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首页> 外文期刊>Journal of neuroinflammation >Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis
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Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis

机译：聚（ADP-核糖）聚合酶2有助于小鼠实验性自身免疫性脑脊髓炎的神经炎症和神经功能障碍

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Background Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by entry of activated T cells and antigen presenting cells into the central nervous system and subsequent autoimmune destruction of nerve myelin. Previous studies revealed that non-selective inhibition of poly(ADP-ribose) polymerases (PARPs) 1 and 2 protect against neuroinflammation and motor dysfunction associated with EAE, but the role of the PARP-2 isoform has not yet been investigated selectively. Results EAE was induced in mice lacking PARP-2, and neurological EAE signs, blood-spine barrier (BSB) permeability, demyelination and inflammatory infiltration were monitored for 35 days after immunization. Mice lacking PARP-2 exhibited significantly reduced overall disease burden and peak neurological dysfunction. PARP-2 deletion also significantly delayed EAE onset and reduced BSB permeability, demyelination and central nervous system (CNS) markers of proinflammatory Th1 and Th17 T helper lymphocytes. Conclusions This study represents the first description of a significant role for PARP-2 in neuroinflammation and neurological dysfunction in EAE.
机译：背景技术实验性自身免疫性脑脊髓炎（EAE）是一种多发性硬化症的动物模型，其特征在于活化的T细胞和抗原呈递细胞进入中枢神经系统，随后发生神经髓磷脂的自身免疫破坏。先前的研究表明，聚（ADP-核糖）聚合酶（PARPs）1和2的非选择性抑制可防止与EAE相关的神经炎症和运动功能障碍，但尚未选择性研究PARP-2同工型的作用。结果：在缺乏PARP-2的小鼠中诱发了EAE，免疫后35天监测其EEA体征，血脊屏障（BSB）的通透性，脱髓鞘和炎症浸润。缺乏PARP-2的小鼠表现出明显降低的总体疾病负担和峰值神经功能障碍。 PARP-2缺失还显着延迟了EAE的发作，并降低了促炎性Th1和Th17 T辅助淋巴细胞的BSB通透性，脱髓鞘和中枢神经系统（CNS）标记。结论本研究首次描述了PARP-2在EAE的神经炎症和神经功能障碍中的重要作用。

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