The cytokine temporal profile in rat cortex after controlled cortical impact.
The cytokine temporal profile in rat cortex after controlled cortical impact.
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DOI：
10.3389/fnmol.2012.00006
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发表时间：
2012
影响因子：
4.8
通讯作者：
Watson WD
中科院分区：
文献类型：
--
作者：
Dalgard CL;Cole JT;Kean WS;Lucky JJ;Sukumar G;McMullen DC;Pollard HB;Watson WD
创伤性脑损伤（TBI）后，脑炎症反应可能引发继发性级联反应。细胞因子和趋化因子表达的变化可能激活、调节和招募与继发性变性相关的先天和适应性免疫细胞，并改变许多其他细胞过程。在这项研究中，我们量化了大鼠脑损伤后皮层组织中大量炎症介质的时间表达。在对年轻成年雄性大鼠进行控制性皮质冲击（CCI）后，在手术后早期（4、12和24小时）和延长（3和7天）时间点采集损伤半球的皮质和海马组织以及匹配的对侧材料。Naïve只接受麻醉的大鼠作为对照。利用基于电化学发光的多重ELISA平台检测处理后的脑匀浆的趋化因子和细胞因子水平。皮层组织样本的时间谱显示脑损伤后的多阶段损伤反应。与naïve或对侧组织相比，CXCL1、IFN-γ、TNF-α水平在损伤后4小时达到峰值。损伤后12小时，观察到CXCL1、IFN-γ和TNF-α水平下降至少3倍。IL-1β、IL-4和IL-13水平在损伤后4小时也显著升高，尽管它们的表达在损伤后24小时内下降不超过3倍。此外，IL-1β和IL-4水平在损伤反应中表现出双相时间谱，这可能表明它们参与了适应性免疫反应。有趣的是，CCL2和CCL20的峰值水平直到损伤后4小时才被观察到。损伤皮质组织中的CCL2水平明显高于任何其他炎症介质的峰值水平，因此可能被用作生物标志物。充分阐明脑损伤后趋化因子和细胞因子信号传导特性，可能有助于深入了解炎症反应引发或调节的一系列次级级联事件。
Cerebral inflammatory responses may initiate secondary cascades following traumatic brain injury (TBI). Changes in the expression of both cytokines and chemokines may activate, regulate, and recruit innate and adaptive immune cells associated with secondary degeneration, as well as alter a host of other cellular processes. In this study, we quantified the temporal expression of a large set of inflammatory mediators in rat cortical tissue after brain injury. Following a controlled cortical impact (CCI) on young adult male rats, cortical and hippocampal tissue of the injured hemisphere and matching contralateral material was harvested at early (4, 12, and 24 hours) and extended (3 and 7 days) time points post-procedure. Naïve rats that received only anesthesia were used as controls. Processed brain homogenates were assayed for chemokine and cytokine levels utilizing an electrochemiluminescence-based multiplex ELISA platform. The temporal profile of cortical tissue samples revealed a multi-phasic injury response following brain injury. CXCL1, IFN-γ, TNF-α levels significantly peaked at four hours post-injury compared to levels found in naïve or contralateral tissue. CXCL1, IFN-γ, and TNF-α levels were then observed to decrease at least 3-fold by 12 hours post-injury. IL-1β, IL-4, and IL-13 levels were also significantly elevated at four hours post-injury although their expression did not decrease more than 3-fold for up to 24 hours post-injury. Additionally, IL-1β and IL-4 levels displayed a biphasic temporal profile in response to injury, which may suggest their involvement in adaptive immune responses. Interestingly, peak levels of CCL2 and CCL20 were not observed until after four hours post-injury. CCL2 levels in injured cortical tissue were significantly higher than peak levels of any other inflammatory mediator measured, thus suggesting a possible use as a biomarker. Fully elucidating chemokine and cytokine signaling properties after brain injury may provide increased insight into a number of secondary cascade events that are initiated or regulated by inflammatory responses.
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影响因子：
3.8
作者：
Harting, Matthew T.;Jimenez, Fernando;Adams, Sasha D.;Mercer, David W.;Cox, Charles S., Jr.
通讯作者：
Cox, Charles S., Jr.
影响因子：
5.8
作者：
Kawanokuchi, J.;Mizuno, T.;Suzumura, A.
通讯作者：
Suzumura, A.
影响因子：
5.3
作者：
Ponomarev, Eugene D.;Maresz, Katarzyna;Dittel, Bonnie N.
通讯作者：
Dittel, Bonnie N.
影响因子：
6.2
作者：
Hulshof, S;Montagne, L;Van der Valk, P
通讯作者：
Van der Valk, P
影响因子：
20.3
作者：
Krzysiek, R;Lefevre, EA;Richard, Y
通讯作者：
Richard, Y