Persistent immune activation associated with a mouse model of Staphylococcus aureus-induced experimental brain abscess
Persistent immune activation associated with a mouse model of Staphylococcus aureus-induced experimental brain abscess
复制标题
DOI：
10.1016/j.jneuroim.2004.02.002
复制
发表时间：
2004-06-01
影响因子：
3.3
通讯作者：
Kielian, T
中科院分区：
文献类型：
--
作者：
Baldwin, AC;Kielian, T
我们使用金黄色葡萄球菌建立了小鼠实验性脑脓肿模型，其中病变部位与初始感染的局部区域相比大大夸大，使人联想到过度活跃的免疫反应。在金黄色葡萄球菌诱导的脑脓肿小鼠中，il -1 β、tnf - α和巨噬细胞炎症蛋白-2 （MIP-2/CXCL2）的表达延长，同时伴有血脑屏障（BBB）的慢性破坏。这些变化与中性粒细胞和巨噬细胞/小胶质细胞的持续浸润有关。总的来说，这些发现表明，脑脓肿导致的过度组织损伤可能部分是由抗菌免疫反应的持续介导的，而抗菌免疫反应没有及时下调。(C) 2004 Elsevier B.V.版权所有
We have established a mouse experimental brain abscess model using Staphylococcus aureus where lesion sites are greatly exaggerated compared to the localized area of initial infection, reminiscent of an overactive immune response. Here we demonstrate the prolonged expression of IL-1beta, TNF-alpha, and macrophage inflammatory protein-2 (MIP-2/CXCL2), concomitant with a chronic disruption of the blood-brain barrier (BBB) in mice with S. aureus-induced brain abscess. These changes correlated with the continued presence of infiltrating neutrophils and macrophages/microglia. Collectively these findings suggest that the excessive tissue damage that often results from brain abscess may be mediated, in part, by the perpetuation of antibacterial immune responses that are not downregulated in a timely manner. (C) 2004 Elsevier B.V. All rights reserved.