Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pleural fluid from an early, active phase of BCG-induced pleurisy was compared with fluid from late, healing phase, characterized by fibrinous adhesions. Exudates were tested for proteolytic activity on chromogenic peptide substrates designed for plasmin, tissue plasminogen activator, factor Xa, thrombin and plasma kallikrein. Considerable activity of active-phase pleural fluid was found on all of these substrates, and significantly lower values in the healing phase. Most exudates from both stages had very low fibrinogen concentration. Fibrinopeptide A, fibrinolytic products and antiplasmin were found in all exudates. Little or no fibrinolytic effect of pleural fluid was demonstrable on plasminogen free fibrin plates, despite the high activities on the low molecular weight substrates. Occurrence of alpha 2-macroglobulin-enzyme complexes is suggested as an explanation. The experimental results indicate that protease of the fibrinolytic and coagulation systems are active in the chronic inflammation of pleurisy, with higher levels of activity in active pleurisy phase.
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PMID:Fibrinolytic and coagulation mechanisms in stages of inflammation: a study of BCG-induced pleural exudate in guinea pig. 622 6

The human pathogen Mycobacterium tuberculosis binds to a variety of host cell proteins, including those of the fibrinolytic system. These observations prompted us to study the expression of components of this system in an animal model of progressive pulmonary tuberculosis. Lung homogenates from BALB/c mice infected with M. tuberculosis H37Rv were analyzed to determine the expression and enzymatic activity of plasmin/plasminogen and tissue plasminogen activator, as well as the mRNA levels for plasminogen, tissue and urokinase plasminogen activators. Plasminogen was also detected in infected lungs with immunohistochemistry. The results show that the expression of molecules of the fibrinolytic system increased gradually over the course of the infection, peaking during the chronic phase of the disease. Furthermore, in vitro experiments showed that both plasminogen activators were specifically induced after the stimulation of spleen cells from BCG-immunized mice with M. tuberculosis proteins. Together, these results show that molecules of the fibrinolytic system are up-regulated in the chronic phase of experimental tuberculosis and suggest that the mycobacterium itself could play an important role in the overexpression of molecules of the fibrinolytic system, contributing to chronic inflammation in tuberculosis.
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PMID:The response of the fibrinolytic system to mycobacteria infection. 2288 83