卵清蛋白
支气管肺泡灌洗
内质网
未折叠蛋白反应
免疫学
巨噬细胞极化
生物
白细胞介素4
哮喘
肺
巨噬细胞
细胞生物学
免疫系统
医学
内科学
生物化学
体外
作者
Yuan Xiao,Huangping Zhang,Yu Liu,Li‐Hua Mo,Yun Liao,Qinmiao Huang,Liteng Yang,Cai-Jie Zhou,Jiang‐Qi Liu,Xizhuo Sun,Hai‐Qiong Yu,Ping‐Chang Yang
标识
DOI:10.1093/jleuko/qiad109
摘要
Abstract Interleukin (IL)-33 is a key driver of T helper 2 (Th2) cell polarization. Endoplasmic reticulum (ER) stress plays a role in the skewed T cell activation. The objective of this project is to elucidate the role of IL-33 derived from macrophages in inducing Th2 polarization in the airways. In this study, bronchoalveolar lavage fluids (BALF) were collected from patients with asthma and healthy control subjects. Macrophages were isolated from the BALF by flow cytometry cell sorting. An asthmatic mouse model was established using the ovalbumin/alum protocol. The results showed that increased IL33 gene activity and ER stress–related molecules in BALF-derived M2a macrophages was observed in asthmatic patients. Levels of IL33 gene activity in M2a cells were positively correlated with levels of asthma response in asthma patients. Sensitization exacerbated the ER stress in the airway macrophages, which increased the expression of IL-33 in macrophages of airway in sensitized mice. Conditional ablation of Il33 or Perk or Atf4 genes in macrophages prevented induction of airway allergy in mice. In conclusion, asthma airway macrophages express high levels of IL-33 and at high ER stress status. Inhibition of IL-33 or ER stress in macrophages can effectively alleviate experimental asthma.
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