Siegel J, Osmand A P, Wilson M F, Gewurz H
J Exp Med. 1975 Sep 1;142(3):709-21. doi: 10.1084/jem.142.3.709.
Cationic homopolymers of poly-L-lysine were found to activate complement (C) via C-reactive protein (CRP) and deplete C3 and C5 as well as early-acting C components. Maximum C consumption was obtained with polymers of 2,000-8,000 daltons; polymers of 1,700, 11,000, and 23,000 daltons were intermediate in reactivity, while L-lysine, lysyl-L-lysine, tetra-L-lysine, and polymers of 70,000-400,000 daltons lacked significant C-consuming activity. Naturally occurring polycations which consumed C in the presence of CRP included myelin basic proteins, cationic proteins of rabbit leukocytes, and both lysine- and arginine-rich histones; poly-L-arginine polymers of 17,000 but not 65,000 daltons also were C-consuming. Polycations without such reactivity included poly-L-orithine (5,000 and 165,000 daltons), egg white and human lysozymes, and Polybrene. The polycations which failed to induce C consumption via CRP, inhibited its consumption by both active polycations and by C-polysaccharide (CPS). The relative inhibitory capacity of phosphorylcholine and polycations in CPS- and polycations-CRP systems was consistent with the concept that phosphate esters and polycations react at the same or an overlapping combining site. The ability of certain polycations to activate C via CRP increases the potential for initiation of host reactions via C. The capacity of other polycations to inhibit C activation via CRP introduces a potential for physiologic or pharmacologic manipulation. These considerations would seem to expand the potential role of CRP in the initiation and modulation of the inflammatory response.
研究发现,聚-L-赖氨酸阳离子均聚物可通过C反应蛋白(CRP)激活补体(C),并消耗C3和C5以及早期作用的补体成分。2000 - 8000道尔顿的聚合物可使补体消耗达到最大值;1700、11000和23000道尔顿的聚合物反应性中等,而L-赖氨酸、赖氨酰-L-赖氨酸、四-L-赖氨酸以及70000 - 400000道尔顿的聚合物则缺乏显著的补体消耗活性。在CRP存在下消耗补体的天然存在的聚阳离子包括髓鞘碱性蛋白、兔白细胞的阳离子蛋白以及富含赖氨酸和精氨酸的组蛋白;17000道尔顿而非65000道尔顿的聚-L-精氨酸聚合物也具有补体消耗活性。不具有这种反应性的聚阳离子包括聚-L-鸟氨酸(5000和165000道尔顿)、蛋清和人溶菌酶以及聚凝胺。未能通过CRP诱导补体消耗的聚阳离子会抑制活性聚阳离子和C-多糖(CPS)引起的补体消耗。磷酸胆碱和聚阳离子在CPS - 和聚阳离子 - CRP系统中的相对抑制能力与磷酸酯和聚阳离子在相同或重叠结合位点发生反应的概念一致。某些聚阳离子通过CRP激活补体的能力增加了通过补体引发宿主反应的可能性。其他聚阳离子通过CRP抑制补体激活的能力为生理或药理操作带来了可能性。这些考虑因素似乎扩展了CRP在炎症反应启动和调节中的潜在作用。