IL-33 induced airways inflammation is partially dependent on IL-9.

• IL-33 induced airways hyperresponsiveness, inflammation, and goblet cell hyperplasia are attenuated in IL-9 deficient mice. • IL-9 is required for IL-33 induced remodelling in asthma. • IL-9 is one downstream cytokine of IL-33 in asthmatic airways. Asthma is an inflammatory disease of the airways and numerous cytokines contribute to this pathogenesis. It is shown that challenge of airways with IL-33 induces asthma-like pathological changes in mice, but the possible downstream cytokines in this process remain to be characterised. To explore this, we compared changes in the airways of wildtype (WT) and IL-9 deficient mice challenged with IL-33. In line with previous report, per-nasal challenge of WT mice with IL-33 significantly increased the responsiveness of the airways along with infiltration of inflammatory cells, goblet cell hyperplasia, collagen deposition and smooth muscle hypertrophy, and the expression of cytokines compared with control group. Surprisingly, all of these pathological changes were significantly attenuated in IL-9 deficient mice following identical IL-33 challenge. These data suggest that IL-9 is one downstream cytokine relevant to the effects of IL-33 in asthmatic airways and consequently a potential therapeutic target for the treatment of asthma. [ABSTRACT FROM AUTHOR]