Abstract
Research on the pathogenesis of asthma has concentrated on initial stimuli, genetic susceptibilities, adaptive immune responses, and end-organ alterations (particularly in airway mucous cells and smooth muscle) as critical steps leading to disease. Recent evidence indicates that the innate immune cell response to respiratory viruses also contributes to the development of inflammatory airway disease. We further develop this concept by raising the issue that the interaction between host airway epithelial cells and respiratory viruses is another aspect of innate immunity that is also a critical determinant of asthma. We also introduce a rationale for how antiviral performance at the epithelial cell level might be improved to prevent acute infectious illness and chronic inflammatory disease caused by respiratory viruses.
Copyright © 2011 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Asthma / etiology
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Asthma / physiopathology*
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Asthma / therapy
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Asthma / virology
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Disease Models, Animal
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Epithelial Cells / physiology*
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Epithelial Cells / virology
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Host-Pathogen Interactions*
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Humans
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Immunity, Innate
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Interferons / physiology
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Macrophages / immunology
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Mice
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Models, Biological*
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Models, Immunological
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Pulmonary Disease, Chronic Obstructive / etiology
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Pulmonary Disease, Chronic Obstructive / immunology
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Pulmonary Disease, Chronic Obstructive / virology
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Respiratory Tract Infections / complications
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Respiratory Tract Infections / immunology
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Respiratory Tract Infections / physiopathology
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Respiratory Tract Infections / virology
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Respirovirus Infections / complications
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Respirovirus Infections / virology
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Sendai virus
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T-Lymphocyte Subsets / immunology
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Virus Diseases / complications
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Virus Diseases / immunology
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Virus Diseases / virology
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Virus Replication / immunology
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Viruses / pathogenicity*