Thaiss F, Batsford S, Mihatsch M J, Heitz P U, Bitter-Suermann D, Vogt A
Lab Invest. 1986 Jun;54(6):624-35.
The pathogenetic roles of complement, polymorphonuclear granulocytes, and monocytes were studied in a model of in situ immune complex glomerulonephritis employing a cationized antigen. Left kidneys of Wistar rats were perfused with 40 micrograms of cationized human IgG (isoelectric point greater than or equal to 9.5) followed by intravenous injection of rabbit anti-human IgG 1 hour later. This resulted in prominent subepithelial deposit formation in the perfused kidney accompanied by massive proteinuria. Groups examined were: (a) no additional treatment, (b) C3 depleted (cobra venom factor, (c) granulocyte depleted (specific antiserum), (d) monocyte depleted (specific antiserum), and (e) granulocyte depleted and monocyte depleted. The quantity of radiolabeled cationized antigen deposited in the left kidney was not affected by any of the treatment schedules. Proteinuria was abolished in all mediator depleted groups (b to e) for 5 to 7 days, thereafter rising to levels seen in the nondepleted group (a). This late onset of proteinuria is noteworthy since the deposits are then located subepithelially and may be less accessible to circulating mediators. C3 depletion, despite inhibition of proteinuria, did not prevent the intraglomerular accumulation of granulocytes and monocytes thereby suggesting that attraction and activation of these cells may occur independently. Apparently all three mediators are required for full expression of the lesion, a finding not paralleled in other experimental models of glomerulonephritis. The relevance of very low levels of inflammatory cell infiltration for provoking glomerular injury was clearly demonstrated.
在采用阳离子化抗原的原位免疫复合物肾小球肾炎模型中，研究了补体、多形核粒细胞和单核细胞的致病作用。用40微克阳离子化人IgG（等电点大于或等于9.5）灌注Wistar大鼠的左肾，1小时后静脉注射兔抗人IgG。这导致灌注肾中出现明显的上皮下沉积物形成，并伴有大量蛋白尿。所检查的组包括：（a）不进行额外处理，（b）C3耗竭（眼镜蛇毒因子），（c）粒细胞耗竭（特异性抗血清），（d）单核细胞耗竭（特异性抗血清），以及（e）粒细胞和单核细胞均耗竭。沉积在左肾中的放射性标记阳离子化抗原的量不受任何处理方案的影响。所有介质耗竭组（b至e）的蛋白尿在5至7天内消失，此后升至未耗竭组（a）所见的水平。这种蛋白尿的延迟出现值得注意，因为此时沉积物位于上皮下，循环介质可能较难接近。尽管C3耗竭抑制了蛋白尿，但并未阻止粒细胞和单核细胞在肾小球内的积聚，从而表明这些细胞的吸引和激活可能独立发生。显然，所有三种介质都是病变充分表达所必需的，这一发现与其他肾小球肾炎实验模型不同。炎症细胞浸润水平极低对引发肾小球损伤的相关性得到了明确证明。
