Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis.
Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis.
复制标题
DOI：
10.1111/j.1750-3639.2009.00354.x
复制
发表时间：
2010-07
期刊：
影响因子：
--
通讯作者：
Cheeran MC
中科院分区：
文献类型：
--
作者：
Armien AG;Hu S;Little MR;Robinson N;Lokensgard JR;Low WC;Cheeran MC
长期神经系统后遗症在单纯疱疹脑炎（HSE）幸存者中很常见。HSE的动物模型被用于研究急性疾病的机制，但很少有研究对HSE的慢性表现进行建模。目前的研究提出了一个详细的，系统的分析慢性神经病理学，包括地形特征和退行性病变和炎症的顺序进展。在鼻内感染1型单纯疱疹病毒后，在受感染的皮层和脑干区域持续存在时间和空间上不同的炎症反应。在感染急性期，中性粒细胞仅存在于嗅球和脑干区域，而慢性炎症以浆细胞、淋巴细胞和活化的小胶质细胞为标志。慢性淋巴细胞浸润、细胞因子产生和活化的小胶质细胞与内嗅皮层和海马皮层神经堆的丧失有关。急性感染后存活的动物表现出一系列慢性病变，从脑容量减少、神经元丧失、星形胶质细胞活化、胶质瘢痕形成到严重的皮质萎缩和空化。这些损伤也与存活动物严重的空间记忆缺陷有关。综上所述，该模型可用于进一步研究HSE后神经系统缺陷的机制。
Long-term neurological sequela is common among herpes simplex encephalitis (HSE) survivors. Animal models for HSE are used to investigate mechanisms of acute disease, but little has been done to model chronic manifestations of HSE. The current study presents a detailed, systematic analysis of chronic neuropathology, including characterization of topography and sequential progression of degenerative lesions and inflammation. Subsequent to intranasal HSV-1 infection, inflammatory responses that were temporally and spatially distinct persisted in infected cortical and brain stem regions. Neutrophils were present exclusively within the olfactory bulb and brain stem regions during the acute phase of infection, while the chronic inflammation was marked by plasma cells, lymphocytes and activated microglia. The chronic lymphocytic infiltrate, cytokine production, and activated microglia were associated with the loss of cortical neuropile in the entorhinal cortex and hippocampus. Animals surviving the acute infection showed a spectrum of chronic lesions from decreased brain volume, neuronal loss, activated astrocytes, and glial scar formation to severe atrophy and cavitations of the cortex. These lesions were also associated with severe spatial memory deficits in surviving animals. Taken together, this model can be utilized to further investigate the mechanisms of neurological defects that follow in the wake of HSE.
登录
查看更多内容
影响因子：
11.2
作者：
DAVIS, LE;JOHNSON, RT
通讯作者：
JOHNSON, RT
影响因子：
3.1
作者：
Canto CB;Wouterlood FG;Witter MP
通讯作者：
Witter MP
DOI：
10.1073/pnas.0803945105
发表时间：
2008-11-25
影响因子：
11.1
作者：
Breckwoldt, Michael O.;Chen, John W.;Weissleder, Ralph
通讯作者：
Weissleder, Ralph
影响因子：
15.3
作者：
Goldsmith, K;Chen, W;Johnson, DC;Hendricks, RL
通讯作者：
Hendricks, RL
影响因子：
3.1
作者：
Cheng, Xiandong;Mukhtar, Muhammad;Parveen, Zahida
通讯作者：
Parveen, Zahida