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在伯氏疏螺旋体实验性感染期间免疫缺陷小鼠中的莱姆心肌炎

Lyme carditis in immunodeficient mice during experimental infection of Borrelia burgdorferi.

作者信息

Zimmer G, Schaible U E, Kramer M D, Mall G, Museteanu C, Simon M M

机构信息

Institut für Rechtsmedizin Heidelberg, FRG.

出版信息

Virchows Arch A Pathol Anat Histopathol. 1990;417(2):129-35. doi: 10.1007/BF02190530.

Abstract

Recently, we described the severe combined immunodeficiency (scid) mouse as a laboratory model for B. burgdorferi infection. Scid mice inoculated with the virulent low-passage tick isolate Borrelia burgdorferi ZS7 developed a severe pancarditis involving endocardium, myocardium and epicardium in the absence of functional B- or T-cells. Soon after inoculation perivascular infiltration was observed, later diffuse infiltration of the interstitium of the subendocardial and subepicardial areas was seen. The infiltrate was mainly mononuclear and predominantly composed of Mac-1+ cells. Concomitantly, fibroblast proliferation and augmented collagen deposition occurred in the interstitium. This was associated with the presence of B. burgdorferi organisms. The histopathological and ultrastructural findings observed in scid mice resemble those observed in human Lyme carditis. The data emphasize the suitability of the scid mouse as a model in which to study the role of the immune system in the pathogenesis of Lyme carditis.

摘要

最近,我们将严重联合免疫缺陷(scid)小鼠描述为伯氏疏螺旋体感染的实验室模型。接种了强毒低传代蜱分离株伯氏疏螺旋体ZS7的scid小鼠,在缺乏功能性B细胞或T细胞的情况下,发生了累及心内膜、心肌和心包膜的严重全心肌炎。接种后不久观察到血管周围浸润,随后可见心内膜下和心包膜下区域间质的弥漫性浸润。浸润主要为单核细胞,主要由Mac-1+细胞组成。同时,间质中出现成纤维细胞增殖和胶原沉积增加。这与伯氏疏螺旋体的存在有关。在scid小鼠中观察到的组织病理学和超微结构发现与人类莱姆心肌炎中观察到的相似。这些数据强调了scid小鼠作为研究免疫系统在莱姆心肌炎发病机制中作用的模型的适用性。

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