Airway smooth muscle may drive mucus hypersecretion in asthma

The contribution of airway smooth muscle (ASM) to asthma is critical but the multiple ways in which it may contribute to its pathobiology is still an active area of exploration. Contractile, proliferative and secretory properties relevant to asthma have been assessed. To date, studies of the contractile properties of isolated ASM have failed to demonstrate alterations in contractile properties that could explain excessive airway narrowing and airway hyperresponsiveness [1, 2], however tempting it is to attribute these features of asthma to intrinsic abnormalities of the muscle. In contrast to studies of tissue strips, cultured ASM cells demonstrate a range of "pro-asthmatic" properties that differ between cells derived from asthmatic subjects and healthy controls. For example, cultured ASM cells show enhanced stiffening when stimulated with contractile agonists [3] and proliferate more rapidly when treated with growth factors [4, 5], a property that would potentially favour a predisposition to remodelling. The pro-inflammatory phenotype is manifest as the expression of cytokines such as the neutrophilic chemoattractant CXCL8, attributable to enhanced NF-κB binding to the promoter site of CXCL8 [6]. Matrix proteins affecting ASM function and other cellular phenotypes are also secreted by ASM and are determinant of the ASM phenotype (reviewed in [7]). New insights into a potential property of airway smooth muscle cells with relevance to asthma