Cigarette smoke affects IL-17A, IL-17F and IL-17 receptor expression in the lung tissue: Ex vivo and in vitro studies
Cigarette smoke affects IL-17A, IL-17F and IL-17 receptor expression in the lung tissue: Ex vivo and in vitro studies
复制标题
DOI：
10.1016/j.cyto.2015.07.013
复制
发表时间：
2015-12-01
期刊：
影响因子：
3.8
通讯作者：
Profita, Mirella
中科院分区：
文献类型：
--
作者：
Montalbano, Angela Marina;Riccobono, Loredana;Profita, Mirella
吸烟是慢性阻塞性肺疾病（COPD）的危险因素。Th-17细胞因子参与COPD的发病机制。我们旨在评估吸烟对COPD患者气道中IL-17A、IL-17F和IL-17R表达的影响。通过免疫组织化学方法评估COPD患者（n = 15）和健康受试者（HC） （n = 10）手术标本中IL-17A、IL-17F和IL-17R的上皮和上皮下免疫反应性。在体外，用香烟烟雾提取物（CSE）（0%、2.5%、5%、10%）刺激人上皮细胞系16HBE、A549和正常供体PBMC，流式细胞术检测IL-17A、IL-17F和IL-17R的表达。进一步观察rhIL-17A和CSE刺激对16HBE和A549细胞增殖和凋亡的影响。在中央和远端气道中，慢阻肺上皮和上皮下IL-17A对IL-17A、IL-17F和IL-17R的免疫反应性明显高于HC。在远端气道中，慢阻肺上皮下IL-17F的免疫反应性高于HC。IL-17A免疫反应性与COPD患者中央和远端气道上皮IL-17R和总包年呈正相关。在体外，CSE刺激显著增加16HBE（2.5%）和A549（5%）中IL-17F和IL-17R，而PBMC中IL-17A和IL-17F（10%）。IL-17A和CSE刺激，而不是单独使用CSE或rhIL-17A，显著增加了16HBE的增殖和A549的凋亡。吸烟增加COPD患者肺组织Th17免疫，促进气道上皮细胞增殖和凋亡的机制。(C) 2015 Elsevier Ltd.版权所有。
Cigarette smoke is a risk factor for Chronic Obstructive Pulmonary Disease (COPD). Th-17 cytokines are involved in the pathogenesis of COPD. We aimed to evaluate the role of cigarette smoke on the expression of IL-17A, IL-17F and IL-17R in airways of COPD patients. Epithelial and subepithelial immunoreactivity for IL-17A, IL-17F and IL-17R was assessed in surgical specimens from COPD patients (n = 15) and from healthy subjects (HC) (n = 10) by immunohistochemistry. In vitro, human epithelial cell line 16HBE and A549 as well as PBMC from normal donors were stimulated with cigarette smoke extract (CSE) (0%, 2.5%, 5%, 10%) to evaluate the IL-17A, IL-17F and IL-17R expression by flow cytometry. Furthermore, rhIL-17A and CSE stimulation was evaluated on proliferation and apoptosis in 16HBE and in A549. In central and distal airways immunoreactivity for IL-17A, IL-17F and IL-17R significantly increased in the epithelium and IL-17A in the subepithelium from COPD than in HC. In distal airway, immunoreactivity for IL-17F increased in the subepithelium of COPD than in HC. IL-17A immunoreactivity positively correlate with IL-17R and total pack years in the epithelium from central and distal airways of COPD patients. In vitro, CSE stimulation significantly increased IL-17F and IL-17R in 16HBE (2.5%) and A549 (5%) while IL-17A and IL-17F in PBMC (10%). IL-17A and CSE stimulation, rather than CSE or rhIL-17A alone, significantly increased proliferation in 16HBE and apoptosis in A549. Cigarette smoke increases Th17 immunity in lung tissue of COPD patients, promoting the mechanism of proliferation and apoptosis in airway epithelial cells. (C) 2015 Elsevier Ltd. All rights reserved.