CC-CHEMOKINE LIGAND 18/PULMONARY ACTIVATION-REGULATED CHEMOKINE EXPRESSION IN THE CNS WITH SPECIAL REFERENCE TO TRAUMATIC BRAIN INJURIES AND NEOPLASTIC DISORDERS
CC-CHEMOKINE LIGAND 18/PULMONARY ACTIVATION-REGULATED CHEMOKINE EXPRESSION IN THE CNS WITH SPECIAL REFERENCE TO TRAUMATIC BRAIN INJURIES AND NEOPLASTIC DISORDERS
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DOI：
10.1016/j.neuroscience.2009.11.050
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发表时间：
2010-02-17
期刊：
影响因子：
3.3
通讯作者：
Wu, C. -H.
中科院分区：
文献类型：
--
作者：
Chang, C. -Y.;Lee, Y. -H.;Wu, C. -H.
肺活化调节趋化因子（PARC）现在被命名为CC-趋化因子配体18（CCL 18），已经显示以促炎或免疫抑制的方式在各种组织损伤和疾病的发病机制中发挥重要作用，以限制或支持炎症或疾病。虽然对CCL 18/PARC在非神经组织中的作用有很多了解，但其在CNS中的表达在很大程度上仍未被探索和有争议。采用逆转录-聚合酶链反应（RT-PCR）和免疫组化双重染色技术，分析了CCL 18/PARC在人脑中的表达，特别是在创伤性脑损伤和肿瘤中的表达。RT-PCR分析显示，CCL 18/PARC mRNA在所检测的脑外伤和胶质瘤组织中均有表达。免疫组化染色结果显示，所有脑外伤患者脑组织中均检测到CCL 18/PARC蛋白的表达。免疫荧光双标记进一步证实了CCL 18/PARC阳性细胞为巨噬细胞/小胶质细胞、星形胶质细胞或神经元。在CCL 18/PARC阴性的胶质母细胞瘤组织中，CCL 18/PARC表达定位于2/8例巨噬细胞样细胞中。出乎意料的是，胶质母细胞瘤细胞系组成型弱表达的CCL 18/PARC mRNA在内毒素刺激后上调。目前的结果表明，CCL 18/PARC的显着生产在不同的中枢神经系统创伤和肿瘤组织的特定细胞成分表达的趋化因子。这些细胞通过CCL 18/PARC共同发挥抗炎机制，可能参与创伤性损伤和肿瘤发生后的CNS免疫。(C)2010年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Pulmonary activation-regulated chemokine (PARC) now designated CC-chemokine ligand 18 (CCL18) has been shown to play a significant role in the pathogenesis of various tissue injuries and diseases in a proinflammatory or immune suppressive way to limit or support the inflammation or disease. While much is known about the roles of CCL18/PARC in non-neural tissues, its expression in the CNS has remained largely unexplored and controversial. Using reverse transcription polymerase chain reaction (RT-PCR) and double immunohistochemical staining, we analyzed the expression of CCL18/PARC in the human brain with special reference to traumatic brain injuries and tumors. The RT-PCR analysis revealed the expression of CCL18/PARC mRNA both in the traumatic brain and glioma tissues examined. Immunoexpression of CCL18/PARC protein was consistently detected in all cases of traumatic brain injuries examined by immunohistochemical staining. Double immunofluorescence labeling has extended the study that CCL18/PARC positive cells were macrophages/microglia, astrocytes or neurons. The CCL18/PARC expression was localized in macrophage-like cells in two of eight glioblastoma tissues whose cancer cells were CCL18/PARC negative. Unexpectedly, CCL18/PARC mRNA weakly and constitutively expressed by glioblastoma cell line was upregulated after endotoxin stimulation. The present results indicated a significant production of CCL18/PARC in different CNS traumatic and neoplasm tissues by specific cellular elements expressing the chemokine. An anti-inflammatory mechanism jointly exerted by these cells via CCL18/PARC may be involved in the CNS immunity after traumatic injury and tumorigenesis. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.