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bronchopulmonary dysplasia/protease
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Imbalance between cysteine proteases and inhibitors in a baboon model of bronchopulmonary dysplasia.
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BACKGROUND
Bronchopulmonary dysplasia (BPD) continues to be a major morbidity in preterm infants. The lung pathology in BPD is characterized by impaired alveolar and capillary development. An imbalance between proteases and protease inhibitors in association with changes in lung elastic fibers has
Role of serine proteases in the regulation of interleukin-877 during the development of bronchopulmonary dysplasia in preterm ventilated infants.
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BACKGROUND
The chemokine interleukin-8 is implicated in the development of bronchopulmonary dysplasia in preterm infants. The 77-amino acid isoform of interleukin-8 (interleukin-877) is a less potent chemoattractant than other shorter isoforms. Although interleukin-877 is abundant in the preterm
Secretory leukocyte protease inhibitor and lung inflammation in developing bronchopulmonary dysplasia.
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OBJECTIVE
To investigate secretory leukocyte protease inhibitor (SLPI) concentrations in tracheal lavage fluids of neonates with an endotracheal tube in place during the first month of life, and to evaluate the relationship of SLPI to neutrophil counts and elastase activity in patients in whom
Tryptase immunoreactive mast cell hyperplasia in bronchopulmonary dysplasia.
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Bronchopulmonary dysplasia (BPD), the most common cause of chronic lung disease in prematurely born infants, is histologically characterized by various degrees of airway and alveolar septal fibrosis. Tryptase, a serine protease specific to mast cells, has been shown to have potent fibroblast
Protease inhibitors in bronchoalveolar lavage fluid from neonates with special reference to secretory leukocyte protease inhibitor.
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An imbalance of proteolytic enzymes and protease inhibitors may contribute to the development of bronchopulmonary dysplasia. We studied secretory leukocyte protease inhibitor (not previously addressed), and alpha 1-antitrypsin, alpha 1-antichymotrypsin, alpha 2-macroglobulin and elastase. Albumin
Elastase inhibitory activity of airway α1-antitrypsin is protected by treatment with a catalytic antioxidant in a baboon model of severe bronchopulmonary dysplasia.
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Recent studies in animal models of bronchopulmonary dysplasia (BPD) suggest that antioxidant treatments may be beneficial for the disease. However, the mechanisms by which these drugs improve the course of BPD are not completely known. Alpha1-antitrypsin (α1-AT) is one of the major serine protease
[Pathogenesis of bronchopulmonary dysplasia].
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Bronchopulmonary dysplasia of preterm infants has a multifactorial etiology. Pulmonary immaturity, oxygen toxicity, formation of oxygen radicals and mechanical lung trauma as well as additional factors (pulmonary hyperhydration, infection a.o.) may contribute to pulmonary damage. A pulmonary
Bronchopulmonary dysplasia and emphysema: in search of common therapeutic targets.
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Bronchopulmonary dysplasia of the premature neonate and emphysema of the adult lung are common diseases that are characterized by increased airspace size and respiratory insufficiency and that presently lack efficient treatment. Although the former leads to impaired alveolar development and the
Oxygen exposure in the newborn guinea pig lung lavage cell populations, chemotactic and elastase response: a possible relationship to neonatal bronchopulmonary dysplasia.
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Neonatal guinea pig pulmonary response to oxygen exposure FiO2 greater than 0.9 resulted in an increase in total cell number in lung lavage. Alveolar macrophages initially increased within 48 h of exposure. Polymorphonuclear leukocytes and macrophages exceeded age-matched neonatal control values by
SERPINB1 upregulation is associated with in vivo complex formation with neutrophil elastase and cathepsin G in a baboon model of bronchopulmonary dysplasia.
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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. Serine protease inhibitor (SERPIN)B1 is an inhibitor of neutrophil proteases, including neutrophil elastase (NE)
Bronchopulmonary dysplasia and inflammatory biomarkers in the premature neonate.
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Bronchopulmonary dysplasia (BPD) is the most common, serious sequela of premature birth. Inflammation is a major contributor to the pathogenesis of BPD. Often initiated by a pulmonary fetal inflammatory response, lung inflammation is exacerbated by mechanical ventilation and exposure to supplemental
Budesonide and Poractant Alfa prevent bronchopulmonary dysplasia via triggering SIRT1 signaling pathway.
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Chorioamnionitis, postnatal factors and proinflammatory response in the pathogenetic sequence of bronchopulmonary dysplasia.
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Pulmonary inflammation has a central role in the multifactorial and complex pathogenesis of bronchopulmonary dysplasia. Pre- and postnatal factors such as chorioamnionitis, oxygen toxicity, mechanical ventilation and postnatal infections can induce and perpetuate an injurious and complex
Pulmonary inflammation and bronchopulmonary dysplasia.
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Various pre- and postnatal risk factors, which act additively or synergistically induce an injurious inflammatory response in the airways and the pulmonary interstitium of preterm infants with bronchopulmonary dysplasia. This inflammatory response is characterized by an accumulation of neutrophils
Inflammation and bronchopulmonary dysplasia: a continuing story.
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Increasing evidence indicates that bronchopulmonary dysplasia (BPD) results, at least in part, from an imbalance between pro-inflammatory and anti-inflammatory mechanisms, with a persistent imbalance that favours pro-inflammatory mechanisms. The inflammatory response is characterised by an
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