title: Consequences of unbalanced protease in the lung: protease involvement in destruction and local defense mechanisms of the lung.
abstract: Complex mechanisms regulate sequestration, retention and migration of neutrophils in the lung. Neutrophils can migrate into the lung without producing significant damage under some circumstances, whereas at other times great structural alteration occurs. A potential explanation lies in the phenomenon of priming, a state of altered responsivity of neutrophils. A wide variety of molecules are able to induce this higher degree of responsiveness including PAF, TNF, GM-CSF, and IL-1. Enhanced cellular responses include secretion, adhesion and synthetic function. Unprimed neutrophils can migrate through lung tissues, secreting but little of their contents, in the context of "normal" inflammatory response. On the other hand neutrophils primed before the emigration phase, injury to the tissue they are migrating through would be likely by virtue of releasing toxic mediators. One of these mediators is neutrophil elastase, a potent protease. It is the purpose of this review to highlight the duality function of neutrophils as (i) one of the bodies highly effective host defense weapons and (ii) mediator of destruction and host defense impairment in the lung by releasing mediators such as neutrophil elastase.
authors: Department of Paediatrics, University of Berne, Inselspital, Switzerland.
authors: P
authors: P
authors: Birrer
mesh_terms: D001997:Bronchopulmonary Dysplasia / Q000201:enzymology / Q000276:immunology; D003550:Cystic Fibrosis / Q000201:enzymology / Q000276:immunology; D006801:Humans; D007231:Infant, Newborn; D008168:Lung / Q000201:enzymology* / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D010447:Peptide Hydrolases / Q000502:physiology*; D012128:Respiratory Distress Syndrome / Q000201:enzymology / Q000276:immunology; D019896:alpha 1-Antitrypsin Deficiency
chemical_list: D010447:Peptide Hydrolases