Human plasma kallikrein releases neutrophil elastase during blood coagulation

Détails

ID Serval
serval:BIB_11C286FE8742
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Human plasma kallikrein releases neutrophil elastase during blood coagulation
Périodique
Journal of Clinical Investigation
Auteur(s)
Wachtfogel  Y. T., Kucich  U., James  H. L., Scott  C. F., Schapira  M., Zimmerman  M., Cohen  A. B., Colman  R. W.
ISSN
0021-9738 (Print)
Statut éditorial
Publié
Date de publication
11/1983
Volume
72
Numéro
5
Pages
1672-7
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Nov
Résumé
Elastase is released from human neutrophils during the early events of blood coagulation. Human plasma kallikrein has been shown to stimulate neutrophil chemotaxis, aggregation, and oxygen consumption. Therefore, the ability of kallikrein to release neutrophil elastase was investigated. Neutrophils were isolated by dextran sedimentation, and elastase release was measured by both an enzyme-linked immunosorbent assay, and an enzymatic assay using t-butoxy-carbonyl-Ala-Ala-Pro-Val-amino methyl coumarin as the substrate. Kallikrein, 0.1-1.0 U/ml, (0.045-0.45 microM), was incubated with neutrophils that were preincubated with cytochalasin B (5 micrograms/ml). The release of elastase was found to be proportional to the kallikrein concentration. Kallikrein released a maximum of 34% of the total elastase content, as measured by solubilizing the neutrophils in the nonionic detergent Triton X-100. A series of experiments was carried out to determine if kallikrein was a major enzyme involved in neutrophil elastase release during blood coagulation. When 10 million neutrophils were incubated in 1 ml of normal plasma in the presence of 30 mM CaCl2 for 90 min, 2.75 micrograms of elastase was released. In contrast, neutrophils incubated in prekallikrein-deficient or Factor XII-deficient plasma released less than half of the elastase, as compared with normal plasma. The addition of purified prekallikrein to prekallikrein-deficient plasma restored neutrophil elastase release to normal levels. Moreover, release of elastase was enhanced in plasma deficient in C1-inhibitor, the major plasma inhibitor of kallikrein. This release was not dependent upon further steps in the coagulation pathway, or on C5a, since levels of elastase, released in Factor XI- or C5-deficient plasma, were similar to that in normal plasma, and an antibody to C5 failed to inhibit elastase release. These data suggest that kallikrein may be a major enzyme responsible for the release of elastase during blood coagulation.
Mots-clé
*Blood Coagulation Complement C1 Inactivator Proteins/deficiency Cytochalasin B/pharmacology Dose-Response Relationship, Drug Factor XII Deficiency/blood Humans Kallikreins/*pharmacology Kinetics Neutrophils/drug effects/*enzymology Pancreatic Elastase/*blood
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 16:27
Dernière modification de la notice
20/08/2019 13:39
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