The Editor takes a closer look at some of this month's articles

Abstract

The Editor takes a closer look at some of this month's articlesSmoking and asthma: amplification or suppression?As many asthmatics smoke as non-asthmatics, a testimony to the addictive effects of tobacco. Smoking asthmatics are generally regarded as more difficult to control than their nonsmoking counterparts and long-term smokers often have a mixed asthma-COPD picture. Decline in lung function is accelerated in asthmatic smokers. However, it is not clear if smoking amplifies, attenuates or just modifies airway inflammation, for example by promoting a more neutrophilic profile. It is sufficiently common for people to say that their respiratory problems started after they stopped smoking to raise the possibility that smoking may be having a suppressive effect on airway inflammation and airway hyperresponsiveness (AHR). Interestingly, Paul O'Byrne's group recently reported in the journal a reduced effect on AHR after allergen challenge, despite no obvious effect on airway inflammation [1]. Two studies in this issue have examined the effect of smoking on the immunology of asthma. Nagasaki and colleagues (pp. 608-615) found that smoking promoted a Th2 pattern of inflammation with more IgE, eosinophils, and TSLP in smoking asthmatics. Similarly, found increased levels of leukotrienes and PGE2 in the sputum of smoking asthmatics the former associated with eosinophils and the latter with neutrophils. Evidence from these two studies therefore supports the expected pro-inflammatory role of smoking in asthma.