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IL-33 increased the level of phosphorylated p38 mitogen-activated protein kinase (MAPK). Chemical inhibition of p38 and genetic siRNA knockdown of p38 beta (p38β), but not p38α, abrogated the I A response induced by IL-33. Moreover, IL-33 increased neuronal excitability of DRG neurons and facilitated peripheral pain sensitivity in mice; both of these effects were occluded by I A blockade. Conclusions Our present study reveals a novel mechanism by which IL-33/ST2 suppresses I A via a Syk-dependent p38β signaling pathway