Host inflammatory response profiling in preeclampsia using an in vitro whole blood stimulation model
Host inflammatory response profiling in preeclampsia using an in vitro whole blood stimulation model
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DOI：
10.1080/10641950701826067
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发表时间：
2008-01-01
影响因子：
1.5
通讯作者：
Walker, J. J.
中科院分区：
文献类型：
--
作者：
Brewster, J. A.;Orsi, N. M.;Walker, J. J.
先兆子痫 (PET) 的病理生理学涉及炎症功能障碍。这项研究通过用脂多糖挑战全血来描述这种宿主反应。多重免疫分析测定白细胞介素 (IL)-1 beta IL-2、IL-4、IL-5、IL-6、IL-7、IL-8、IL-10、IL-12(p70)、IL-13、IL-17、粒细胞/粒细胞巨噬细胞集落刺激因子 (G-CSF/GM-SCF)、干扰素 (IFN)-γ 单核细胞趋化蛋白 (MCP)-1、巨噬细胞炎症蛋白 1 β 和肿瘤坏死因子 (TNF) α 水平。分泌能力以皮克/百万白细胞或单核细胞 (SEM) 表示。 PET 具有显着更高的 IL-1、IL-2、IL-10、IL-13、G-CSF、IFN-γ MCP-1 和 TNF-α 单核细胞分泌能力 (p < 0.05)。 PET 组表现出炎症高反应性 (p < 0.01)，传统的 Th1:Th2 二分法很难描述这一点。
The pathophysiology of preeclampsia (PET) implicates an inflammatory dysfunction. This study profiled this host response by challenging whole blood with lipopolysaccharide. Multiplex immunoassays determined interleukin (IL)-1 beta IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12(p70), IL-13, IL-17, granulocyte/granulocyte macrophage-colony stimulating factors (G-CSF/GM-SCF), interferon(IFN)-gamma monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein-1 beta and tumor necrosis factor (TNF)-alpha levels. Secretory capacity was expressed in pg/million white cells or monocytes (SEM). PET featured significantly higher IL-1, IL-2, IL-10, IL-13, G-CSF, IFN-gamma MCP-1 and TNF-alpha monocyte secretory capacities (p < 0.05). The PET group exhibited an inflammatory hyper-responsiveness (p < 0.01) which was poorly described by the traditional Th1:Th2 dichotomy.