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Clara cell secretory protein oxidation and expression in premature infants who develop bronchopulmonary dysplasia
P L Ramsay1, F J DeMayo, S E Hegemier
1Department of Pediatrics, Baylor College of Medicine, Houston Texas, USA.
Insights
Infants who develop bronchopulmonary dysplasia (BPD) show increased oxidation and lower levels of Clara cell secretory protein (CCSP) in early respiratory samples. This suggests CCSP
Area of Science:
- Neonatal Medicine
- Pulmonology
- Biochemistry
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants.
- Early lung inflammation is implicated in BPD development.
- Inflammation is linked to protein and lipid oxidation in respiratory fluids.
Purpose of the Study:
- To test if specific protein oxidation and expression changes in tracheal aspirates predict BPD development in preterm infants.
- To investigate the role of Clara cell secretory protein (CCSP) in BPD pathogenesis.
Main Methods:
- Tracheal aspirate fluids collected on Days 1, 3, and 6 from infants born at < 29 weeks gestation.
- Proteins incubated with 2,4-dinitrophenylhydrazine (DNPH) and separated by electrophoresis.
- DNPH reactivity assessed by immunoblotting to detect protein oxidation.
Main Results:
- Increased DNPH reactivity (oxidation) of CCSP was observed in infants who later developed BPD.
- Lower levels of immunoreactive CCSP were found on Day 1 in infants who developed BPD.
- CCSP oxidation and reduced expression correlate with subsequent BPD diagnosis.
Conclusions:
- Altered CCSP expression and increased oxidation in early respiratory samples may indicate BPD risk.
- CCSP function is crucial for maintaining lung fluid balance in neonates.
- Targeting CCSP expression and function could be a therapeutic strategy for preventing BPD.
Abstract:
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that affects prematurely born infants and appears to evolve in part from early inflammatory responses in the lung. The inflammatory responses have been associated with protein and lipid oxidation in tracheal aspirate fluids. The present study was designed to test the hypothesis that in the first week of life specific oxidations and/ or altered expressions of proteins would be observed in tracheal aspirate fluids in infants who would subsequently develop BPD. We obtained tracheal aspirate fluids on Days of life 1, 3, and 6 from infants born at < or = 29 wk gestation, incubated the fluids with 2,4-dinitrophenylhyrazine (DNPH), separated the proteins electrophoretically, and assessed DNPH reactivity by immunonblots. DNPH reactivity of a protein that was identified as Clara cell secretory protein (CCSP) was observed more consistently in tracheal aspirate fluids from infants who later developed BPD than from infants who did not develop BPD. Tracheal aspirate fluid levels of immunoreactive CCSP were also lower on Day of life 1 in infants who developed BPD than in those who did not develop BPD. Increased CCSP oxidation and decreased immunoreactive CCSP expression in infants who subsequently developed BPD suggest that Clara cell function and CCSP expression may be critical for normal bronchoalveolar fluid homeostasis and that maintaining CCSP expression and function may be useful goals for targeted therapies for inhibition of the development of BPD.