实验性神经元肌囊虫感染对马模型免疫的影响。

Journal of veterinary medicine Pub Date : 2014-01-01 Epub Date: 2014-11-12 DOI:10.1155/2014/239495
S Rochelle Lewis, Siobhan P Ellison, John J Dascanio, David S Lindsay, Robert M Gogal, Stephen R Werre, Naveen Surendran, Meghan E Breen, Bettina M Heid, Frank M Andrews, Virginia A Buechner-Maxwell, Sharon G Witonsky
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引用次数: 11

摘要

神经元性肌囊虫病是马原生动物髓脑炎(EPM)最常见的病因,在美国有0.5-1%的马在其一生中受到影响。本研究的目的是评估马在实验诱导的神经元肌囊虫感染模型中的免疫反应。在70天的研究之前和整个研究过程中,由盲法研究人员记录神经参数。血清和脑脊液的重组SnSAG1 ELISA用于确认和跟踪疾病进展。所有实验感染的马在感染后都表现出神经症状。感染马的中性粒细胞、单核细胞和淋巴细胞在某些时间点表现出明显延迟的凋亡。与对照组相比,非特异性PMA/I刺激神经元链球菌感染马的细胞增殖显著增加,而神经元链球菌刺激马的细胞增殖显著减少。总的来说,我们的研究结果表明,实验感染神经索菌的马表现出对神经索菌的抗原特异性反应受损,这可能是抗原呈递改变的功能,缺乏抗原识别,或两者兼而有之。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effects of Experimental Sarcocystis neurona-Induced Infection on Immunity in an Equine Model.

Effects of Experimental Sarcocystis neurona-Induced Infection on Immunity in an Equine Model.

Effects of Experimental Sarcocystis neurona-Induced Infection on Immunity in an Equine Model.

Effects of Experimental Sarcocystis neurona-Induced Infection on Immunity in an Equine Model.

Sarcocystis neurona is the most common cause of Equine Protozoal Myeloencephalitis (EPM), affecting 0.5-1% horses in the United States during their lifetimes. The objective of this study was to evaluate the equine immune responses in an experimentally induced Sarcocystis neurona infection model. Neurologic parameters were recorded prior to and throughout the 70-day study by blinded investigators. Recombinant SnSAG1 ELISA for serum and CSF were used to confirm and track disease progression. All experimentally infected horses displayed neurologic signs after infection. Neutrophils, monocytes, and lymphocytes from infected horses displayed significantly delayed apoptosis at some time points. Cell proliferation was significantly increased in S. neurona-infected horses when stimulated nonspecifically with PMA/I but significantly decreased when stimulated with S. neurona compared to controls. Collectively, our results suggest that horses experimentally infected with S. neurona manifest impaired antigen specific response to S. neurona, which could be a function of altered antigen presentation, lack of antigen recognition, or both.

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