Migration of the contractile phenotype of human airway smooth muscle cells in response to supernatants from rhinovirus infected human bronchial epithelial cells

Rationale Human rhinovirus (HRV) infections during early childhood are associated with a significantly increased risk of developing asthma in subsequent years [1]. There is published evidence that airway remodeling is present in pre-school children, often before the diagnosis of asthma is established [1]. It is thought that this increased risk relates to the fact that HRV infections facilitate airway remodeling in asthma [2]. A feature of airway remodeling is the proximity of airway smooth muscle (ASM) to the subepithelial region among other pathological changes [3]. Smooth muscle is also known to exist in two distinct phenotypes: secretory and contractile [4]. We have recently shown that HRV infection of Human Bronchial Epithelial Cells (HBEC), both in vitro and in vivo, results in the up-regulation of a number of airway remodeling mediators [5]. We now sought to determine which ASM phenotype (contractile or secretory) results in migration to supernatants from HRV infected HBE cells.