Cook H T, Smith J, Salmon J A, Cattell V
Department of Pathology, St. Mary's Hospital Medical School, London, England.
Am J Pathol. 1989 Feb;134(2):431-7.
Macrophage infiltration is important in the pathogenesis of acute proliferative glomerulonephritis (gn). The state of activation of macrophages during gn may be central to their role in injury. To study this, a method for extracting macrophages from nephritic glomeruli in active in situ gn was developed. MHC Class II (Ia) antigen expression, superoxide (O2-) generation, and eicosanoid synthesis were compared with thioglycollate elicited peritoneal macrophages (TEM). At the height of inflammation there were 407 +/- 83 macrophages/glomerulus. Compared with TEM, Ia expression, and in vitro production of O2- were enhanced. Synthesis of prostaglandin E2 was greatly reduced (day 6 gn, 62 +/- 10 ng/mg; TEM 663 +/- 128 ng/mg cell protein). Thromboxane synthesis was relatively conserved (day 6 gn, 109 +/- 28 ng/mg; TEM 201 +/- 53 ng/mg). Leukotriene B4 (LTB4) was undetectable (day 6 gn, less than 13 ng/mg; TEM 119 +/- 56 ng/mg). This large influx of activated macrophages in glomeruli may be fundamental to pathogenesis of glomerular inflammation.
巨噬细胞浸润在急性增生性肾小球肾炎（GN）的发病机制中起重要作用。GN期间巨噬细胞的激活状态可能是其损伤作用的核心。为研究此问题，开发了一种从活动性原位GN的肾炎性肾小球中提取巨噬细胞的方法。将MHC II类（Ia）抗原表达、超氧化物（O2-）生成和类花生酸合成与巯基乙酸诱导的腹腔巨噬细胞（TEM）进行比较。在炎症高峰期，每个肾小球有407±83个巨噬细胞。与TEM相比，Ia表达和O2-的体外生成增强。前列腺素E2的合成大大减少（GN第6天，62±10 ng/mg；TEM 663±128 ng/mg细胞蛋白）。血栓素合成相对保守（GN第6天，109±28 ng/mg；TEM 201±53 ng/mg）。白三烯B4（LTB4）检测不到（GN第6天，小于13 ng/mg；TEM 119±56 ng/mg）。肾小球中大量活化巨噬细胞的涌入可能是肾小球炎症发病机制的基础。
