Department of Respiratory and Critical Care Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Guangdong Provincial Geriatrics Institute, First Clinical Medicine Institute of South China University of Technology, Guangzhou, Guangdong, China.
Department of Respiratory and Critical Care Medicine, Yan'an Hospital of Kunming, Kunming, China.
Can Respir J. 2020 Feb 10;2020:1350872. doi: 10.1155/2020/1350872. eCollection 2020.
. Some studies have found that cilia were shorter in COPD smokers than in nonsmokers or healthy smokers. However, the structural abnormalities of cilia and the cause of such abnormalities in COPD patients still remain unknown. Tumor necrosis factor alpha receptor 3 interacting protein 1 (MIP-T3) may play an important role in the progress of ciliary protein transporting.
This study aimed at exploring the dominated structural abnormalities of cilia and the involvement of MIP-T3 in the pathogenesis of cilia of COPD patients.
Patients who accepted pulmonary lobectomy were divided into 3 groups: the chronic obstructive pulmonary disease (COPD) smoker group, the healthy smoker group, and the nonsmoker group, according to smoking history and pulmonary function. The ultrastructure of cilia and the percentage of abnormal cilia were analyzed using a transmission electron microscope. Real-time PCR, immunohistochemical staining, and western blotting in bronchial epithelium were used to determine MIP-T3 mRNA and protein expression. The relationship between the percentage of abnormal cilia and lung function and MIP-T3 protein expression was analyzed.
Patients in the COPD smoker group had increased percentage of abnormal cilia comparing to both the healthy smoker group and the nonsmoker group (both values <0.05). MIP-T3 expression was significantly declined in the COPD smoker group ( values <0.05). MIP-T3 expression was significantly declined in the COPD smoker group ( values <0.05). MIP-T3 expression was significantly declined in the COPD smoker group ( values <0.05). MIP-T3 expression was significantly declined in the COPD smoker group (.
Our results suggested that the abnormal ciliary ultrastructure, which was common in COPD patients, might be due to MIP-T3 downregulation.
本研究旨在探讨 COPD 患者纤毛的主要结构异常及 MIP-T3 在纤毛发病机制中的作用。
根据吸烟史和肺功能，将接受肺叶切除术的患者分为慢性阻塞性肺疾病（COPD）吸烟者组、健康吸烟者组和非吸烟者组。使用透射电子显微镜分析纤毛的超微结构和异常纤毛的比例。采用实时 PCR、免疫组织化学染色和支气管上皮细胞的 Western blot 检测 MIP-T3 mRNA 和蛋白表达。分析异常纤毛的比例与肺功能和 MIP-T3 蛋白表达的关系。
与健康吸烟者组和非吸烟者组相比，COPD 吸烟者组异常纤毛的比例明显增加（均 P<0.05）。COPD 吸烟者组 MIP-T3 表达明显下降（均 P<0.05）。
我们的结果表明，COPD 患者常见的纤毛超微结构异常可能与 MIP-T3 下调有关。
