The STAT6 inhibitor AS1517499 reduces the risk of asthma in mice with 2,4-dinitrochlorobenzene-induced atopic dermatitis by blocking the STAT6 signaling pathway

STAT6 卵清蛋白 嗜酸性粒细胞 特应性皮炎 哮喘 免疫学 医学 信号转导 FOXP3型 免疫球蛋白E 细胞因子 白细胞介素4 生物 免疫系统 细胞生物学 抗体
作者
Xueying Li,Zhaoqing Han,Wang Feng,Jianou Qiao
出处
期刊:Allergy, Asthma & Clinical Immunology [BioMed Central]
卷期号:18 (1) 被引量:12
标识
DOI:10.1186/s13223-022-00652-8
摘要

Epidemiological studies have revealed a link between atopic dermatitis (AD) and asthma. AS1517499, a selective signal transducer and activation of transcription 6 (STAT6) inhibitor, has been shown to effectively block this connection. In this study, we further explored the underlying mechanism by constructing an AD mouse model.Female BALB/c mice were randomly divided into four groups (n = 10/group). The AD mouse model was established by 2,4-dinitrochlorobenzene induction with repeated ovalbumin challenge. AS1517499 and corn oil were used as treatment interventions. The features of airway inflammation, remodeling, and hyperactivity were analyzed.Active use of AS1517499 in AD mice effectively reduced Th2-related cytokine levels, alleviated airway eosinophil and lymphocyte infiltration, and regulated GATA3/Foxp3 levels and subepithelial collagen deposition. These changes might be due to specific blockade of the STAT6 signaling pathway.AS1517499 could partially block the association between AD and asthma by specifically inhibiting the STAT6 signaling pathway.
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