Virus Infection-Induced Bronchial Asthma Exacerbation

Infection with respiratory viruses, including rhinoviruses, influenza virus, and respiratory syncytial virus, exacerbates asthma, which is associated with processes such as airway inflammation, airway hyperresponsiveness, and mucus hypersecretion. In patients with viral infections and with infection...

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Main Author: Mutsuo Yamaya
Format: Article
Language:English
Published: Hindawi Limited 2012-01-01
Series:Pulmonary Medicine
Online Access:http://dx.doi.org/10.1155/2012/834826
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spelling doaj-268208dc1fb54cde94ec3bf119efbe5b2020-11-25T00:04:50ZengHindawi LimitedPulmonary Medicine2090-18362090-18442012-01-01201210.1155/2012/834826834826Virus Infection-Induced Bronchial Asthma ExacerbationMutsuo Yamaya0Department of Advanced Preventive, Medicine for Infectious Disease, Tohoku University Graduate School of Medicine, Sendai 980-8575, JapanInfection with respiratory viruses, including rhinoviruses, influenza virus, and respiratory syncytial virus, exacerbates asthma, which is associated with processes such as airway inflammation, airway hyperresponsiveness, and mucus hypersecretion. In patients with viral infections and with infection-induced asthma exacerbation, inflammatory mediators and substances, including interleukins (ILs), leukotrienes and histamine, have been identified in the airway secretions, serum, plasma, and urine. Viral infections induce an accumulation of inflammatory cells in the airway mucosa and submucosa, including neutrophils, lymphocytes and eosinophils. Viral infections also enhance the production of inflammatory mediators and substances in airway epithelial cells, mast cells, and other inflammatory cells, such as IL-1, IL-6, IL-8, GM-CSF, RANTES, histamine, and intercellular adhesion molecule-1. Viral infections affect the barrier function of the airway epithelial cells and vascular endothelial cells. Recent reports have demonstrated augmented viral production mediated by an impaired interferon response in the airway epithelial cells of asthma patients. Several drugs used for the treatment of bronchial asthma reduce viral and pro-inflammatory cytokine release from airway epithelial cells infected with viruses. Here, I review the literature on the pathogenesis of the viral infection-induced exacerbation of asthma and on the modulation of viral infection-induced airway inflammation.http://dx.doi.org/10.1155/2012/834826
collection DOAJ
language English
format Article
sources DOAJ
author Mutsuo Yamaya
spellingShingle Mutsuo Yamaya
Virus Infection-Induced Bronchial Asthma Exacerbation
Pulmonary Medicine
author_facet Mutsuo Yamaya
author_sort Mutsuo Yamaya
title Virus Infection-Induced Bronchial Asthma Exacerbation
title_short Virus Infection-Induced Bronchial Asthma Exacerbation
title_full Virus Infection-Induced Bronchial Asthma Exacerbation
title_fullStr Virus Infection-Induced Bronchial Asthma Exacerbation
title_full_unstemmed Virus Infection-Induced Bronchial Asthma Exacerbation
title_sort virus infection-induced bronchial asthma exacerbation
publisher Hindawi Limited
series Pulmonary Medicine
issn 2090-1836
2090-1844
publishDate 2012-01-01
description Infection with respiratory viruses, including rhinoviruses, influenza virus, and respiratory syncytial virus, exacerbates asthma, which is associated with processes such as airway inflammation, airway hyperresponsiveness, and mucus hypersecretion. In patients with viral infections and with infection-induced asthma exacerbation, inflammatory mediators and substances, including interleukins (ILs), leukotrienes and histamine, have been identified in the airway secretions, serum, plasma, and urine. Viral infections induce an accumulation of inflammatory cells in the airway mucosa and submucosa, including neutrophils, lymphocytes and eosinophils. Viral infections also enhance the production of inflammatory mediators and substances in airway epithelial cells, mast cells, and other inflammatory cells, such as IL-1, IL-6, IL-8, GM-CSF, RANTES, histamine, and intercellular adhesion molecule-1. Viral infections affect the barrier function of the airway epithelial cells and vascular endothelial cells. Recent reports have demonstrated augmented viral production mediated by an impaired interferon response in the airway epithelial cells of asthma patients. Several drugs used for the treatment of bronchial asthma reduce viral and pro-inflammatory cytokine release from airway epithelial cells infected with viruses. Here, I review the literature on the pathogenesis of the viral infection-induced exacerbation of asthma and on the modulation of viral infection-induced airway inflammation.
url http://dx.doi.org/10.1155/2012/834826
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