Robin M, Dong P, Hermans C, Bernard A, Bersten A D, Doyle I R
Industrial Toxicology and Occupational Medicine Unit, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium.
Eur Respir J. 2002 Nov;20(5):1152-61. doi: 10.1183/09031936.02.02042001.
Since the 16-kDa bronchiolar Clara cell protein (CC16) and the alveolar surfactant-associated proteins (SP)-A and -B leak into the circulation when parenchymal health is disturbed, the aim of this study was to determine whether their serum levels could serve as early peripheral markers of tobacco smoke-induced epithelial injury. Sixty-nine (51 yrs (32-54) median (25-75th percentile)) nonsmokers and 54 (42 yrs (31-53)) asymptomatic smokers were enrolled in the study. Serum levels of SP-A did not differ between subjects (270 (208-389) versus 259 (168-392) microg x L(-1)), however, CC16 levels decreased (10.6 (8.7-14.6) versus 7.6 (6.0-11.2) microg x L(-1)) and SP-B levels increased (2,529 (2,091-2,943) versus 3,053 (2,613-4,188) microg x L(-1)) in the smokers. When tobacco smoke exposure, serum creatinine (renal index), age and sex were used as independent variables, CC16 was negatively influenced by cumulative smoking and positively influenced by age. SP-A and -B were negatively influenced by creatinine and positively influenced by cumulative smoking. Serum SP-B was inversely correlated with forced expiratory volume in one second/vital capacity, suggesting an association between obstructive disease and parenchymal lung health. The authors suggest that serum surfactant-associated proteins-A and -B reflect increased alveolocapillary leakage whereas Clara cell secretory protein 16 reflects tobacco smoke-induced Clara cell toxicity. Their evaluation may allow the effects of tobacco smoke on different levels of the respiratory tract, cellular toxicity and epithelial leakage to be distinguished.
由于当实质健康受到干扰时,16 kDa细支气管 Clara 细胞蛋白(CC16)以及肺泡表面活性物质相关蛋白(SP)-A和-B会漏入循环系统,因此本研究的目的是确定它们的血清水平是否可作为烟草烟雾诱导的上皮损伤的早期外周标志物。69名(年龄中位数51岁(25-75百分位数为32-54岁))非吸烟者和54名(年龄42岁(25-75百分位数为31-53岁))无症状吸烟者参与了本研究。受试者之间的SP-A血清水平无差异(分别为270(208-389)与259(168-392)μg·L⁻¹),然而,吸烟者的CC16水平降低(分别为10.6(8.7-14.6)与7.6(6.0-11.2)μg·L⁻¹),SP-B水平升高(分别为2529(2091-2943)与3053(2613-4188)μg·L⁻¹)。当将烟草烟雾暴露、血清肌酐(肾脏指标)、年龄和性别作为自变量时,CC16受到累积吸烟的负面影响,并受到年龄的正面影响。SP-A和SP-B受到肌酐的负面影响,并受到累积吸烟的正面影响。血清SP-B与一秒用力呼气量/肺活量呈负相关,提示阻塞性疾病与肺实质健康之间存在关联。作者认为,血清表面活性物质相关蛋白-A和-B反映了肺泡毛细血管渗漏增加,而 Clara 细胞分泌蛋白16反映了烟草烟雾诱导的 Clara 细胞毒性。对它们的评估可能有助于区分烟草烟雾对呼吸道不同水平、细胞毒性和上皮渗漏的影响。