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1 Newborn Medicine, Children's Hospital, Boston, Massachusetts, United States
2 CBR Institute for Biomedical Research and Department of Pediatrics, Boston, Massachusetts, United States
3 Department of Pediatrics, Harvard Medical School, CBR Institute for Biomedical Research, Boston, Massachusetts, United States
4 Newborn Medicine, Children's Hospital, Boston, Massachusetts, United States; Newborn Medicine, Brigham and Women's Hospital, Boston, Massachusetts, United States
* To whom correspondence should be addressed. E-mail: sule.cataltepe{at}childrens.harvard.edu.
Bronchopulmonary dysplasia (BPD) continues to be a major cause of morbidity in premature infants. An imbalance between neutrophil elastase and its inhibitors has been implicated in BPD. SERPINB1 is an inhibitor of neutrophil proteases, including neutrophil elastase (NE) and cathepsin G (cat G). Recent studies suggest that SERPINB1 could provide protection in the airways by regulating excess protease activity associated with inflammatory lung disorders. In this study, we determined the distribution and ontogeny of SERPINB1 in the baboon lung, and characterized the expression of SERPINB1 in baboon models of BPD. SERPINB1 expression was detected in the conducting airway and glandular epithelial cells in addition to neutrophils, macrophages, and mast cells. SERPINB1 mRNA and protein expression increased with advancing gestational age and in the new BPD model. In contrast, SERPINB1 expression levels were decreased in the old BPD model. Furthermore, SERPINB1 was detected as a high molecular mass (HMM) complex in lung tissue and bronchoalveolar lavage fluid samples from the BPD group. Analysis of the HMM complex by co-immunoprecipitation showed that these complexes were formed between SERPINB1 and NE or cat G. HPLC ion trap mass spectrometry (LC-MS/MS) verified the presence of SERPINB1 in HMM complexes. Finally, NE activity level was compared between new and old baboon models of BPD and was found to be significantly lower in new BPD. Thus, SERPINB1 up-regulation in new BPD may be protective by contributing to the regulation of neutrophil proteases, NE and cat G.
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