Loss of Endothelial Barrier Antigen Immunoreactivity as a Marker of Clostridium perfringens Type D Epsilon Toxin-induced Microvascular Damage in Rat Brain

被引:17
作者
Finnie, J. W. [1 ,2 ]
Manavis, J. [1 ]
Chidlow, G. [3 ,4 ]
机构
[1] SA Pathol, Hanson Inst Ctr Neurol Dis, Adelaide, SA, Australia
[2] Univ Adelaide, Sch Vet Sci, Adelaide, SA, Australia
[3] Hanson Inst Ctr Neurol Dis, South Australian Inst Ophthalmol, Ophthalm Res Labs, Adelaide, SA, Australia
[4] Univ Adelaide, Dept Ophthalmol & Visual Sci, Adelaide, SA, Australia
关键词
Clostridium perfringens type D epsilon toxin; endothelial barrier antigen; microvascular injury; rat brain; SHEEP;
D O I
10.1016/j.jcpa.2014.04.010
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The epsilon toxin elaborated by Clostridium perfringens type D in the intestine of domestic livestock is principally responsible for the neurological disease produced after its absorption in excessive quantities into the systemic circulation. The fundamental basis of the cerebral damage induced by epsilon toxin appears to be microvascular injury with ensuing severe, diffuse vasogenic oedema. Endothelial barrier antigen (EBA), which is normally expressed by virtually all capillaries and venules in the rat brain, was used in this study as a marker of blood-brain barrier (BBB) integrity. After exposure to high levels of circulating epsilon toxin, there was substantial loss of EBA in many brain microvessels, attended by widespread plasma albumin extravasation. These results support microvascular injury and subsequent BBB breakdown as a key factor in the pathogenesis of epsilon toxin-induced neurological disease. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:153 / 156
页数:4
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