Acute, regional inflammatory response after traumatic brain injury: Implications for cellular therapy.
Acute, regional inflammatory response after traumatic brain injury: Implications for cellular therapy.
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DOI：
10.1016/j.surg.2008.05.017
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发表时间：
2008-11
期刊：
影响因子：
3.8
通讯作者：
Cox, Charles S., Jr.
中科院分区：
文献类型：
--
作者：
Harting, Matthew T.;Jimenez, Fernando;Adams, Sasha D.;Mercer, David W.;Cox, Charles S., Jr.
虽然细胞治疗在创伤性脑损伤（TBI）的管理中显示出了希望，但对脑内环境和治疗性干细胞之间的微环境相互作用知之甚少。我们试图描述TBI后急性局部炎症反应的特征。在6、12、24、48和72小时处死大鼠，并从直接损伤、半影、同侧额叶、对侧区域分离脑内液（IF）。还分离了皮质和海马区。测量局部细胞因子水平。在与IF孵育后评估PMN氧化爆发和标志物表达。免疫组织化学鉴定脑内CD 68+细胞（小胶质细胞/巨噬细胞）。CCI后损伤区和半暗区促炎细胞因子IL-1α、IL-1β、IL-6和TNF-α显著升高。相同细胞因子的增加局限于皮质和海马。在与损伤或半影区IF孵育后，鉴定了PMN的CD 11b和L-选择素表达增加，而PMN氧化爆发没有变化。CD 68+细胞在直接损伤区和半影区可见。TBI后最初48小时内的局部脑环境是高度促炎的。这种反应在直接损伤处或邻近直接损伤的区域中最明显。TBI后的局部急性促炎反应可作为早期细胞治疗的治疗靶点，或者相反，可产生不利的局部环境，限制早期细胞治疗的功效。
While cellular therapy has shown promise in the management of traumatic brain injury (TBI), microenvironment interactions between the intracerebral milieu and therapeutic stem cells are poorly understood. We sought to characterize the acute, regional inflammatory response after TBI. Rats underwent a controlled cortical impact (CCI) injury or sham injury, were sacrificed at 6, 12, 24, 48, and 72 hours, and intracerebral fluid (IF) was isolated from the direct injury, penumbral, ipsilateral frontal, contralateral regions. Cortical and hippocampal areas were also isolated. Regional cytokine levels were measured. PMN oxidative burst and marker expression were assessed after incubation with the IF. Immunohistochemistry identified intracerebral CD68+ cells (microglia/macrophages). The pro-inflammatory cytokines IL-1α, IL-1β, IL-6, and TNF-α were significantly elevated after CCI in the injury and penumbral regions. Increases in the same cytokines were localized to the cortex and the hippocampus. Increased PMN expression of CD11b and L-selectin was identified after incubation with injury or penumbral area IF, without change in PMN oxidative burst. CD68+ cells were noted in the direct injury and penumbral areas. The local cerebral milieu in the first 48 hrs after TBI is highly pro-inflammatory. This response is most pronounced in areas at or proximal to the direct injury. The local, acute pro-inflammatory response after TBI may serve as a therapeutic target of early cell therapy or, conversely, may create an unfavorable local milieu, limiting the efficacy of early cellular therapy.
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