Coutinho M, Zahedi K, Whitehead A S, Davis A E
Division of Nephrology, Children's Hospital Research Foundation, Cincinnati, OH.
Eur J Immunogenet. 1992 Dec;19(6):419-23. doi: 10.1111/j.1744-313x.1992.tb00085.x.
The aim of the study was to determine whether C5 deficiency in the mouse is associated with resistance to the development of secondary amyloidosis. Chronic inflammation was induced in the F2 progeny, derived from matings between amyloid-susceptible and amyloid-resistance mice, by daily injections of azocasein for thirty days. Using a restriction fragment length polymorphism generated by digestion of genomic DNA with the restriction enzyme HindIII, C5 sufficient and deficient DNA can be clearly differentiated. Eight mice were found to be C5 sufficient, 32 were heterozygotes and 14 were found to be C5 deficient. Grading of the splenic amyloid load from negative to 4+ was performed after staining tissue squashes with Congo red and viewing them under a polarizing microscope. Seventeen mice were noted to have negative to trace, 18 had moderate (1+ - 2+) and 19 had heavy (3+ - 4+) amyloid deposition. There was no correlation between splenic amyloid load and C5 deficiency. Based on these results it is clear that C5 deficiency and resistance to secondary amyloidosis are not associated.
本研究的目的是确定小鼠中的C5缺陷是否与对继发性淀粉样变性发展的抗性相关。通过每天注射偶氮酪蛋白，持续三十天，在淀粉样变性易感小鼠和抗淀粉样变性小鼠交配产生的F2后代中诱导慢性炎症。使用由限制性内切酶HindIII消化基因组DNA产生的限制性片段长度多态性，可以清楚地区分C5充足和缺陷的DNA。发现8只小鼠C5充足，32只为杂合子，14只C5缺陷。在用刚果红对组织压片进行染色并在偏光显微镜下观察后，对脾脏淀粉样蛋白负荷进行从阴性到4 +的分级。注意到17只小鼠呈阴性至微量，18只具有中度（1 + - 2 +），19只具有重度（3 + - 4 +）淀粉样蛋白沉积。脾脏淀粉样蛋白负荷与C5缺陷之间没有相关性。基于这些结果，很明显C5缺陷与对继发性淀粉样变性的抗性无关。
