Aziz K A, Cawley J C, Kamiguti A S, Zuzel M
Department of Haematology, University of Liverpool.
Br J Haematol. 1995 Sep;91(1):46-54. doi: 10.1111/j.1365-2141.1995.tb05243.x.
Mutual interactions between neutrophils (PMN) and platelets are recognized to be important in modulating the respective functions of these two cell types. Here we show that primary granule secretion from appropriately-stimulated PMN can lead to complete proteolytic removal of GPIb from the platelet surface. Thus, when the PMN in PMN/platelet mixtures were stimulated by FMLP, platelets lost GPIb as measured by ristocetin-induced aggregation, flow cytometry and SDS-PAGE analysis. This loss was most marked when PMN were primed by GM-CSF, and could be inhibited by a specific elastase inhibitor. As expected, the alpha 1-antiproteinase in plasma inhibited GPIb loss, but when PMN were strongly stimulated by FMLP and GM-CSF in the presence of platelets this inhibition was incomplete or absent. It is concluded that joint priming of PMN with GM-CSF and platelets can cause a previously unrecognized degree of primary granule secretion which, via elastase, leads to platelet GPIb loss. We suggest that this loss is likely to be of physiological and pathophysiological importance.
中性粒细胞（PMN）与血小板之间的相互作用被认为在调节这两种细胞类型各自的功能中起着重要作用。在此我们表明，适当刺激的PMN的初级颗粒分泌可导致血小板表面的GPIb被完全蛋白水解去除。因此，当用FMLP刺激PMN/血小板混合物中的PMN时，通过瑞斯托霉素诱导的聚集、流式细胞术和SDS-PAGE分析测量，血小板失去了GPIb。当PMN用GM-CSF预处理时，这种损失最为明显，并且可以被一种特异性弹性蛋白酶抑制剂抑制。正如预期的那样，血浆中的α1-抗蛋白酶抑制了GPIb的损失，但是当在血小板存在的情况下用FMLP和GM-CSF强烈刺激PMN时，这种抑制不完全或不存在。结论是，用GM-CSF和血小板对PMN进行联合预处理可导致先前未被认识到的初级颗粒分泌程度，这通过弹性蛋白酶导致血小板GPIb丢失。我们认为这种丢失可能具有生理和病理生理重要性。
