scholarly journals Human lysosomal elastase. Catalytic and immunological properties

1976 ◽  
Vol 155 (2) ◽  
pp. 265-271 ◽  
Author(s):  
P M. Starkey ◽  
A J. Barrett
Keyword(s):  
Human Neutrophil ◽  
Serine Proteinase ◽  
Ph Optimum ◽  
Human Spleen ◽  
Pancreatic Elastase ◽  
Good Substrate ◽  
Endopeptidase Activity ◽  
Specific Antisera ◽  
Porcine Pancreatic Elastase ◽  
Effect Of Inhibitors

1. The elastase of human spleen was shown to exhibit endopeptidase activity against azo-casein and elastin. 2. Activity against several synthetic substrates was detected, and benzyloxycarbonyl-L-alanine 2-naphthyl ester was found to be a good substrate for routine use. 3. The enzyme showed a broad pH optimum in the range of 8.2-9.2 against azo-casein and the synthetic substrate. 4. The effect of inhibitors on the spleen elastase showed it to be a serine proteinase with a specificity similar to that of porcine pancreatic elastase. 5. Specific antisera were raised against the enzyme, and it was shown to be immunologically identical with the lysosomal elastase of human neutrophil leucocytes.

Defenses of the Hamster Lung against Human Neutrophil and Porcine Pancreatic Elastase

Respiration ◽  
1988 ◽  
Vol 54 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Phillip J. Stone ◽  
Edgar C. Lucey ◽  
James D. Calore ◽  
Mary P. McMahon ◽  
Gordon L. Snider ◽  
...  
Keyword(s):  
Human Neutrophil ◽  
Pancreatic Elastase ◽  
Porcine Pancreatic Elastase

Inhaled porcine pancreatic elastase causes bronchoconstriction via a bradykinin-mediated mechanism

2000 ◽  
Vol 89 (4) ◽  
pp. 1397-1402 ◽  
Author(s):  
M. Scuri ◽  
R. Forteza ◽  
I. Lauredo ◽  
J. R. Sabater ◽  
Y. Botvinnikova ◽  
...  
Keyword(s):  
Neutrophil Elastase ◽  
Human Neutrophil ◽  
Inflammatory Diseases ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Human Neutrophil Elastase ◽  
Elastase Inhibitor ◽  
Pancreatic Elastase ◽  
Asthmatic Patients ◽  
Porcine Pancreatic Elastase

Neutrophil elastase has been linked to inflammatory lung diseases such as chronic obstructive pulmonary disease, adult respiratory distress syndrome, emphysema, and cystic fibrosis. In guinea pigs, aerosol challenge with human neutrophil elastase causes bronchoconstriction, but the mechanism by which this occurs is not completely understood. Our laboratory previously showed that human neutrophil elastase releases tissue kallikrein (TK) from cultured tracheal gland cells. TK has been identified as the major kininogenase of the airway and cleaves both high- and low-molecular weight kininogen to yield lysyl-bradykinin. Because inhaled bradykinin causes bronchoconstriction and airway hyperresponsiveness in asthmatic patients and allergic sheep, we hypothesized that elastase-induced bronchoconstriction could be mediated by bradykinin. To test this hypothesis, we measured lung resistance (Rl) in sheep before and after inhalation of porcine pancreatic elastase (PPE) alone and after pretreatment with a bradykinin B2 antagonist (NPC-567), the specific human elastase inhibitor ICI 200,355, the histamine H1-antagonist diphenhydramine hydrochloride, the cysteinyl leukotriene 1 receptor antagonist montelukast, or the cyclooxygenase inhibitor indomethacin. Inhaled PPE (125–1,000 μg) caused a dose-dependent increase in Rl. Aerosol challenge with a single 500 μg dose of PPE increased Rlby 132 ± 8% over baseline. This response was blocked by pretreatment with NPC-567 and ICI-200,355 ( n = 6; P < 0.001), whereas treatment with dyphenhydramine hydrochloride, montelukast, or indomethacin failed to block the PPE-induced bronchoconstriction. Consistent with pharmacological data, TK activity in bronchial lavage fluid increased 134 ± 57% over baseline ( n = 5; P < 0.02). We conclude that, in sheep, PPE-induced bronchoconstriction is in part mediated by the generation of bradykinin. Our findings suggest that elastase-kinin interactions may contribute to changes in bronchial tone during inflammatory diseases of the airways.

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