Skoglund Caroline, Wetterö Jonas, Skogh Thomas, Sjöwall Christopher, Tengvall Pentti, Bengtsson Torbjörn
Department of Physics, Chemistry and Biology, Materials in Medicine, Division of Applied Physics, Linköping University, Linköping, Sweden.
Immunol Cell Biol. 2008 Jul;86(5):466-74. doi: 10.1038/icb.2008.9. Epub 2008 Mar 11.
Blood platelets and C-reactive protein (CRP) are both used clinically as markers of ongoing inflammation, and both participate actively in inflammatory responses, although the biological effects are still incompletely understood. Rapidly adhering platelets express receptors for complement factor 1q (C1q) and the Fc part of immunoglobulin G (IgG), and CRP is known to activate/regulate complement via C1q binding, and to ligate FcgammaRs. In the present study, we used normal human IgG pre-adsorbed to a well-characterized methylated surface as a model solid-phase immune complex when investigating the effects of CRP and C1q on platelet adhesion and activation. Protein adsorption was characterized using ellipsometry and polyclonal antibodies, and human serum albumin (HSA) and non-coated surfaces were used as reference surfaces. Platelet adhesion to IgG and HSA was inhibited by both C1q and CRP. Furthermore, CRP (moderately) and C1q (markedly) decreased the spreading of adhering platelets. The combination of C1q and CRP was slightly more potent in reducing cell adhesion to IgG, and also impaired the adhesion to HSA and non-coated surfaces. Platelet production of thromboxane B2 (TXB(2)) was also reduced by C1q both in the presence and absence of CRP, whereas CRP alone had no effect on TXB(2) production. We conclude that CRP and C1q regulate the behaviour of platelets, and that this may be an important immunoregulatory mechanism during inflammatory conditions.
血小板和C反应蛋白（CRP）在临床上均被用作炎症持续的标志物，并且二者均积极参与炎症反应，尽管其生物学效应仍未被完全了解。快速黏附的血小板表达补体因子1q（C1q）和免疫球蛋白G（IgG）的Fc部分的受体，并且已知CRP通过与C1q结合来激活/调节补体，并连接Fcγ受体。在本研究中，我们使用预先吸附到特征明确的甲基化表面上的正常人IgG作为模型固相免疫复合物，来研究CRP和C1q对血小板黏附和激活的影响。使用椭圆偏振光法和多克隆抗体对蛋白质吸附进行表征，并使用人血清白蛋白（HSA）和未包被的表面作为参考表面。C1q和CRP均抑制血小板对IgG和HSA的黏附。此外，CRP（中度）和C1q（显著）减少了黏附血小板的铺展。C1q和CRP的组合在降低细胞对IgG的黏附方面稍强，并且也损害了对HSA和未包被表面的黏附。无论有无CRP存在，C1q均降低血小板血栓素B2（TXB₂）的产生，而单独的CRP对TXB₂的产生没有影响。我们得出结论，CRP和C1q调节血小板的行为，并且这可能是炎症状态下一种重要的免疫调节机制。
