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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human neutrophil elastase and other neutrophil granule constituents are internalized by human alveolar macrophages in vitro via receptor-mediated endocytosis, and immunoreactive neutrophil elastase is detectable within alveolar macrophages freshly harvested from human smokers. To gain insight into the potential role of neutrophil elastase bound by alveolar macrophages in the pathogenesis of connective tissue proteolysis, we have chosen hypoxia as a model of macrophage injury and have studied its effect upon the fate of bound neutrophil elastase. We found (1) that in a 3-h incubation after brief exposure to neutrophil elastase, control alveolar macrophages partially degraded bound enzyme, but they also released intact, enzymatically active, elastase in small amounts; (2) that release of TCA-insoluble radiolabeled elastase and elastase activity was enhanced fivefold and twofold over control, respectively, by alveolar macrophage injury during a 3-h incubation in humidified nitrogen; (3) that enzymatic activity of bound neutrophil elastase was largely masked by human neutrophil elastase-inhibitory activity of macrophage cell extracts. The data suggest (1) that the fate of neutrophil elastase bound to alveolar macrophages may be modulated by the local tissue environment; (2) that noxious agents may cause proteolytic tissue injury in the vicinity of alveolar macrophages by enhancing release of bound neutrophil elastase; (3) that alveolar macrophages may participate in the pathogenesis of centrilobular pulmonary emphysema by serving as a vector for neutrophil elastase, even if elastase activity is not detectable in alveolar macrophage lysates.
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PMID:Hypoxic injury to human alveolar macrophages accelerates release of previously bound neutrophil elastase. Implications for lung connective tissue injury including pulmonary emphysema. 634 81

In collagen content of four emphysematous lungs as defined by radiological, physiological and anatomical tests were studied. They were compared to three control lungs and five lungs removed from patients with relapsing pneumothorax (PNO). Morphologically, emphysematous lungs were characterized by patchy disorganization of collagen fibers, involving microfibrillar areas or elastoid laminae. Elastic fibers were at times found in plugs. Such abnormalities were also present, but less frequently in the PNO group. Biochemically, emphysematous lungs showed an increase of soluble proteins removed by CaCl2 extraction, which were associated with a decrease in insoluble proteins in extracted by TCA. Total hydroxyproline, expressed as a fraction of deoxyribonucleic acid (DNA) content, was not modified, but an increase of dialyzable and undialyzable fraction was observed in MEM medium. The PNO group showed the same modifications in terms of mean values, but individual results were more scattered. Results of in vitro 14C-proline incorporation did not show any modification of collagen biosynthesis, except in 2 emphysematous lungs. The results indicate that the PNO group is nearer to the emphysematous group than the controls. This suggests that patients with relapsing PNO may develop emphysema but it has to be further substantiated. The results here presented indicate that soluble hydroxyproline is an index either of abnormal synthesis or of excessive collagenolysis.
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PMID:Biochemical and anatomical study of collagen and associated macromolecules in pulmonary panacinar emphysema and spontaneous pneumothorax. 738 18