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首页> 外文期刊>Amyloid: the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis >Phagocyte depletion inhibits AA amyloid accumulation in AEF-induced huIL-6 transgenic mice
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Phagocyte depletion inhibits AA amyloid accumulation in AEF-induced huIL-6 transgenic mice

机译：吞噬细胞耗竭抑制AEF诱导的huIL-6转基因小鼠的AA淀粉样蛋白积累

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Objective: Determine the role of phagocytosis in the deposition of acute phase SAA protein in peripheral organs as AA amyloid. Methods: AA amyloidosis was induced by injection of amyloid enhancing factor (AEF) in huIL-6 transgenic mice. Clodronate liposomes were injected at different times, and the amyloid load evaluated by Congo red birefringence staining and monitoring with the amyloid specific probe 125I-labeled peptide p5R. Results: Injection of clodronate containing liposomes depleted Iba-1 positive and F4/80 positive phagocytic cells in liver and spleen for up to 5 days. Treatment prior to administration of intravenous AEF did not alter the pattern of deposition of the AEF in spleen, but inhibited the catabolism of the 125I-labeled AEF. Clodronate treatment 1 day before or 1 day after AEF administration had little effect on AA amyloid accumulation at 2 weeks; however, mice treated with clodronate liposomes 5 days after AEF induction and evaluated at 2 weeks post-AEF induction showed reduced amyloid load relative to controls. At 6 weeks post-AEF there was no significant effect on amyloid load following a single clodronate treatment. Conclusion: Macrophages have been shown to be instrumental in both accumulation and clearance of AA amyloid after cessation of inflammation. Our data indicate that when SAA protein is continuously present, depletion of phagocytic cells during the early course of the disease progression temporarily reduces amyloid load.
机译：目的：确定吞噬作用在急性期SAA蛋白在外周器官中作为AA淀粉样蛋白沉积的作用。方法：注射淀粉样蛋白增强因子（AEF）诱导转染huIL-6的小鼠AA淀粉样变性。在不同时间注射氯膦酸盐脂质体，并通过刚果红双折射染色评估淀粉样蛋白负荷，并用淀粉样蛋白特异性探针125 I标记的肽p5R进行监测。结果：注射含氯膦酸盐的脂质体最多可耗尽肝脏和脾脏中Iba-1阳性和F4 / 80阳性吞噬细胞。静脉内AEF给药前的治疗并未改变AEF在脾脏中的沉积方式，但抑制了125I标记的AEF的分解代谢。服用AEF前1天或服用后1天的氯膦酸盐治疗对2周时AA淀粉样蛋白的积累影响很小;但是，在AEF诱导后5天用氯膦酸盐脂质体处理的小鼠，并在AEF诱导后2周进行了评估，显示相对于对照，淀粉样蛋白负荷降低。 AEF后6周，单次氯膦酸盐治疗对淀粉样蛋白负荷无明显影响。结论：已经证明巨噬细胞在炎症停止后对AA淀粉样蛋白的积累和清除均起作用。我们的数据表明，当SAA蛋白持续存在时，在疾病进展的早期阶段吞噬细胞的消耗会暂时减少淀粉样蛋白的负荷。

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