Our results identified that: 1) Apical dsRNA exposure induces bidirectional (apical/basolateral) secretion of TSLP in HBEC; 2) Asthmatic HBEC exhibit an exaggerated apical, but not basal, secretion of TSLP after dsRNA exposure; 3) TSLP exposure induces unidirectional (apical) secretion of CCL11/eotaxin-1 in asthmatic HBEC and enhanced CCL11/eotaxin-1 secretion in asthmatic HASMC; and 4) Rhinovirus-induced asthma exacerbations in children are associated with in vivo airway secretion of TSLP and CCL11/eotaxin-1. This evidence concerns the gene TSLP and asthma.