Johnson R J, Couser W G, Alpers C E, Vissers M, Schulze M, Klebanoff S J
Department of Medicine, University of Washington, Seattle 98195.
J Exp Med. 1988 Sep 1;168(3):1169-74. doi: 10.1084/jem.168.3.1169.
We infused microgram quantities of active or inactive PMN elastase and cathepsin G into the renal arteries of rats. Both active and inactive elastase localized to the glomerular capillary wall equally, and in amounts that could be achieved physiologically in GN. However, elastase-perfused rats developed marked proteinuria (196 +/- 32 mg/24 h) compared with control rats receiving inactive elastase (19 +/- 2 mg/24 h, p less than 0.005). Similar results were seen with active and inactive cathepsin G. Neither elastase nor cathepsin G infusion was associated with histologic evidence of glomerular injury. We conclude that the PMN neutral serine proteinases elastase and cathepsin G can mediate marked changes in glomerular permeability in vivo due to their proteolytic activity, and thus, may contribute to the proteinuria observed in PMN-dependent models of GN.
我们将微克量的活性或非活性中性粒细胞弹性蛋白酶和组织蛋白酶G注入大鼠肾动脉。活性和非活性弹性蛋白酶均同等程度地定位于肾小球毛细血管壁，且其含量在肾小球肾炎（GN）的生理状态下可以达到。然而，与接受非活性弹性蛋白酶的对照大鼠（19±2mg/24h，p<0.005）相比，灌注弹性蛋白酶的大鼠出现明显的蛋白尿（196±32mg/24h）。活性和非活性组织蛋白酶G也观察到类似结果。注入弹性蛋白酶和组织蛋白酶G均未伴有肾小球损伤的组织学证据。我们得出结论，中性粒细胞中性丝氨酸蛋白酶弹性蛋白酶和组织蛋白酶G因其蛋白水解活性可在体内介导肾小球通透性的显著变化，因此，可能导致在依赖中性粒细胞的肾小球肾炎模型中观察到的蛋白尿。
