1 Department of Surgical Intensive Care Unit, Beijing An Zhen Hospital, Capital Medical University, Beijing 100029, China.
2 Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, National Clinical Research Center for Respiratory Disease, Beijing 100029, China.
Exp Biol Med (Maywood). 2019 Jun;244(9):770-780. doi: 10.1177/1535370219843827. Epub 2019 Apr 18.
Our work focused on alveolar epithelial cells (AECs)-derived type-2 cytokine (interleukin [IL]-25) in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We showed that IL-25 and IL-17BR (IL-25's receptor) is upregulated in lung tissues (especially in AECs and lung fibroblasts) of IPF patients and contributes to lung fibrosis by directly activating lung fibroblasts and modulating epithelial-mesenchymal transition (EMT) of AECs. We suggest that IL-25 may be one of the master switches hidden in the milieu of abnormal epithelial-mesenchymal crosstalk. Treatment targeting IL-25 may be the potential and novel method for IPF patients.
我们的工作重点是特发性肺纤维化（IPF）发病机制中的肺泡上皮细胞（AEC）衍生的 2 型细胞因子（白细胞介素[IL]-25）。我们表明，IL-25 和 IL-17BR（IL-25 的受体）在 IPF 患者的肺组织（特别是 AEC 和肺成纤维细胞中）上调，并通过直接激活肺成纤维细胞和调节 AEC 的上皮-间充质转化（EMT）来导致肺纤维化。我们认为，IL-25 可能是异常上皮-间充质相互作用环境中隐藏的主开关之一。针对 IL-25 的治疗可能是 IPF 患者的潜在新方法。
