Abstract
The prevailing current concept is that airway mucus expression is dependent on STAT6 signaling. However, IL-17A has recently been reported to induce airway mucus expression and is not known to signal through STAT6. We hypothesized that IL-17A induces airway mucus in a STAT6-independent manner. To test this hypothesis, we used a mouse model of RSV infection of STAT1 knock out (KO) mice in which there is abundant lung IL-17A protein expression. We created STAT1/STAT6 double KO (DKO) mice to determine if the mucus in the RSV-infected STAT1 KO mice was dependent upon STAT6 signaling, and STAT1/STAT6/IL-17RA TKO to confirm the role of IL-17A.
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