老年C57BL/Ka小鼠胃肠道AAPOAII和系统性aa -淀粉样变性长期免疫抑制治疗的淀粉样蛋白依赖效应。

H HogenEsch, T A Niewold, K Higuchi, P C Tooten, E Gruys, J Radl
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引用次数: 12

摘要

本文描述了C57BL/Ka小鼠胃肠道中一种新的局限性老年性淀粉样变性的光镜和免疫组织化学特征。老年性胃肠道淀粉样变主要发生在回肠、盲肠和胃固有层,在胃肠道其他部位少见。老年性淀粉样蛋白的刚果红亲和力对高锰酸钾预处理敏感。淀粉样蛋白与抗aa和抗免疫球蛋白抗血清无反应,但高密度脂蛋白的主要载脂蛋白apoAII染色阳性。一种类似的淀粉样蛋白,被称为AApoAII,最近被描述为小鼠老年性淀粉样变性的系统性形式。在本研究中,我们研究了长期免疫抑制治疗对老年C57BL/Ka小鼠系统性aa -淀粉样变性和胃肠道aapoaii -淀粉样变性发病率的影响。60%的对照组小鼠发生了胃肠道淀粉样变,但免疫抑制组小鼠的发生率明显降低。相比之下,全身性aa免疫反应性淀粉样变性仅在给予免疫抑制治疗的小鼠中发现。AA与aapoaii -淀粉样蛋白无共沉积。这些结果表明,免疫抑制药物对C57BL/Ka小鼠淀粉样变性的发病率和类型有深远的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gastrointestinal AAPOAII and systemic AA-amyloidosis in aged C57BL/Ka mice. Amyloid-type dependent effect of long-term immunosuppressive treatment.

The light microscopic and immunohistochemical features of a novel localized senile amyloidosis in the gastrointestinal tract of C57BL/Ka mice are described. Senile gastrointestinal amyloidosis was predominantly found in the lamina propria of the ileum, cecum and stomach and infrequently in other segments of the gastrointestinal tract. The Congo red affinity of the senile amyloid was sensitive to potassium permanganate pretreatment. The amyloid did not react with anti-AA and anti-immunoglobulin antisera, but stained positively for apoAII, a major apolipoprotein of high density lipoproteins. A similar type of amyloid, termed AApoAII, has recently been described in a systemic form of senile amyloidosis in mice. In the present study, we investigated the effect of long-term immunosuppressive treatment on the incidence of systemic AA-amyloidosis and gastrointestinal AApoAII-amyloidosis in aged C57BL/Ka mice. Gastrointestinal amyloidosis occurred in 60% of the control mice, but significantly less in mice of the immunosuppressed groups. In contrast, systemic AA-immunoreactive amyloidosis was only found in mice that were given immunosuppressive treatment. There was no codeposition of AA and AApoAII-amyloid. These findings indicate that immunosuppressive drugs have a profound effect on the incidence as well as the type of amyloidosis in C57BL/Ka mice.

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