Camussi G, Tetta C, Meroni M, Torri-Tarelli L, Roffinello C, Alberton A, Deregibus C, Sessa A
Lab Invest. 1986 Jul;55(1):56-62.
The localization of cationic proteins (CP) derived from platelets and from polymorphonuclear neutrophils (PMN) in glomeruli of 42 rabbits injected i.v. with a large amount of bovine serum albumin, was investigated in sequential biopsies by immunofluorescence, using goat-anti-platelet CP and anti-PMN CP sera. Platelet CP deposits became detectable within 7 to 8 days after the i.v. injection of bovine serum albumin, before or coincident with the onset of proteinuria. The intensity and the extent of linear and segmental deposits of platelet CP along the glomerular capillary walls reached a peak at day 9 to 10, when proteinuria was maximal. The anti PMN-CP serum stained the cytoplasm of the few PMN present in glomeruli and only occasionally at day 11 and 12 identified focal deposits of PMN-CP along the glomerular capillary walls. The kinetic study of glomerular immune deposits showed that the first appearance of immune deposits in antigen excess was preceded by, or was concomitant, with the detection of platelet-CP in glomeruli. In the later stages of serum sickness, the immune deposits showed a progressive increase in rabbit IgG and C3. The glomerular polyanions were studied by light microscopy, using the colloidal iron technique, and by electron microscopy using polyethyleneimine as a cationic probe. The glomerular deposits of platelet-CP were associated with a reduction of colloidal iron staining, which was maximal 9 to 11 days after the i.v. injection of bovine serum albumin. At day 15, colloidal iron staining was almost completely restored. At day 9 in rabbits with acute serum sickness the anionic sites of glomerular basement membrane evidenced by polyethyleneimine, were segmentally decreased, mainly in the lamina rara interna. In rabbit studied at day 15 the anionic sites were decreased only at the base of the subepithelial electron dense deposits (humps). These results suggest that in rabbits with experimentally-induced acute serum sickness, during the early stages of glomerular immune deposit formation endogenous CP, released mainly from platelets, bind to glomerular capillary walls and possibly contribute to the neutralization of glomerular polyanions.
通过免疫荧光法，使用山羊抗血小板阳离子蛋白（CP）血清和抗多形核中性粒细胞（PMN）CP血清，对42只静脉注射大量牛血清白蛋白的兔子肾小球中源自血小板和多形核中性粒细胞的阳离子蛋白（CP）定位进行了连续活检研究。静脉注射牛血清白蛋白后7至8天内，在蛋白尿出现之前或同时，可检测到血小板CP沉积。沿着肾小球毛细血管壁的血小板CP线性和节段性沉积的强度和范围在第9至10天达到峰值，此时蛋白尿最为严重。抗PMN-CP血清使肾小球中存在的少数PMN的细胞质染色，仅在第11天和12天偶尔识别出沿着肾小球毛细血管壁的PMN-CP局灶性沉积。肾小球免疫沉积物的动力学研究表明，在抗原过量情况下免疫沉积物的首次出现之前或同时，在肾小球中检测到血小板-CP。在血清病后期，免疫沉积物显示兔IgG和C3逐渐增加。使用胶体铁技术通过光学显微镜以及使用聚乙烯亚胺作为阳离子探针通过电子显微镜研究肾小球多阴离子。血小板-CP的肾小球沉积物与胶体铁染色减少有关，静脉注射牛血清白蛋白后9至11天减少最为明显。在第15天，胶体铁染色几乎完全恢复。在患有急性血清病的兔子中，第9天通过聚乙烯亚胺证明的肾小球基底膜阴离子位点节段性减少，主要在内疏松层。在第15天研究的兔子中，阴离子位点仅在 subepithelial电子致密沉积物（驼峰）底部减少。这些结果表明，在实验性诱导的急性血清病兔子中，在肾小球免疫沉积物形成的早期阶段，主要从血小板释放的内源性CP与肾小球毛细血管壁结合，并可能有助于中和肾小球多阴离子。
