Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
Cytokine. 2017 Nov;99:114-123. doi: 10.1016/j.cyto.2017.08.022. Epub 2017 Sep 3.
IL-36α, IL-36β and IL-36γ are cytokine members of IL-1 family. Although IL-36 expression was observed in human lung during pulmonary infections, it remains unknown whether IL-36 could act directly on lung tissue cells during pulmonary inflammatory responses. In this study, we showed that IL-36 receptor was expressed in human lung fibroblasts and bronchial epithelial cells. Correspondingly, IL-36α, IL-36β or IL-36γ up-regulated gene expression of cytokine IL-6 and chemokine CXCL8 in human lung fibroblasts and bronchial epithelial cells, and promoted IL-6 and CXCL8 release from human lung fibroblasts and bronchial epithelial cells. The production of IL-6 and CXCL8 in these lung tissues cells induced by IL-36α, IL-36β or IL-36γ was regulated by p38MAPK, ERK or Akt signaling pathways. Taken together, the above results suggest that IL-36-mediated IL-6 and CXCL8 production in human lung fibroblasts and bronchial epithelial cells may be involved in pulmonary inflammation especially caused by bacterial or viral infections.
IL-36α、IL-36β 和 IL-36γ 是白细胞介素 1 家族的细胞因子成员。虽然在肺部感染期间观察到 IL-36 在人肺中表达，但尚不清楚 IL-36 是否可以在肺部炎症反应期间直接作用于肺组织细胞。在这项研究中，我们表明 IL-36 受体在人肺成纤维细胞和支气管上皮细胞中表达。相应地，IL-36α、IL-36β 或 IL-36γ 上调了人肺成纤维细胞和支气管上皮细胞中细胞因子 IL-6 和趋化因子 CXCL8 的基因表达，并促进了人肺成纤维细胞和支气管上皮细胞中 IL-6 和 CXCL8 的释放。IL-36α、IL-36β 或 IL-36γ 诱导的这些肺组织细胞中 IL-6 和 CXCL8 的产生受 p38MAPK、ERK 或 Akt 信号通路调节。总之，上述结果表明，IL-36 介导的人肺成纤维细胞和支气管上皮细胞中 IL-6 和 CXCL8 的产生可能参与肺部炎症，特别是由细菌或病毒感染引起的炎症。
