Asthma Remission
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Date
2010-04-09
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Thai Journal of Tuberculosis Chest Diseases and Critical Care
Abstract
Treatment with inhaled corticosteroids could induce asthma remission at clinical levels but could only reduce Th2 cytokine-mediated airway inflammation therefore ongoing airway inflammation still exists and asthmatic symptoms may be relapse in patients with severe asthma. Mechanisms underlying ongoing airway inflammation are associated with environmental epigenitics, Th2 polarization, suppression of indoleamine 2, 3 dioxygenase (IDO) after allergen exposure, and ICS-resistant neutrophilic airway inflammation induced by Th17 cells. Environment epigenetics is induced by appropriate environment stimuli including cigarette smoking which result in favour of Th2 cytokine production but reduce Th1 cytokines. Th2 polarization is rather irreversible process, which causes the increase of Th2 cell numbers and Th2 cytokine release. Aeroallergen in particular house dust mite could suppress immunosuppressive activity of IDO in dendritic cells, thus enhancing airway inflammation. Th17 cells are a major source of interleukin-17 which is chemoattractant for neutrophil therefore induces neutrophilic airway inflammation. Recent study has demonstrated that there is an increase in Th17 cells in patients with steroid-resistant severe asthma in association with neutrophilic airway inflammation, possibly contributing to the mechanism responsible for steroid-resistance in asthma.
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Thai Journal of Tuberculosis Chest Diseases and Critical Care; Vol.30 No.2 April-June 2009; 74-83