Serum Clara cell protein (CC16), a marker of the integrity of the air-blood barrier in sarcoidosis
Serum Clara cell protein (CC16), a marker of the integrity of the air-blood barrier in sarcoidosis
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DOI：
10.1183/09031936.01.99102601
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发表时间：
2001-09-01
影响因子：
24.3
通讯作者：
Bernard, A
中科院分区：
文献类型：
--
作者：
Hermans, C;Petrek, M;Bernard, A
为了检验结节病与肺上皮分泌蛋白的血管内渗漏相关的假设，结节病患者血清中CC 16的发生和决定因素，CC 16是一种小尺寸且易于扩散的肺特异性蛋白，由细支气管Clara细胞分泌，通过敏感的乳胶免疫测定法测定了117例确诊结节病患者和117例年龄匹配的健康受试者血清中的CC 16，性别和吸烟状况。采用逐步回归分析确定血清CC 16变化的肺外变量。然后将这些变化与支气管肺泡灌洗液（BALF）中的生化和细胞参数以及支气管或肺活检样本中CC 16免疫染色细胞的数量进行比较。结节病患者血清中的CC 16浓度与其匹配的对照组相比显著升高（25.9 ± 16.2 μ g/ml对13.9 ± 5.2 μ g/ml）。L（-1））。在无明显肾损害的非吸烟患者中，血清CC 16随胸片和计算机断层扫描改变的严重程度而增加，平均为50- 100%，当存在实质受累时更高。然而，结节病患者BALF中CC 16水平正常，肺活检样品中CC 16免疫阳性细胞数量不变，表明结节病肺中CC 16分泌增加是非常不可能的，结节病中CC 16的升高是由于该蛋白质通过空气的血管内渗漏增加所致，本研究表明，血清中的CC 16可能提供一种有用的工具，以非侵入性地评估与结节病相关的空气-血液屏障的蛋白质的损伤和增加的渗透性。
To test the hypothesis that sarcoidosis is associated with an intravascular leakage of lung epithelium secretory proteins, the occurrence and determinants in serum of sarcoid patients of CC16, a small size and readily diffusible lung-specific protein of 16 kDa secreted by bronchiolar Clara cells, was investigated.CC16 was measured by a sensitive latex immunoassay in the serum of 117 patients with established sarcoidosis and of 117 healthy subjects matched for age, sex and smoking status. Stepwise regression analysis was used to identify extrapulmonary variables of CC16 changes in serum. These changes were then compared with biochemical and cellular parameters in bronchoalveolar lavage fluid (BALF) as well as with the number of CC16 immunostaining cells on bronchial or pulmonary biopsy samples.CC16 concentration in serum of sarcoid patients was significantly increased, compared to their matched controls (25.9 +/- 16.2 versus 13.9 +/-5.2 mug(.)L(-1)). In nonsmoking patients without significant renal impairment, CC16 in serum increased with the severity of the chest radiograph and computed tomography changes, and was on average 50-100%, higher when parenchymal involvement was present. Sarcoid patients had, however, normal levels of CC16 in BALF and an unchanged number of CC16-immunopositive cells in lung biopsy samples, suggesting that an increased secretion of CC16 in the sarcoid lung is very unlikely, and that the elevation of CC16 in sarcoidosis results from an increased intravascular leakage of the protein across the air-blood barrier.The present study suggests that CC16 in serum might provide a useful tool to noninvasively evaluate the damage and increased permeability to proteins of the air-blood barrier associated with sarcoidosis.