Lin Xue-Feng, Zhang Lei, Shi Shu-Yuan, Fan Yi-Chu, Wu Zhen-Lin, Zhang Xun, Sun Da-Qiang
Department of Nursing, Tianjin Medical College, Tianjin 300222, P.R. China.
Graduate School of Tianjin Medical University, Tianjin 300070, P.R. China.
Mol Med Rep. 2016 Feb;13(2):1667-72. doi: 10.3892/mmr.2015.4702. Epub 2015 Dec 22.
Pulmonary surfactant protein A (SP-A) has been associated with host defense in the lung, and contributes to the pathogenesis of chronic obstructive pulmonary disease (COPD). The present study aimed to determine a non‑invasive method of measurement of SP‑A, and further examine the expression levels of SP‑A in patients with COPD. SP‑A was detected in the exhaled breath condensate (EBC) obtained from patients with COPD and from non‑COPD subjects. The individuals recruited for the present study comprised 60 subjects with and without COPD, who underwent lobectomy for a solitary peripheral lung nodule. EBC was collected using a condenser, and an enzyme‑linked immunosorbent assay (ELISA) was used to measure the levels of SP‑A. Tissue samples were obtained during lobectomy through resection of the adjacent lung tissues, located >5 cm from the nodule. Western blot analysis and immunohistochemistry were used to measure SP‑A and SP‑A‑positive type II pneumocytes. The results demonstrated that SP‑A was detectable in the EBC of all subjects. The results of the ELISA and western blotting demonstrated that the expression levels of SP‑A were significantly decreased in patients with COPD, compared with the non‑COPD subjects. The reduction of SP‑A‑positive type II pneumocytes was associated with the expression levels of SP‑A. Decreased expression levels of SP‑A in EBC were associated with a higher degree of airway limitation. These results suggested that the measurement of SP‑A levels in the EBC may serve as a method for monitoring airway obstruction in patients with COPD. Further investigations are required in order to examine these observations further and to elucidate the underlying mechanisms.
肺表面活性物质蛋白A(SP-A)与肺部的宿主防御相关,并在慢性阻塞性肺疾病(COPD)的发病机制中起作用。本研究旨在确定一种测量SP-A的非侵入性方法,并进一步检测COPD患者中SP-A的表达水平。在从COPD患者和非COPD受试者获得的呼出气冷凝液(EBC)中检测SP-A。本研究招募的个体包括60名有或无COPD的受试者,他们因孤立性周围型肺结节接受了肺叶切除术。使用冷凝器收集EBC,并采用酶联免疫吸附测定(ELISA)测量SP-A水平。在肺叶切除术中通过切除距结节>5 cm的相邻肺组织获取组织样本。采用蛋白质免疫印迹分析和免疫组织化学检测SP-A和SP-A阳性的II型肺细胞。结果表明,所有受试者的EBC中均可检测到SP-A。ELISA和蛋白质免疫印迹结果显示,与非COPD受试者相比,COPD患者中SP-A的表达水平显著降低。SP-A阳性II型肺细胞的减少与SP-A的表达水平相关。EBC中SP-A表达水平降低与气道受限程度较高相关。这些结果表明,测量EBC中SP-A水平可作为监测COPD患者气道阻塞的一种方法。为了进一步研究这些观察结果并阐明潜在机制,还需要进行进一步的研究。