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首页> 外文期刊>The European Journal of Neuroscience >Complete Freunds adjuvant-induced peripheral inflammation evokes glial activation and proinflammatory cytokine expression in the CNS.
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Complete Freunds adjuvant-induced peripheral inflammation evokes glial activation and proinflammatory cytokine expression in the CNS.

机译：完全弗氏佐剂诱导的周围炎症引起中枢神经系统中神经胶质的活化和促炎细胞因子的表达。

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Abstract Peripheral inflammation induces central sensitization characterized by the development of allodynia and hyperalgesia to mechanical and thermal stimuli. Recent evidence suggests that activation of glial cells and a subsequent increase in proinflammatory cytokines contribute to the development of behavioral hypersensitivity after nerve injury or peripheral inflammation. In the present study, we examined mRNA and protein expression of glial markers and proinflammatory cytokines at the lumbar spinal cord, brainstem and forebrain following intraplantar administration of complete Freunds adjuvant (CFA) in rats. Gene expression studied by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for microglial markers (Mac-1, TLR4 and CD14) showed a significant increase in their expression during all phases (acute, subacute and chronic) of inflammation. Conversely, up-regulation of astroglial markers [glial fibrillary acidic protein (GFAP) and S100B] was observed only at the subacute and chronic phases of inflammation. Increased immunoreactivity for OX-42 (CR3/CD11b) and GFAP at various brain regions was also observed after the acute and subacute phases of the inflammation, respectively. Quantification of proinflammatory cytokines (IL-1beta, IL-6 and TNF-alpha) at the mRNA (by real-time RT-PCR) and protein level (by ELISA) revealed enhanced expression during the acute, subacute and chronic phases of CFA-induced peripheral inflammation. This study demonstrates that CFA-induced peripheral inflammation induces robust glial activation and proinflammatory cytokines both spinally and supraspinally. In addition, similar to nerve injury-induced behavioral hypersensitivity microglial activation preceded astrocytic activation following CFA-induced peripheral inflammation, supporting a role of microglia in the initiation phase and astrocytes in maintaining hypersensitivity. These findings further support a unifying theory that glial activation and enhanced cytokine expression at the CNS have a role in eliciting behavioral hypersensitivity.
机译：摘要周围炎症引起中枢敏化，其特征在于对机械和热刺激的异常性疼痛和痛觉过敏的发展。最近的证据表明，神经胶质细胞的激活和随后促炎性细胞因子的增加有助于神经损伤或周围炎症后行为超敏反应的发展。在本研究中，我们在大鼠足底内给予完全弗氏佐剂（CFA）后，检查了腰椎脊髓，脑干和前脑的神经胶质标志物和促炎细胞因子的mRNA和蛋白表达。通过实时逆转录聚合酶链反应（RT-PCR）研究的神经胶质标记（Mac-1，TLR4和CD14）的基因表达在炎症的所有阶段（急性，亚急性和慢性）均显着增加。相反，仅在炎症的亚急性和慢性阶段才观察到星形胶质标记[胶质纤维酸性蛋白（GFAP）和S100B]的上调。在炎症的急性期和亚急性期之后，还分别观察到了大脑各个部位对OX-42（CR3 / CD11b）和GFAP的免疫反应性增加。在mRNA（通过实时RT-PCR）和蛋白水平（通过ELISA）对促炎细胞因子（IL-1beta，IL-6和TNF-α）的定量显示在CFA-的急性，亚急性和慢性期表达增强引起外周炎症。这项研究表明，CFA诱导的周围炎症在脊髓和脊髓上均诱导强大的神经胶质活化和促炎细胞因子。此外，类似于神经损伤引起的行为超敏反应，小胶质细胞活化先于CFA引起的周围炎症后的星形胶质细胞活化，从而支持小胶质细胞在起始阶段和星形胶质细胞维持超敏反应的作用。这些发现进一步支持了统一的理论，即中枢神经系统的神经胶质激活和细胞因子表达增强在引起行为超敏反应中起作用。

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