The NIH-3 immunodeficient mouse is a model for Lyme borreliosis myositis and carditis.
The NIH-3 immunodeficient mouse is a model for Lyme borreliosis myositis and carditis.
复制标题
DOI：
--
复制
发表时间：
1992-07
期刊：
影响因子：
--
通讯作者：
D. Defosse;P. Duray;R. C. Johnson
中科院分区：
文献类型：
--
作者：
D. Defosse;P. Duray;R. C. Johnson
免疫缺陷 NIH-3 (N:NIH-bg-nu-xid) 小鼠实验性感染伯氏疏螺旋体被发现会导致多系统组织病理学病变。除了裸突变导致的 T 细胞缺陷外，这些小鼠还存在影响 B 细胞成熟的 X 连锁缺陷和导致 NK 细胞缺失的米色突变。 NIH-3 小鼠易受伯氏疏螺旋体进行性感染，导致全心炎、滑膜炎和骨骼间质性肌炎，而对照组则保持正常。心肌病的特征是炎性单核细胞浸润和纤维状坏死。胫跗关节和尺腕关节可见滑膜增生和炎症。在周围骨骼肌中观察到晚期肌炎。胃肠粘膜下层、心脏和骨骼肌大量定殖伯氏疏螺旋体。该小鼠被提议作为莱姆疏螺旋体病心脏炎、滑膜炎和肌炎的模型。
Experimental infection of immunodeficient NIH-3 (N:NIH-bg-nu-xid) mice with Borrelia burgdorferi was found to result in multisystem histopathologic lesions. In addition to T-cell deficiency due to the nude mutation, these mice have an x-linked defect affecting the B-cell maturation and the beige mutation resulting in the absence of NK cells. NIH-3 mice were susceptible to progressive infection with B. burgdorferi resulting in pancarditis, synovitis, and skeletal interstitial myositis whereas controls remained normal. Cardiomyopathy was characterized by inflammatory mononuclear infiltration and fibrillar necrosis. Synovial hyperplasia and inflammation were seen in the tibiotarsal and ulna-carpal joints. Advanced myositis was observed in peripheral skeletal muscle. Gastrointestinal submucosa, heart, and skeletal muscle were heavily colonized with B. burgdorferi. This mouse is proposed as a model for Lyme borreliosis carditis, synovitis, and myositis.