Department of Clinical Chemistry, F-1-219, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, The Netherlands.
Placenta. 2007 Aug-Sep;28(8-9):928-35. doi: 10.1016/j.placenta.2007.02.008. Epub 2007 Apr 12.
Inflammation plays a major role in the vascular dysfunction seen in preeclampsia, and several studies suggest involvement of the complement system.
To investigate whether complement activation on the surface of microparticles is increased in plasma of preeclamptic patients versus healthy pregnant controls.
Microparticles from plasma of preeclamptic (n=10), healthy pregnant (n=10) and healthy nonpregnant (n=10) women were analyzed by flow cytometry for bound complement components (C1q, C4, C3) and complement activator molecules (C-reactive protein [CRP], serum amyloid P component [SAP], immunoglobulin [Ig]M, IgG). Fluid phase complement activation products and activator molecules were also determined.
Levels of microparticles with bound complement components showed no increase in complement activation on the microparticle surface in preeclamptic women, in line with levels of fluid phase complement activation products. In healthy nonpregnant and pregnant women, bound CRP was associated with classical pathway activation on the microparticle surface, and in healthy pregnant women IgM and IgG molecules also contributed. In preeclamptic women, microparticles with bound SAP and those with IgG seemed to contribute to C1q binding without a clear association to further classical pathway activation. Furthermore, significantly increased levels of microparticles with bound CRP were present in preeclamptic compared with healthy pregnant women (median 178x10(6)/L versus 47x10(6)/L, P<0.01), but without concomitant increases in complement activation.
We found no evidence of increased complement activation on the microparticle surface in preeclamptic women. Microparticles with bound CRP were significantly increased, but in contrast to healthy pregnant and nonpregnant women, this was not associated with increased classical pathway activation on the surface of the microparticles.
炎症在子痫前期患者的血管功能障碍中起主要作用，有几项研究表明补体系统的参与。
研究子痫前期患者血浆中微粒上的补体激活是否高于健康孕妇对照。
通过流式细胞术分析来自子痫前期（n=10）、健康妊娠（n=10）和健康非妊娠（n=10）妇女的血浆中的微粒，以分析结合的补体成分（C1q、C4、C3）和补体激活分子（C 反应蛋白[CRP]、血清淀粉样蛋白 P 成分[SAP]、免疫球蛋白[Ig]M、IgG）。还测定了体液相补体激活产物和激活分子。
子痫前期妇女微粒上结合的补体成分水平没有增加补体在微粒表面的激活，与体液相补体激活产物水平一致。在健康非妊娠和妊娠妇女中，结合的 CRP 与微粒表面的经典途径激活有关，而在健康妊娠妇女中，IgM 和 IgG 分子也有贡献。在子痫前期妇女中，结合的 SAP 和 IgG 的微粒似乎有助于 C1q 结合，但与进一步的经典途径激活没有明确关联。此外，与健康妊娠妇女相比，子痫前期妇女结合 CRP 的微粒水平显著升高（中位数 178x10(6)/L 与 47x10(6)/L，P<0.01），但补体激活没有增加。
我们没有发现子痫前期妇女微粒表面补体激活增加的证据。结合 CRP 的微粒显著增加，但与健康妊娠和非妊娠妇女不同，这与微粒表面经典途径激活没有增加有关。
