Elevated levels of bronchoalveolar lavage vitronectin in hypersensitivity pneumonitis.
Elevated levels of bronchoalveolar lavage vitronectin in hypersensitivity pneumonitis.
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过敏性肺炎中支气管肺泡灌洗玻连蛋白水平升高。
DOI：
10.1164/ajrccm/147.2.332
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Rennard,SI
中科院分区：
文献类型：
--
作者：
Teschler,H;Pohl,WR;Thompson,AB;Konietzko,N;Mosher,DF;Costabel,U;Rennard,SI
玻连蛋白是一种存在于血浆和细胞外基质中的粘附糖蛋白。过敏性肺炎（HP）的特点是肺部炎症和细胞外基质损伤。已发现 HP 患者下呼吸道中的纤连蛋白升高，也许反映了这一点。玻连蛋白与纤连蛋白一样，与细胞外基质成分和细胞结合，并可能介导组织重塑。因此，研究了 HP 患者的支气管肺泡灌洗 (SAL) 液中玻连蛋白是否可能增加。通过酶联免疫吸附测定，对 16 名 HP 患者和 9 名健康对照受试者的 SAL 液中的玻连蛋白和纤连蛋白进行了测量。与对照组（58.4±11.1 ng/ml，p<0.001）相比，HP组的玻连蛋白显着增加（658.4±121.8ng/ml），并且与纤连蛋白呈正相关。最后一次接触抗原是在 SAL 前 4 天或更少天的患者比最后一次接触是在 SAL 前 5 天或更多天的患者具有统计学上显着更高的 SAL 玻连蛋白和纤连蛋白。血清玻连蛋白水平没有差异。 HP 中灌洗液玻连蛋白和纤连蛋白水平与 SAL 细胞谱之间没有显着关系。本研究证实，玻连蛋白与纤连蛋白一样，是下呼吸道的正常成分，并表明玻连蛋白在 HP 患者的下呼吸道中升高，可能在该疾病的组织重塑和纤维化中发挥作用。过敏性肺炎 (HP) 的特点是肺实质中炎症细胞积聚，并可能进展为纤维化 (1-3)。据推测，纤维化过程涉及肺泡巨噬细胞释放特定介质，包括介导细胞募集粘附和生长的糖蛋白纤连蛋白，并被认为有助于损伤后的直接修复 (4-6)。玻连蛋白与纤连蛋白一样，是一种糖蛋白，是细胞外基质的组成部分。在体外，玻连蛋白介导细胞粘附和扩散 (7)。凭借这些功能，玻连蛋白还可以帮助指导组织炎症后的修复过程。支气管肺泡灌洗 (SAL) 是从下呼吸道获取细胞和液体的一种有价值的方法 (8)。该方法允许对炎症细胞特征进行表征，并对可能调节多种疾病中炎症和修复的细胞机制的介质进行定量 (2, 9-12)。例如，纤连蛋白水平升高与肺纤维化有关 (6, 9)。此外，间质性肺疾病患者的肺泡巨噬细胞已被
Vitronectin is an adhesive glycoprotein that is present in plasma and the extracellular matrix. Hypersensitivity pneumonitis (HP) is characterized by pulmonary inflammation and damage to the extracellular matrix. Perhaps reflecting this, fibronectin has been found to be elevated in the lower respiratory tract of subjects with HP. Vitronectin, like fibronectin, binds to both extracellular matrix components and cells and may mediate tissue remodeling. Thus, it was investigated whether vitronectin might be increased in bronchoalveolar lavage (SAL) fluid of patients with HP. Vitronectin and, for comparison, fibronectin were measured in SAL fluid from 16 patients with HP and nine healthy control subjects by enzyme-linked immunosorbent assay. Vitronectin was significantly increased in the HP group (658.4±121.8ng/ml) compared with the controls (58.4±11.1 ng/ml, p< 0.001) and was found to be positively correlated with fibronectin. Patients whose last antigenic exposure was 4 or fewer days before the SAL had statistically significantly higher SAL vitronectin and fibronectin than did patients whose last exposure was 5 or more days before the SAL. The serum vitronectin levels did not differ. There was no significant relationship between the lavage fluid vitronectin and fibronectin levels and the SAL cell profile in HP. This study confirms that vitronectin, like fibronectin, is a normal constituent of the lower respiratory tract, and demonstrates that vitronectin is elevated in the lower respiratory tract of patients with HP and may playa role in tissue remodeling and fibrosis in this disease.Hypersensitivity pneumonitis (HP) is characterized byaccumulation of inflammatory cells in the lung parenchyma and may progress to fibrosis (1-3). The fibrotic process has been postulated to involve alveolar macrophage release of specific mediators, including the glycoprotein fibronectin that mediates cellular recruitment adhesion and growth and is thought to help direct repair following injury (4-6). Vitronectin, like fibronectin, is a glycoprotein, which is a component of the extracellular matrix. In vitro, vitronectin mediates cell adhesion and spreading (7). Sy virtue of these functions, vitronectin may also help direct the repair processes that follow tissue inflammation. Sronchoalveolar lavage (SAL) is a valuable method of obtaining cells and fluid from the lower respiratory tract (8). This method has permitted the characterization of the inflammatory cell profiles and the quantification of mediators that may modulate cellular mechanisms of inflammation and repair in a variety of diseases (2, 9-12). Increased levels of fibronectin, for example, have been associated with pulmonary fibrosis (6, 9). Moreover, alveolar macrophages of patients with interstitial lung disease have been