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.