Miyoshi N, Miyoshi S, Sugiyama K, Suzuki Y, Furuta H, Shinoda S
Infect Immun. 1987 Aug;55(8):1936-9. doi: 10.1128/iai.55.8.1936-1939.1987.
Vibrio vulnificus protease enhanced hypodermic vascular permeability when injected into the dorsal skin of a guinea pig. Enhancement of permeability was observed within 2 min, and the permeability-enhancing reaction terminated at about 10 min postinjection. The permeability-enhancing reaction was greatly augmented by simultaneous injection of a kininase II inhibitor, whereas the reaction was inhibited by soybean trypsin inhibitor, a well-known inhibitor of plasma kallikrein. Furthermore, in vitro activation of plasma prekallikrein to kallikrein by V. vulnificus protease was observed. These results indicate that V. vulnificus protease enhances vascular permeability through activation of the plasma kallikrein-kinin system which generates bradykinin, factor in edema formation.
创伤弧菌蛋白酶注入豚鼠背部皮肤后可增强皮下血管通透性。注射后2分钟内即可观察到通透性增强,且通透性增强反应在注射后约10分钟终止。同时注射激肽释放酶II抑制剂可极大增强通透性增强反应,而该反应则受到大豆胰蛋白酶抑制剂(一种众所周知的血浆激肽释放酶抑制剂)的抑制。此外,还观察到创伤弧菌蛋白酶在体外可将血浆前激肽释放酶激活为激肽释放酶。这些结果表明,创伤弧菌蛋白酶通过激活血浆激肽释放酶-激肽系统来增强血管通透性,该系统可产生缓激肽,而缓激肽是水肿形成的一个因素。