These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: IL33/ST2 contributes to airway remodeling via p-JNK MAPK/STAT3 signaling pathway in OVA-induced allergic airway inflammation in mice.
    Author: Zhang Y, Li S, Huang S, Cao L, Liu T, Zhao J, Wu J, Wang J, Cao L, Xu J, Dong L.
    Journal: Exp Lung Res; 2019; 45(3-4):65-75. PubMed ID: 31112061.
    Abstract:
    Aim of this study: Airway remodeling, which encompasses structural changes in airway is a main feature of asthma. Interleukin-33 (IL-33) has been reported to be a vital cytokine in airway remodeling in asthma, but the underlying mechanisms are not clear yet. This study focused on discussing the role of IL-33 in airway remodeling in asthma. Material and methods: Female BALB/c mice were divided into a control group, an OVA induced allergic airway disease group and an anti-ST2 antibody intervention group. Immunohistochemistry and western blot were performed to detect IL-33, ST2 expression in addition to airway remodeling markers a-smooth muscle actin (a-SMA) and type 1 collagen in OVA-induced mice model. Levels of p-JNK and p-STAT3 activation in mice were detected by western blot. Human lung fibroblast (HLF) were stimulated with rhIL-33, anti-ST2 antibody and JNK inhibitor sp600125 and levels of JNK and STAT3 activation were determined via western blot and immunofluorescence staining. Results: Anti-ST2 treatment inhibited JNK/STAT3 phosphorylation and airway remodeling in OVA-induced mouse model. IL-33 induced a-SMA and collagen 1 expression was inhibited by anti-ST2 antibody and sp600125 treatment via decreased JNK/STAT3 phosphorylation in human lung fibroblast. Conclusions: IL-33 promoted airway remodeling by interacting with ST2 to activate the JNK/STAT3 signaling pathway in asthma.
    [Abstract] [Full Text] [Related] [New Search]