Janette Kay Burgess

Comments on Point:Counterpoint: Alterations in airway smooth muscle phenotype do/do not cause airway hyperresponsiveness in asthma.

TO THE EDITOR: We just witnessed an interesting debate, with lowdown punches, on the potential role of airway smooth muscle (ASM) in asthmatic airway hyperresponsiveness (AHR) when the ASM proponents Drs. Gunst and Panettieri faced the ASM opponents Drs. Paré and Mitzner (2). However, part of the disagreement seems to lie upon the vocabulary used. On one hand, the proponents reported that several molecules that are overexpressed in asthma have the ability to affect ASM contractility. IL17A can now be added to this list (3). These observations suggest that the contractile properties of ASM are malleable. In asthmatic lungs, where the ASM is bombarded by many of those molecules, it seems reasonable to infer that the ASM may become stronger, stiffer, quicker, and/or less likely to relax, which may all contribute to AHR. On the other hand, the opponents can argue that nonasthmatic ASM would behave similarly under these aberrant circumstances. Therefore, the ASM of asthmatics is not abnormal. The term “alterations” in the title of this debate is a source of ambiguity, because it can either mean that the alterations are innate (genetically determined) or acquired due to both the abnormal environment in which asthmatic ASM operates and the recognized malleability of ASM contractility. If my little 10 years of experience is worth anything, I don’t think there is convincing evidence of innate differences in contractility between asthmatic and non-asthmatic ASM in humans. The hypercontractile phenotype observed by Ma et al. (4), Matsumoto et al. (5), and more recently Sutcliffe et al. (6) in isolated cells could have been acquired and simply maintained in culture; not mentioning that those findings are plagued with the lack of consistency (1).