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Dept of Respiratory Medicine, Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK.
CORRESPONDENCE: N.C. Thomson, Dept of Respiratory Medicine, Division of Immunology, Infection and Inflammation, Western Infirmary & University of Glasgow, Glasgow, G11 6NT, UK. Fax: 44 1412113464. E-mail: n.c.thomson@clinmed.gla.ac.uk
Keywords: Asthma, corticosteroid resistance, smokers, smoking cessation
Received: April 1, 2004
Accepted July 6, 2004
Abstract
In most developed countries
Cigarette smoking may modify inflammation that is associated with asthma, although there is limited published data on airway pathology in smokers with asthma. To date, the evidence points towards a combination of both heightened and suppressed inflammatory responses in smokers compared with nonsmokers with asthma.
The mechanisms of corticosteroid resistance in asthmatic smokers are unexplained, but could be as a result of alterations in airway inflammatory cell phenotypes (e.g. increased neutrophils or reduced eosinophils), changes in the glucocorticoid receptor-
In conclusion, every effort should be made to encourage asthmatics who smoke to stop, although the effects of smoking cessation upon reversing the adverse effects of tobacco smoke on asthma control, therapeutic response to corticosteroids and airway pathology have yet to be fully elucidated. Alternative or additional therapies to inhaled corticosteroids are needed for asthmatic patients who are unable to quit smoking.
25% of adults with asthma are current cigarette smokers. Asthma and active cigarette smoking interact to cause more severe symptoms, accelerated decline in lung function, and impaired short-term therapeutic response to corticosteroids. 
to -ß ratio (e.g. overexpression of glucocorticoid receptor ß), and increased activation of pro-inflammatory transcription factors (e.g. nuclear factor-
B) or reduced histone deacetylase activity.
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