johnston, Sebastian L. Powell, Robert Puddicombe, Sarah Davies, Donna E. Holgate, Stephen T. Bucchieri, Fabio |
| AuthorAffiliation | 1 The Brooke Laboratories, University of Southampton, Southampton SO16 6YD, UK 2 Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London W2 IPG, England, UK 3 Department of Experimental Medicine, Human Anatomy Division, University of Palermo, Palermo 90127, Italy |
| AuthorAffiliation_xml | – name: 3 Department of Experimental Medicine, Human Anatomy Division, University of Palermo, Palermo 90127, Italy – name: 1 The Brooke Laboratories, University of Southampton, Southampton SO16 6YD, UK – name: 2 Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London W2 IPG, England, UK |
| Author_xml | – sequence: 1 givenname: Peter A.B. surname: Wark fullname: Wark, Peter A.B. – sequence: 2 givenname: Sebastian L. surname: Johnston fullname: Johnston, Sebastian L. – sequence: 3 givenname: Fabio surname: Bucchieri fullname: Bucchieri, Fabio – sequence: 4 givenname: Robert surname: Powell fullname: Powell, Robert – sequence: 5 givenname: Sarah surname: Puddicombe fullname: Puddicombe, Sarah – sequence: 6 givenname: Vasile surname: Laza-Stanca fullname: Laza-Stanca, Vasile – sequence: 7 givenname: Stephen T. surname: Holgate fullname: Holgate, Stephen T. – sequence: 8 givenname: Donna E. surname: Davies fullname: Davies, Donna E. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15781584$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 P.A.B. Wark and S.L. Johnston contributed equally to this work. CORRESPONDENCE Peter Wark: p.wark@soton.ac.uk Abbreviations used: AxV, annexin-V; BEC, bronchial epithelial cell; ICS, inhaled corticosteroid; IQR, interquartile range; LDH, lactate dehydrogenase; MFI, mean fluorescence intensity; RV, rhinovirus. |
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| Snippet | Rhinoviruses are the major trigger of acute asthma exacerbations and asthmatic subjects are more susceptible to these infections. To investigate the underlying... |
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| SubjectTerms | Adult Antiviral Agents - immunology Antiviral Agents - therapeutic use Apoptosis - immunology Asthma - drug therapy Asthma - immunology Asthma - virology Bronchi - cytology Bronchi - immunology Bronchi - virology Caspase 3 Caspase 7 Caspases - immunology Cells, Cultured Epithelial Cells - immunology Epithelial Cells - virology Female Gene Expression Regulation - immunology Humans Immunity, Innate Interferon-beta - immunology Interferon-beta - therapeutic use Male Middle Aged Picornaviridae Infections - complications Picornaviridae Infections - drug therapy Picornaviridae Infections - immunology Rhinovirus Rhinovirus - immunology RNA, Viral - biosynthesis Virus Replication - immunology |
| Title | Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus |
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