Description
Title: Chronic Lung Disease and Neutrophil Elastase
Abstract: In the airways of patients with cystic fibrosis (CF), chronic obstructive pulmonary disease, non-CF bronchiectasis, and bronchopulmonary dysplasia, neutrophils release neutrophil elastase (NE), a significant inflammatory protease. NE promotes leukocyte transmigration to the site of infection and is necessary for the removal of Gram-negative bacteria, but when released into the airway milieu in chronic inflammatory airway diseases, it also activates inflammation. Airway remodeling brought on by NE exposure includes increased mucin expression and secretion as well as reduced ciliary motility. By encouraging cellular apoptosis and senescence, NE prevents epithelial repair. It also activates inflammation indirectly by causing extracellular trap release and exosome release, which intensify protease activity and inflammation in the airway. By breaking down opsonins and opsonin receptors, destroying innate immune proteins like lactoferrin, and preventing macrophage phagocytosis, NE prevents the innate immune system from functioning. It’s significant to note that NE-directed therapies have not yet proven successful in preventing the pathologic consequences of NE exposure, but brand-new treatments are being created that have both direct antiprotease activity and multifunctional anti-inflammatory properties.
Keywords: neutrophil elastase; cystic fibrosis; chronic obstructive pulmonary disease; bronchiectasis; bronchopulmonary dysplasia; antiprotease; glycosaminoglycan
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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