Results
Poly (I:C) stimulated NHBE and BEAS-2B cells to produce CCL5. Poly (I:C) and IL-13 increased CCL5 production. Poly (I:C)-induced CCL5 production occurred via the TLR3-IRF3 and IFNAR/JAK1-PI3K pathways, but not the IFNAR/JAK1-STATs pathway. In addition, IL-13 did not augment poly (I:C)-induced CCL5 production via the canonical IL-13R/IL-4R/JAK1-STAT6 pathway but likely via subsequent TLR3-IRF3-IFNAR/JAK1-PI3K pathways. JAK1 was identified to be a potential therapeutic target for severe eosinophilic asthma. The JAK1/2 inhibitor, ruxolitinib, was demonstrated to more effectively decrease CCL5 production in BEAS-2B cells than fluticasone propionate.