Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling
Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling
复制标题
香烟和 IL-17A 通过激活 IL-17R/NF-κ B 信号协同诱导支气管上皮间质转化
DOI：
10.1186/s12890-020-1057-6
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发表时间：
2020-01-30
影响因子：
3.1
通讯作者：
Chu, Shuyuan
中科院分区：
文献类型：
--
作者：
Ma, Libing;Jiang, Ming;Chu, Shuyuan
背景IL-17 A直接诱导肺泡上皮细胞的上皮-间质转化（EMT）。结论：本品能协同香烟烟雾提取物（CSE）促进支气管上皮细胞增殖。本研究旨在探讨IL-17 A和CSE对支气管上皮细胞EMT的直接影响。方法分离C57 BL/6小鼠支气管上皮细胞，与CSE或/和IL-17 A共培养。免疫荧光染色检测细胞中E-cadherin和Vimentin的表达。免疫组化法检测IL-17 R的表达。使用蛋白质印迹法评估NF-κ B表达。当BAY 11-7821抑制NF-κ B时，测量NF-κ B、E-钙粘蛋白和波形蛋白的表达。结果CSE + IL-17 A组支气管上皮细胞E-cadherin蛋白表达最低，CSE组次之。CSE + IL-17 A组Vimentin蛋白表达最高，CSE组次之。同样，IL-17 R和NF-κ B B表达在CSE + IL-17 A组中最高，其次是CSE组和IL-17 A组。NF-κ B抑制剂可抑制E-钙粘蛋白和Vimentin的表达。结论香烟和IL-17 A可通过激活IL-17 R/NF-κ B信号通路协同诱导支气管上皮细胞发生EMT。我们的研究结果有助于更好地了解气道EMT和呼吸系统疾病的发病机制，这涉及IL-17 A和吸烟。这些将为肺部疾病的免疫治疗提供新的途径。
Background IL-17A directly induces epithelial-mesenchymal transition (EMT) in alveolar epithelial cells. It could coordinate with cigarette smoke extract (CSE) to promote proliferation of bronchial epithelial cells. In this study, we aim to explore the direct effect of IL-17A and CSE on EMT in bronchial epithelial cells. Methods Bronchial epithelial cells were isolated from C57BL/6 mice, and cocultured with CSE or/and IL-17A. E-cadherin and Vimentin expressions in cells were detected using immunofluorescence staining. IL-17R expression was detected using immunohistochemistry staining. NF-kappa B expression was assessed using western blotting. When NF-kappa B was inhibited by BAY 11-7821, expressions of NF-kappa B, E-cadherin and Vimentin were measured. Results The protein expression of E-cadherin in bronchial epithelial cells was lowest in CSE + IL-17A group, followed by CSE group. In contrast, the protein expression of Vimentin was highest in CSE + IL-17A group, followed by CSE group. Similarly, IL-17R and NF-kappa B expressions were highest in CSE + IL-17A group, followed by CSE group and IL-17A group. NF-kappa B inhibitor could inhibit the expressions of E-cadherin and Vimentin. Conclusions Cigarette and IL-17A could synergistically induce EMT in bronchial epithelial cells through activating IL17R/NF-kappa B signaling. Our findings contribute to a better understanding in airway EMT and pathogenesis of respiratory diseases, which are involved IL-17A and cigarette smoking. Those will provide novel avenues in the immunotherapy of lung diseases.