Sobh M, Moustafa F, Hamid S, Ghoneim M
Urology and Nephrology Center, University of Mansoura, Egypt.
Nephrol Dial Transplant. 1996 Nov;11(11):2178-84. doi: 10.1093/oxfordjournals.ndt.a027134.
One hundred and twenty Syrian golden hamsters were infected with Schistosoma mansoni cercariae and 20 served as negative controls (group I). Of the S. mansoni-infected hamsters, 20 served as positive controls (group II) and 100 hamsters were treated for 12 weeks post-infection by loading with S. mansoni adult worm antigen. Animals were divided into groups according to the dose of adult worm antigen injected: group III (5-fold increase in circulating antigen concentration), group IV (10-fold increase), group V (20-fold increase), group VI (40-fold increase), and group VII (80-fold increase). Each of the groups was subdivided into four groups (sacrificed at 1, 2, 4 or 7 days after initiation of antigen loading or the corresponding time points in the case of the control groups). At sacrifice, blood and urine were obtained for laboratory assessment (serum creatinine, protein, albumin, cholesterol and urinary proteins). Kidney, liver and spleen tissue specimens were obtained for light, immunofluorescent and electron microscopic examinations. At sacrifice, significant proteinuria, hypoalbuminaemia and hypercholesterolaemia were observed in S. mansoni-infected hamsters when compared with negative control animals. Histopathologic assessment showed changes compatible with those previously reported, mainly immune complex glomerular deposits, mesangial proliferation and renal amyloid deposits. Significant laboratory improvement was observed in animals treated with antigen loading, especially those treated with 80-fold antigen excess and sacrificed at 7 days postinitiation of treatment. Histopathologic evaluation showed significantly less immune complex glomerular deposits, less mesangial hyperplasia, and less amyloid deposits in hamsters treated with antigen loading. It is concluded that induction of antigen excess by antigen loading induces biochemical and histopathologic regression of schistosomal-specific nephropathy in S. mansoni-infected Syrian golden hamsters.
120只叙利亚金黄地鼠感染曼氏血吸虫尾蚴,20只作为阴性对照(第一组)。在感染曼氏血吸虫的地鼠中,20只作为阳性对照(第二组),100只地鼠在感染后通过注射曼氏血吸虫成虫抗原进行为期12周的治疗。根据注射成虫抗原的剂量将动物分为几组:第三组(循环抗原浓度增加5倍)、第四组(增加10倍)、第五组(增加20倍)、第六组(增加40倍)和第七组(增加80倍)。每组再细分为四组(在抗原注射开始后1、2、4或7天处死,对照组为相应时间点)。处死时,采集血液和尿液进行实验室评估(血清肌酐、蛋白质、白蛋白、胆固醇和尿蛋白)。获取肾脏、肝脏和脾脏组织标本进行光镜、免疫荧光和电子显微镜检查。处死时,与阴性对照动物相比,感染曼氏血吸虫的地鼠出现明显的蛋白尿、低白蛋白血症和高胆固醇血症。组织病理学评估显示的变化与先前报道的相符,主要为免疫复合物肾小球沉积、系膜增生和肾淀粉样沉积。在接受抗原注射治疗的动物中观察到明显的实验室指标改善,尤其是那些接受80倍过量抗原注射并在治疗开始后7天处死的动物。组织病理学评估显示,接受抗原注射治疗的地鼠肾小球免疫复合物沉积明显减少,系膜增生减轻,淀粉样沉积减少。结论是,通过抗原注射诱导抗原过量可导致感染曼氏血吸虫的叙利亚金黄地鼠血吸虫特异性肾病的生化和组织病理学逆转。