Division of Molecular Surface Physics and Nanoscience, Department of Physics, Chemistry and Biology, Linköping University, SE-581 83 Linköping, Sweden.
Immunol Lett. 2012 Feb 29;142(1-2):28-33. doi: 10.1016/j.imlet.2011.11.003. Epub 2011 Nov 28.
Blood platelets express several receptors involved in immunity (e.g. complement-, toll-like- and Fcγ-receptors) and release inflammatory mediators. Furthermore, formation of platelet-leukocyte aggregates has an important role during inflammatory conditions such as coronary artery disease. Thus, apart from their well-known role in haemostasis, platelets are today also recognized as cells with immuno-modulatory properties. We have previously reported regulatory effects of complement protein 1q (C1q) on platelet activation in experimental setups using isolated cells. In the present study we have proceeded by investigating effects of C1q on collagen-induced aggregation, production of reactive oxygen species (ROS), formation of platelet-leukocyte aggregates and levels of soluble P-selectin in whole blood. Impedance measurements showed that C1q inhibited collagen-induced aggregation whereas it potentiated the collagen-provoked production of ROS in a luminol-dependent chemiluminescence assay. The effects of C1q on aggregation and ROS-production were dependent upon platelets, as they were no longer observed in presence of the platelet (GpIIb/IIIa) inhibitor Reopro. Furthermore, the levels of soluble P-selectin were found to be lowered upon treatment with C1q prior to addition of collagen. There was also a trend towards a decreased formation of large platelet-leukocyte aggregates in collagen-stimulated whole blood following C1q treatment. In conclusion, our data indicate that C1q could have a role in regulating platelet activation and associated leukocyte recruitment during vessel wall injury. This has implications for inflammatory disorders such as coronary artery disease.
血小板表达几种参与免疫的受体（例如补体、 toll 样和 Fcγ 受体），并释放炎症介质。此外，血小板-白细胞聚集体的形成在炎症状态下（如冠状动脉疾病）具有重要作用。因此，除了在止血方面的众所周知的作用外，血小板现在也被认为具有免疫调节特性的细胞。我们之前已经报道了补体蛋白 1q（C1q）对使用分离细胞的实验设置中的血小板活化的调节作用。在本研究中，我们通过研究 C1q 对胶原诱导的聚集、活性氧物质（ROS）的产生、血小板-白细胞聚集体的形成以及全血中可溶性 P-选择素水平的影响来进行研究。阻抗测量表明 C1q 抑制胶原诱导的聚集，而在发光依赖性化学发光测定中增强胶原引起的 ROS 的产生。C1q 对聚集和 ROS 产生的作用取决于血小板，因为在存在血小板（GpIIb/IIIa）抑制剂 Reopro 的情况下，这些作用不再观察到。此外，在添加胶原之前用 C1q 处理可降低可溶性 P-选择素的水平。胶原刺激的全血中 C1q 处理后，大血小板-白细胞聚集体的形成也呈下降趋势。总之，我们的数据表明 C1q 可能在调节血管壁损伤期间的血小板活化和相关白细胞募集中起作用。这对炎症性疾病（如冠状动脉疾病）有影响。
