['To explore the role of IL-33 in asthmatic airway remodeling.', 'Male BALB/c mice were randomly divided into 3 groups: a control group, an ovalbumin (OVA) group, and an anti-IL-33 antibody combined with OVA group. The airway remodeling features in mice were observed by HE staining. In addition, the expressions of IL-33, alpha smooth muscle actin (α-SMA), and type 1 collagen (Col1) in the airway of mice were detected by immunohistochemistry and Western blotting. Finally, Western blotting was used to determine the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and mitogen- and stress-activated protein kinase 1 (MSK1) in the lungs of mice. In vitro, human lung fibroblasts (HLF-1) were pretreated with the ERK1/2 inhibitor U0126 or the MSK1 inhibitor H89 respectively, and then treated with the human recombinant IL-33 (rIL-33). Then real-time quantitative PCR and Western blotting were used to test the expressions of α-SMA and Col1. Immunofluorescence cytochemistry and Western blotting were also used to observe the phosphorylation of ERK1/2 and MSK1 in HLF-1 cells.', 'The pre-treatment with the ERK1/2 inhibitor U0126 or anti-IL-33 antibody significantly abolished the OVA-induced airway remodeling, increased expressions of IL-33, α-SMA, Col1, and phosphorylation of ERK1/2 and MSK1 in the airway of mice. In vitro, the increased expressions of α-SMA and Col1 and the phosphorylation of ERK1/2 and MSK1 induced by rIL-33 in HLF-1 cells were markedly inhibited by the pre-treatment with U0126 or H89.'] Does [ IL-33 promote airway remodeling in a mouse model of asthma via ERK1/2 signaling pathway ]?