Intracerebroventricular injection of the terminal complement complex causes inflammatory reaction in the rat brain

Intracerebroventricular injection of the terminal complement complex causes inflammatory reaction in the rat brain
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DOI:
10.1002/eji.200323574
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发表时间:
2003-05-01
影响因子:
5.4
通讯作者:
Tedesco, F
Tedesco, F
中科院分区:
医学3区
文献类型:
--
作者:
Casarsa, C;De Luigi, A;Tedesco, F

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为了研究末端补体复合体(TCC)对中枢神经系统的影响,我们将细胞溶解活性复合体和非活性复合体同时注入大鼠侧脑室。两种复合体均促进白细胞在注射后4~6h积聚到脑脊液中。此时恢复的细胞主要是多形核白细胞(PMN),在12h时被单核细胞部分取代。由于它们不能对大鼠PMN趋化,因此排除了它们对白细胞在体内迁移的直接贡献。污染C5a不太可能是TCC影响的原因,因为当注射到侧脑室时,C5a无法动员白细胞。TCC注射后6h脑组织学观察发现,脉络丛内有明显的白细胞浸润,细胞间黏附分子-1表达增加,白细胞从脑膜血管中渗出。经TCC处理的大鼠脑脊液对大鼠PMN具有趋化活性,并在白细胞聚集之前增加了生长相关癌基因/细胞因子诱导的中性粒细胞趋化因子-1和单核细胞趋化蛋白-1的水平。接受TCC治疗的大鼠脑脊液和脑室周围也发现IL-1β浓度升高。
To investigate the effect of the terminal complement complex (TCC) on the central nervous system, we injected both the cytolytically active and the inactive complexes into the lateral ventricle of rats. Both complexes promoted accumulation of leukocytes into the cerebrospinal fluid at 4-6 h post-injection. The cells recovered at this time were mostly polymorphonuclear leukocytes (PMN) that were partially replaced by mononuclear cells at 12 h. A direct contribution of the complexes to the in-vivo migration of leukocytes was ruled out by their inability to be chemotactic for rat PMN. Contaminating C5a is unlikely to be responsible for the effect of TCC because it failed to mobilize leukocytes when injected into the lateral ventricle. Histological analysis of rat brains 6 hours after injection of TCC revealed marked leukocyte infiltration of the choroid plexus, increased expression of intercellular adhesion molecule-1 and egression of leukocytes out of the meningeal vessels. The cerebrospinal fluid of rats treated with TCC exhibited chemotactic activity for rat PMN and increased levels of growth related oncogen/cytokine-induced neutrophil chemoattractant-1 and monocyte chemoattractant protein-1 preceding the accumulation of leukocytes. Elevated concentration of IL-1beta was also found in the cerebrospinal fluid and in periventricular areas of rats treated with TCC.