Requirements for leukocyte adhesion molecules in nephrotoxic nephritis.
Requirements for leukocyte adhesion molecules in nephrotoxic nephritis.
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肾毒性肾炎对白细胞粘附分子的要求。
DOI：
10.1172/jci116237
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Ward,PA
中科院分区：
文献类型：
--
作者：
Mulligan,MS;Johnson,KJ;Todd3rd,RF;Issekutz,TB;Miyasaka,M;Tamatani,T;Smith,CW;Anderson,DC;Ward,PA
白细胞粘附分子以及细胞因子的要求已被确定在大鼠急性肾毒性肾炎模型。蛋白尿（24 h）和肾小球中性粒细胞蓄积（6 h）用作终点。对于中性粒细胞在肾小球中的完全积累以及蛋白尿的完全发展，已经证明需要TNF α（而不是IL-1）、CD 11b（而不是CD 11 a）、非常晚产生的-4（CD 49 d/CD 29）和细胞间粘附分子-1，而不是内皮白细胞粘附分子-1（E-选择素）。通过免疫组化方法，肾小球基底膜抗体的输注诱导肾小球细胞间粘附分子-1，内皮白细胞粘附分子-1，血管粘附分子-1的上调。用抗TNF α或可溶性重组人TNF受体-1治疗大鼠可阻断这种表达。肾动脉灌注TNF α可诱导肾小球表达所有三种内皮粘附分子，但灌注IL-1 β则无此作用。这些数据表明，在中性粒细胞和补体依赖性抗肾小球基底膜诱导的大鼠急性肾炎，有选择性的要求细胞因子，β 1和β 2整合素，和内皮细胞粘附分子。这些要求与在其他血管床中发现的要求形成对比，在其他血管床中，补体和嗜中性粒细胞诱导的血管损伤是由免疫复合物的沉积诱导的。
Requirements for leukocyte adhesion molecules as well as cytokines have been determined in the rat model of acute nephrotoxic nephritis. Proteinuria (at 24 h) and neutrophil accumulation in renal glomeruli (at 6 h) have been used as the endpoints. For full accumulation in glomeruli of neutrophils as well as full development of proteinuria, requirements have been demonstrated for TNF alpha, (but not IL-1), CD11b (but not CD11a), very late arising-4 (CD49d/CD29), and intercellular adhesion molecule-1 but not endothelial leukocyte adhesion molecule-1 (E-selectin). By immunohistochemical approaches, infusion of antibody to glomerular basement membrane induced glomerular upregulation of intercellular adhesion molecule-1, endothelial leukocyte adhesion molecule-1, and vascular adhesion molecule-1. Treatment of rats with anti-TNF alpha or soluble recombinant human TNF receptor-1 blocked this expression. Renal arterial infusion of TNF alpha induced glomerular expression of all three endothelial adhesion molecules, but infusion of IL-1 beta did not. These data suggest that, in neutrophil and complement-dependent anti-glomerular basement membrane-induced acute nephritis in rats, there are selective requirements for cytokines, beta 1 and beta 2 integrins, and endothelial adhesion molecules. These requirements contrast with those found in other vascular beds in which complement and neutrophil-induced vascular injury has been induced by deposition of immune complexes.Images