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Matrix metalloproteinases-2, -8, and -9 and TIMP-2 in tracheal aspirates from preterm infants with respiratory
K Cederqvist1, T Sorsa, T Tervahartiala
1Hospital for Children and Adolescents, Helsinki University Central Hospital, Finland. katariina.cederqvist@hus.fi
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.
Insights
Matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMP)-2 levels in tracheal aspirate fluid (TAF) are linked to lung injury in preterm infants. An imbalance of MMP-8 and TIMP-2 may contribute to bronchopulmonary dysplasia (BPD) development.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Biochemistry
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants characterized by inflammation and disordered repair.
- Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) play critical roles in tissue remodeling and inflammation.
Purpose of the Study:
- To investigate the presence and levels of MMP-2, MMP-8, MMP-9, and TIMP-2 in the lungs of preterm infants during early postnatal development.
- To determine the association between MMPs and TIMP-2 levels in tracheal aspirate fluid (TAF) and acute or chronic lung morbidity in preterm infants.
Main Methods:
- Tracheal aspirate fluid (TAF) samples were collected from 16 intubated preterm infants within the first 5 postnatal days.
- Western immunoblotting and densitometric scanning were used to identify and quantify MMPs and TIMP-2.
Main Results:
- MMP-8 levels were elevated in infants requiring surfactant treatment and those who developed BPD.
- TIMP-2 levels were lower in infants with poor oxygenation (arterial to alveolar oxygen tension ratio <0.22) and those requiring prolonged mechanical ventilation (>1 week).
Conclusions:
- Pulmonary MMP-8 and TIMP-2 levels are altered in preterm infants with respiratory distress syndrome.
- An imbalance between MMP-8 and TIMP-2 may contribute to the acute inflammatory process and the development of chronic lung injury, including BPD, in preterm infants.
