Clava cell specific protein (CC16) expression after acute lung inflammation induced by intratracheal lipopolysaccharide administration
Clava cell specific protein (CC16) expression after acute lung inflammation induced by intratracheal lipopolysaccharide administration
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DOI：
10.1164/ajrccm.161.5.9812157
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发表时间：
2000-05-01
影响因子：
24.7
通讯作者：
Bernard, A
中科院分区：
文献类型：
--
作者：
Arsalane, K;Broeckaert, F;Bernard, A
Clara细胞分泌蛋白（CC 16、CC 10或CCSP）是Clara细胞的主要分泌蛋白，具有多种生物学特性，提示其可能对肺内炎症过程起保护作用。本研究旨在观察脂多糖（LPS）诱导的大鼠急性肺损伤（ALI）时肺、支气管肺泡灌洗液（BALF）和血清中CC 16浓度的变化。将这些变化与Clara细胞密度、肺中CC 16 mRNA水平和BALF中经典炎症指数进行比较。以10、100或200 μ g/100 g体重的剂量注射LPS，通过BALF中细胞和白蛋白的流入增加来估计，LPS诱导急性肺部炎症。这种炎症反应与BALF和肺匀浆中CC 16浓度以及肺中CC 16 mRNA水平的显著降低相关。在最高剂量的LPS下，细支气管上皮中的CC 16阳性细胞密度也降低。相比之下，在血清中，CC 16的浓度升高是由于气道通透性增加。腹腔注射地塞米松（2 mg/kg）可明显抑制BALF中白细胞内流和白蛋白升高。然而，地塞米松未能阻止气道对CC 16的渗透性增加，这表明在炎症期间，不同的机制调节蛋白质穿过肺泡-毛细血管屏障的渗漏，这取决于蛋白质的通过方向和/或大小。我们的研究结果表明，在LPS诱导的急性肺部炎症过程中，CC 16的分泌和合成显着减少。
Clara cell secretory protein (CC16, CC10, or CCSP), the major secretory protein of the Clara cell, presents several biologic properties, suggesting that it may play a protective role against intrapulmonary inflammatory processes. The aim of the present study was to investigate the changes of CC16 concentrations in the lung, bronchoalveolar lavage fluid (BALF), and serum of rats with acute lung injury induced by lipopolysaccharide (LPS). These changes were compared with Clara cell density, CC16 mRNA level in the lung and classic indices of inflammation in BALF. Injected at doses of 10,100, or 200 mu g/100 g body weight, LPS induced an acute lung inflammation as estimated by an increased influx of cells and albumin in the BALF. This inflammatory response was associated with a marked reduction of CC16 concentrations in BALF and lung homogenate as well as of the CC16 mRNA levels in the lung. At the highest dose of LPS, the CC16-positive cell density in the bronchiolar epithelium was also decreased. In serum, by contrast, the concentration of CC16 was elevated as a consequence of increased airway permeability. Pretreating rats intraperitoneally with dexamethasone (2 mg/kg) significantly towered the leukocyte influx and attenuated the albumin increase in BALF. Dexamethasone, however, failed to prevent the increased airway permeability to CC16, suggesting that during inflammation different mechanisms regulate the leakage of proteins across the alveolo-capillary barrier depending on the direction of passage and/or the size of the protein. Our results show a marked decrease of the secretion and synthesis of CC16 during LPS-induced acute lung inflammation.