Viruses are associated with the majority of exacerbations of asthma and COPD. Virus induction of neutrophil and lymphocyte chemokines in bronchial epithelium is important in exacerbation pathogenesis. Combined corticosteroid/₂ agonists synergistically suppress airway smooth muscle chemokine production. As bronchial epithelium expresses both glucocorticoid and ₂ receptors, we investigated whether combination therapy can synergistically suppress rhinovirus induced bronchial epithelial cell neutrophil (CXCL5, CXCL8) and lymphocyte (CCL5, CXCL10) chemokine production. We investigated modulation of rhinovirus and IL-1 induced bronchial epithelial cell chemokine production by salmeterol and fluticasone propionate, used at therapeutic concentrations, both alone and in combination. After only 1h pre-treatment, combined treatment significantly inhibited rhinovirus 16, 1B and IL-1 induced CCL5 and CXCL8 protein and mRNA production in BEAS-2B cells, compared to fluticasone alone. When used 4h post treatment, the combination significantly reduced virus induced CCL5, but not CXCL8. Salmeterol alone had no effect, therefore this inhibition was synergistic. Kinetic analysis demonstrated that combination therapy reduced by 5-fold the concentration of corticosteroid required to inhibit CXCL8 mRNA expression. In primary cells, salmeterol alone reduced rhinovirus induced CCL5 and CXCL10 and increased CXCL5 production in a dose dependent manner, but had no effect on CXCL8. Fluticasone alone reduced CCL5, CXCL8 and CXCL10, but had no effect on CXCL5. Combination therapy augmented inhibition of CXCL8, CCL5 and CXCL10, but had no effect on CXCL5. Corticosteroids and ₂ agonists suppress rhinovirus induced chemokines in bronchial epithelial cells through both synergistic and additive mechanisms. This effect was greater for lymphocyte than for neutrophil related chemokines.