title: [IL-33 promotes airway remodeling in a mouse model of asthma via ERK1/2 signaling pathway].
abstract: OBJECTIVE
  To explore the role of IL-33 in asthmatic airway remodeling.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  IL-33 promotes airway remodeling in asthmatic mice via the ERK1/2-MSK1 signaling pathway.
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Jidong Section, Yankuang Group General Hospital, Jining 272072, China.
authors.forename: Cuixia
authors.initials: C
authors.lastname: Bian
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China.
authors.forename: Jinxiang
authors.initials: J
authors.lastname: Wu
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China.
authors.forename: Jiping
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China.
authors.forename: Junfei
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China.
authors.forename: Tian
authors.initials: T
authors.lastname: Liu
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan 250012, China. *Corresponding author, E-mail: dl5506@126.com.
authors.forename: Liang
authors.initials: L
authors.lastname: Dong
mesh_terms: D056151:Airway Remodeling; D000818:Animals; D001249:Asthma / Q000473:pathology*; D002070:Butadienes / Q000494:pharmacology; D004195:Disease Models, Animal; D006801:Humans; D000067596:Interleukin-33 / Q000502:physiology*; D020935:MAP Kinase Signaling System / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009570:Nitriles / Q000494:pharmacology; D038744:Ribosomal Protein S6 Kinases, 90-kDa / Q000502:physiology
chemical_list: D002070:Butadienes; C506535:Il33 protein, mouse; D000067596:Interleukin-33; D009570:Nitriles; C113580:U 0126; D038744:Ribosomal Protein S6 Kinases, 90-kDa; C116919:mitogen and stress-activated protein kinase 1