IL-36 induces cytokine IL-6 and chemokine CXCL8 expression in human lung tissue cells: Implications for pulmonary inflammatory responses
IL-36 induces cytokine IL-6 and chemokine CXCL8 expression in human lung tissue cells: Implications for pulmonary inflammatory responses
复制标题
IL-36 诱导人肺组织细胞中细胞因子 IL-6 和趋化因子 CXCL8 的表达：对肺部炎症反应的影响
DOI：
10.1016/j.cyto.2017.08.022
复制
发表时间：
2017-11-01
期刊：
影响因子：
3.8
通讯作者：
Cao, Ju
中科院分区：
文献类型：
--
作者：
Zhang, Juan;Yin, Yibing;Cao, Ju
IL-36α、IL-36β和IL-36γ是IL-1家族的细胞因子成员。尽管在肺部感染过程中观察到了IL-36在人肺组织中的表达，但目前尚不清楚IL-36在肺部炎症反应中是否直接作用于肺组织细胞。在本研究中，我们发现人肺成纤维细胞和支气管上皮细胞表达IL-36受体。相应地，IL-36α、IL-36β或IL-36γ上调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，促进人肺成纤维细胞和支气管上皮细胞释放IL-6和CXCL8。IL-36α、IL-36β或IL-36γ诱导的肺组织细胞产生IL-6和CXCL8受p38MAPK、ERK或Akt信号通路的调节。综上所述，上述结果提示IL-36介导的人肺成纤维细胞和支气管上皮细胞产生IL-6和CXCL8可能参与了肺部炎症，尤其是细菌或病毒感染引起的肺部炎症。
IL-36 alpha, IL-36 beta and IL-36 gamma 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-36 alpha, IL-36 beta or IL-36 gamma 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-36 alpha, IL-36 beta or IL-36 gamma 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.