Changes in collagen turnover in early acute respiratory distress syndrome
Changes in collagen turnover in early acute respiratory distress syndrome
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DOI：
10.1164/ajrccm.160.6.9811084
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发表时间：
1999-12-01
影响因子：
24.7
通讯作者：
Millar, AB
中科院分区：
文献类型：
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作者：
Armstrong, L;Thickett, DR;Millar, AB
肺纤维化是公认的急性呼吸窘迫综合征（ARDS）的特征。使用支气管肺泡损伤（BAL）、液体的免疫测定，我们研究了患有ARDS、急性肺损伤（ALI）的患者、具有ARDS危险因素的受试者（处于危险中）和健康/通气对照受试者中I型前胶原（PICP）和I/II型胶原降解产物（COL 2 -3/4C（短）新表位）的合成。通过ELISA测量PICP作为I型前胶原合成的标志物。通过抑制ELISA测量COL 2 -3/4C（短）新表位作为I/II型胶原的胶原酶降解的标志物。最初在通气后48小时内（第1天）进行BAL，随后在第4天进行。上皮细胞衬液（ELF）的稀释通过血浆尿素比较进行校正。与处于危险中的受试者相比，在第1天，在来自ARDS和ALI受试者的ELF中观察到PICP水平增加（中值分别为124.9和95.0ng/ml对38.0ng/ml，p < 0.0005）。相比之下，与处于风险中的受试者相比，患有ARDS的受试者中COL 2 -3/4C（短）新表位的水平显著降低（13.22 ng/ml对32.33 ng/ml，p < 0.0005）。这转化为在患有ARDS的受试者中PICP：COL 2 -3/4C（短）比率大大增加（p < 0.0001）。在第1天和第4天之间，患有ARDS的受试者中的PICP水平显著下降（n = 15，p < 0.05）。线性回归分析显示PICP与ARDS受试者的肺损伤评分之间存在显著相关性（p = 0.01）。我们的数据表明，早期转移的平衡之间的I型胶原蛋白的合成和降解的胶原酶。I型胶原蛋白的增加有利于基质沉积和ARDS患者肺纤维化的发展。
Pulmonary fibrosis is a well-recognized feature of acute respiratory distress syndrome (ARDS). Using immunoassays of bronchoalveolar ravage (BAL), fluid we investigated the synthesis of type I procollagen (PICP) and type I/II collagen degradation products (COL2-3/4C(short) neoepitope) in patients with ARDS, acute lung injury (ALI), subjects with risk factors for ARDS (At Risk), and healthy/ventilated control subjects. PICP was measured by ELISA as a marker of type I procollagen synthesis. COL2-3/4C(short) neoepitope was measured by an inhibition ELISA as a marker of collagenase degradation of type I/II collagen. BAL was performed initially within 48 h of ventilation (Day 1) and then subsequently on Day 4. Dilution of epithelial lining fluid (ELF) was corrected for by plasma urea comparison. increased PICP levels were observed in the ELF from ARDS and ALI subjects on Day 1 compared with subjects At Risk (median values, 124.9 and 95.0 ng/ml versus 38.0 ng/ml, respectively, p < 0.0005). By contrast, the levels of COL2-3/4C(short) neoepitope were significantly reduced in the subjects with ARDS versus the At Risk subjects (13.22 ng/ml versus 32.33 ng/ml, p < 0.0005). This translated into a greatly increased PICP:COL2-3/4C(short) ratio in the subjects with ARDS (p < 0.0001). There was a significant decline in the PICP level in the subjects with ARDS between Days 1 and 4 (n = 15, p < 0.05). Linear regression analysis showed a significant association between PICP and lung injury score in the subjects with ARDS (p = 0.01). Our data suggests an early shift in balance between type I collagen synthesis and degradation by collagenase. The resultant increase in type I collagen would favor matrix deposition and the development of pulmonary fibrosis in the lungs of subjects with ARDS.