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W2051635103 abstract "Studies of both emphysema and adult respiratory distress syndrome (ARDS) support the premise that lung injury is due to unregulated host defense mechanisms. A major mediator of host defense and injury is the neutrophil, which is relatively incapable of regulating its own function. Accordingly, defects in regulatory mechanisms allow neutrophils to damage the lungs. Emphysema serves as a prime example of this link between host defense and injury. Hereditary emphysema is caused by a deficiency in α1-antitrypsin (α1-AT), a protease inhibitor. The decreased levels of this enzyme in affected individuals result in inadequate protection against neutrophil elastase and other proteolytic enzymes, leading to lung damage. Patients with acquired emphysema, associated with cigarette smoking, have normal levels of α1-AT in their lungs. However, the α1-AT in these patients has a reduced ability to associate with and inhibit the action of neutrophil elastase. Thus, both types of emphysema involve an alteration in the balance between proteases and antiproteases. The lung damage observed in patients with ARDS also appears to involve neutrophils, but in this case elastase may not be the culprit. In these patients, neutrophil elastase appears to be inactivated by high levels of α1-AT, thus preventing excess protease action. It is hoped that a more complete understanding of the mechanisms involved in host defense and injury will enable the development of specific therapeutic interventions, such as the α1-AT replacement therapy that is being used to treat patients with hereditary emphysema." @default.
W2051635103 created "2016-06-24" @default.
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W2051635103 date "1992-06-01" @default.
W2051635103 modified "2023-10-18" @default.
W2051635103 title "Adverse effects of neutrophils on the lung" @default.
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W2051635103 doi "https://doi.org/10.1016/0002-9343(92)90604-a" @default.
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