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在患有实验性变应性脑脊髓炎的小鼠中,星形胶质细胞和小胶质细胞表达诱导型一氧化氮合酶。

Astrocytes and microglia express inducible nitric oxide synthase in mice with experimental allergic encephalomyelitis.

作者信息

Tran E H, Hardin-Pouzet H, Verge G, Owens T

机构信息

Neuroimmunology Unit, Montréal Neurological Institute, Que., Canada.

出版信息

J Neuroimmunol. 1997 Apr;74(1-2):121-9. doi: 10.1016/s0165-5728(96)00215-9.

Abstract

Nitric oxide (NO), produced by inducible NO synthase (iNOS), may play a role in inflammatory demyelinating diseases of the central nervous system (CNS). We show upregulation of iNOS mRNA in CNS of SJL/J mice with experimental allergic encephalomyelitis (EAE). Using antibodies against mouse iNOS, GFAP (a marker for astrocytes) and Mac-1/CD11b (a marker for macrophages/microglia), both astrocytes and macrophages/microglia were identified as iNOS-expressing cells in situ in EAE lesions. GFAP + astrocytes not associated with inflammatory infiltrates were also found to express iNOS. Because microglia rather than astrocytes are implicated in demyelinating pathology, we propose that microglial NO may be cytopathic whereas astrocyte-derived NO may be protective in EAE.

摘要

由诱导型一氧化氮合酶(iNOS)产生的一氧化氮(NO)可能在中枢神经系统(CNS)的炎性脱髓鞘疾病中发挥作用。我们发现,患有实验性变应性脑脊髓炎(EAE)的SJL/J小鼠的中枢神经系统中iNOS mRNA上调。使用抗小鼠iNOS、GFAP(星形胶质细胞标志物)和Mac-1/CD11b(巨噬细胞/小胶质细胞标志物)的抗体,在EAE病变中原位鉴定出星形胶质细胞和巨噬细胞/小胶质细胞均为iNOS表达细胞。还发现未与炎性浸润相关的GFAP+星形胶质细胞也表达iNOS。由于脱髓鞘病变与小胶质细胞而非星形胶质细胞有关,我们提出小胶质细胞源性NO可能具有细胞毒性,而星形胶质细胞源性NO在EAE中可能具有保护作用。

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