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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Matrix metalloproteinases-2, -8, and -9 and TIMP-2 in tracheal aspirates from preterm infants with respiratory distress.
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Matrix metalloproteinases-2, -8, and -9 and TIMP-2 in tracheal aspirates from preterm infants with respiratory distress.

机译：呼吸窘迫早产儿气管抽吸物中基质金属蛋白酶2，-8和-9以及TIMP-2。

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OBJECTIVES: Matrix metalloproteinases (MMPs) are a family endoproteinases that act in degradation of extracellular matrix and basement membranes. The development of bronchopulmonary dysplasia (BPD) is characterized by early pulmonary inflammation, increased microvascular permeability, and subsequently by disordered repair. The aims of our study were to characterize the presence and molecular weight forms of MMP-2, -8, and -9 and their specific inhibitor, tissue inhibitor of metalloproteinases (TIMP)-2, in lungs of preterm infants during the early postnatal period and to determine whether levels of these MMPs and TIMP-2 in tracheal aspirate fluid (TAF) are associated with acute or chronic lung morbidity of the preterm infant. METHODS: TAF samples were collected from 16 intubated preterm infants (gestational age 27.0 +/- 2.0 weeks; birth weight 875 +/- 246 g) during their first 5 postnatal days. The presence and molecular weight forms of MMPs and TIMP-2 were identified by Western immunoblotting, and their levels were evaluated by densitometric scanning. RESULTS: MMP-8 in TAF was higher in infants who needed treatment with surfactant (25.4 +/- 6.3 vs 10.6 +/- 1.5 arbitrary unit/secretory component of immunoglobulin A [AU/SC]) and in whom BPD developed (N = 6; 27.6 +/- 5.2 vs 15.1 +/- 5.0 AU/SC). TIMP-2 levels were lower in infants with initial arterial to alveolar oxygen tension ratios <0.22 (2.7 +/- 1.1 vs 16.8 +/- 7.4 AU/SC) and in infants needing mechanical ventilation for >1 week (5.2 +/- 2.1 vs 22.8 +/- 11.7 AU/SC). CONCLUSIONS: In preterm infants, an imbalance between pulmonary MMP-8 and TIMP-2 participates in the acute inflammatory process in respiratory distress syndrome and may contribute to the development of chronic lung injury.
机译：目的：基质金属蛋白酶（MMPs）是一种家族内蛋白酶，可降解细胞外基质和基底膜。支气管肺发育不良（BPD）的发展特征是早期肺部炎症，微血管通透性增加以及随后的修复失调。我们研究的目的是鉴定早产儿肺中MMP-2，-8和-9及其特异性抑制剂金属蛋白酶组织抑制剂（TIMP）-2的存在和分子量形式并确定气管吸出液（TAF）中这些MMP和TIMP-2的水平是否与早产儿的急性或慢性肺部疾病相关。方法：从出生后前5天的16例插管早产儿（胎龄27.0 +/- 2.0周;出生体重875 +/- 246 g）中收集TAF样品。通过Western免疫印迹法鉴定MMP和TIMP-2的存在和分子量形式，并通过光密度扫描评估其水平。结果：需要用表面活性剂治疗的婴儿中TAF中的MMP-8较高（25.4 +/- 6.3对10.6 +/- 1.5免疫球蛋白A [AU / SC]的任意单位/分泌成分）并且BPD发生（N = 6; 27.6 +/- 5.2与15.1 +/- 5.0 AU / SC）。初始动脉与肺泡氧张力比<0.22（2.7 +/- 1.1与16.8 +/- 7.4 AU / SC）的婴儿和需要机械通气> 1周的婴儿（5.2 +/- 2.1），TIMP-2水平较低vs 22.8 +/- 11.7 AU / SC）。结论：在早产儿中，肺MMP-8和TIMP-2之间的失衡参与呼吸窘迫综合征的急性炎症过程，并可能导致慢性肺损伤的发展。

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