Pillitteri Daniele, Bassus Steffen, Boller Klaus, Mahnel René, Scholz Thomas, Westrup Dagmar, Wegert Wolfgang, Kirchmaier Carl M
Deutsche Klinik für Diagnostik, Wiesbaden, Germany.
Platelets. 2007 Mar;18(2):119-27. doi: 10.1080/09537100600800792.
A controversial discussion as to whether human platelets are capable of regulated protein synthesis has been ongoing for over half a century. A previous study has suggested that human platelets synthesize large amounts of interleukin 1beta (IL-1beta) in response to external cues and in a physiologically significant manner. However, cytokines such as IL-1beta are generally considered to be products of leukocytes and it could not be completely excluded that contaminating leukocytes may have contributed to the IL-1beta results in platelet preparations. It was therefore our intention to investigate whether residual leukocytes had an impact on thrombin-induced IL-1beta synthesis. Using various methods to reduce the level of contaminating leukocytes, we found that IL-1beta production in platelet-rich suspensions is dependent on the presence of leukocytes, as it was decreased by reducing the number of leukocytes. In addition, we found that thrombin-induced IL-1beta synthesis was completely eliminated in leukocyte-free platelet preparations and could be restored by adding leukocytes. IL-1beta synthesis could be detected in platelet suspensions contaminated with at least 1 leukocyte per 10(5) platelets. This study demonstrated that platelets are incapable of synthesizing detectable amounts of IL-1beta on their own. We suggest that any IL-1beta synthesis detected is a by-product of leukocytes contaminating the platelet preparations. Thus, the hypothesis that platelets producing IL-1beta, provide a new link between thrombosis and inflammation needs to be reconsidered.
关于人类血小板是否能够进行调节性蛋白质合成的争议性讨论已经持续了半个多世纪。先前的一项研究表明,人类血小板会响应外部信号并以生理上有意义的方式合成大量白细胞介素1β(IL-1β)。然而,诸如IL-1β之类的细胞因子通常被认为是白细胞的产物,并且不能完全排除污染的白细胞可能对血小板制剂中的IL-1β结果有所贡献。因此,我们的目的是研究残留白细胞是否对凝血酶诱导的IL-1β合成有影响。通过使用各种方法降低污染白细胞的水平,我们发现富含血小板的悬浮液中IL-1β的产生依赖于白细胞的存在,因为通过减少白细胞数量其会降低。此外,我们发现无白细胞的血小板制剂中凝血酶诱导的IL-1β合成完全消除,并且通过添加白细胞可以恢复。在每10(5)个血小板中至少污染1个白细胞的血小板悬浮液中可以检测到IL-1β合成。这项研究表明血小板自身无法合成可检测量的IL-1β。我们认为检测到的任何IL-1β合成都是污染血小板制剂的白细胞的副产物。因此,血小板产生IL-1β从而在血栓形成和炎症之间提供新联系的假设需要重新考虑。