清除机体细菌，特别是血液循环中的细菌，是治疗感染的关键。我们的前期研究发现，血小板和其释放物质均能够通过促进中性粒细胞胞外诱捕网(NET) 形成提高捕获循环细菌的能力。由于血小板含有丰富高迁移率族蛋白（HMGB-1），它能够结合DNA而促进NET形成，提示血小板可能通过HMGB-1释放而促进NET形成。为此，本研究拟利用细胞培养和在体模型，研究血小板是否通过释放胞内物质而促进NET形成；通过分析不同细胞来源HMGB-1的氨基酸组成、功能，研究血小板源性HMGB-1的结构和功能特异性；通过体内、外三维立体动态观察、超分辨显微镜观察，并通过阻断HMGB-1，研究HMGB-1在血小板诱导NET形成中的作用；分别阻断反应体系中TLR和RAGE，研究HMGB-1的释放机制，以及介导NET形成机制。本课题的顺利实施将为NET的形成机制提供理论依据，并为临床抗感染治疗提供可行途径。

To eliminate the invaded bacteria, especial circulating bacteria, is key to improve the prognosis of patients with infection. Our pilot studies found that both platelet and the substances released from platelet can enhance the ability of capturing circulating bacteria via promoting the formation of neutrophil extracellular traps (NET). Because high mobility group box-1 protein (HMGB-1), which also plays a critical role in promoting the formation of NET, is reached in platelet, we therefore hypothesize that the formation of NET can be promoted by platelets via HMGB-1. To test this hypothesis, cell culture and in vivo models would be used to test whether platelets promote NET formation by releasing its intracellular substances; the structure (amino acid sequence) and function of HMGB-1 from both platelet and other types of cells would be analyzed. To identify the role of HMGB-1 in NET formation induced by platelet, HMGB-1 would be blocked in vivo and in vitro, and NET formation would be investigated under confocal and super-resolution microscopy. To elucidate the involved mechanisms, Toll like receptors and RAGE would be blocked in the reaction system respectively, and the release of HMGB-1 and the formation of NET would be observed. This study would provide a theoretical and experimental evidence to understand the elimination of bacteria after their invasion of the body. Therefore, it may provide a feasible approach to improve the prognosis of sepsis patients.