Simultaneous detections of 27 cytokines during cerebral wound healing by multiplexed bead-based immunoassay for wound age estimation

Simultaneous detections of 27 cytokines during cerebral wound healing by multiplexed bead-based immunoassay for wound age estimation
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DOI:
10.1089/neu.2007.0336
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发表时间:
2007-12-01
影响因子:
4.2
通讯作者:
Aoki, Yasuhiro
Aoki, Yasuhiro
中科院分区:
医学2区
文献类型:
--
作者:
Takamiya, Masataka;Fujita, Sachiko;Aoki, Yasuhiro

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定量脑损伤后的27种细胞因子用于伤口年龄估计。所评估的细胞因子包括白细胞介素(IL)-la、IL-1 β、IL-2、IL-3、IL-4、IL-5、IL-6、IL-10、IL-12 p40、IL-12 p70、IL-15、IL-17、IL-18、碱性成纤维细胞生长因子(bFGF)、粒细胞集落刺激因子(G-CSF)、粒细胞巨噬细胞集落刺激因子(GM-CSF)、干扰素-γ(IFN-γ)、白细胞介素(IL)-1 α、IL-1 β、IL-2、IL-3、IL-4、IL-5、IL-6、IL-10、IL-12 p40、IL-12 p70、IL-15、IL-17、IL-18、碱性成纤维细胞生长因子(bFGF)、粒细胞集落刺激因子(G-CSF)、粒细胞巨噬细胞集落刺激因子(GM-CSF)、干扰素-γ(IFN-γ)、白细胞介素(IL)-1 α(IFN-γ)、角质形成细胞衍生的细胞因子(KC)、白血病抑制因子(LIF)、巨噬细胞集落刺激因子(M-CSF)、干扰素γ诱导的单核因子(IFN-γ)、巨噬细胞炎性蛋白(MIP)-1 α、MIP 2、血小板衍生的生长因子BB(PDGF BB),在活化时调节,正常T细胞表达和分泌(Rantes),肿瘤坏死因子-α(TNF-α)和血管内皮生长因子(VEGF)。同时观察神经胶质细胞增殖和炎性细胞浸润情况。虽然星形胶质细胞从损伤后72小时开始增殖,但炎性细胞动力学通常是稳定的。在本研究分析的细胞因子中,IL-1 β、IL-5、IL-6、IL-12 p40、G-CSF、IFN-γ、KC、LIF、MIP 2和PDGF BB在脑创伤愈合的早期阶段增加,M-CSF在中期阶段增加,而IL-15、IL-18和TNF在晚期阶段增加。相反,IL-1 α、IL-10、IL-12 p70和TNF-α在整个脑创伤愈合过程中受到抑制。根据我们的研究结果,定量细胞因子分析在脑伤口部位可能是一个有用的工具,伤口年龄估计。此外,本研究表明,使用单一方法从同一样本获得的多重数据表明,在脑伤口愈合过程中,细胞因子相互作用高度准确。
Quantification of 27 cytokines following cerebral wounding was performed for wound age estimation. The cytokines evaluated included interleukin (IL)-1 alpha, IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12 p40, IL-12 p70, IL-15, IL-17, IL-18, basic fibroblast growth factor (bFGF), granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage-colony stimulating factor (GM-CSF), Interferon-gamma (IFN-gamma), keratinocyte derived cytokine (KC), leukemia inhibitory factor (LIF), macrophage-colony stimulating factor (M-CSF), monokine inducible by interferon gamma (MIG), macrophage inflammatory protein (MIP)-1 alpha, MIP 2, platelet-derived growth factor BB (PDGF BB), regulated upon activation, normal T-cell expressed, and secreted (Rantes), tumor necrosis factor -alpha (TNF-alpha), and vascular endothelial growth factor (VEGF). The proliferation of glial cells as well as the infiltration of inflammatory cells were also evaluated. Although astroglia proliferated from 72 hours post-injury, inflammatory cell dynamics were generally steady. Among cytokines analyzed in the present study, IL-1 beta, IL-5, IL-6, IL-12 p40, G-CSF, IFN-gamma, KC, LIF, MIP 2, and PDGF BB increased during the early phase of cerebral wound healing, and M-CSF increased during the middle phase, while IL-15, IL-18, and MIG increased during the late phase. In contrast, IL-1 alpha, IL-10, IL-12 p70, and TNF-alpha were suppressed throughout the cerebral wound healing process. Based on our findings, quantitative cytokine analyses at the cerebral wound site may be a useful tool for wound age estimation. Further, this study suggests that multiplex data gained from the same sample using a single methodology demonstrates highly accurate cytokine interactions during the process of cerebral wound healing.