Neutrophil swarms protect healthy tissues by sealing off sites of infection. In the absence of swarming, microbial invasion of surrounding tissues can result in severe infections. Recent observations in animal models have shown that swarming requires rapid neutrophil responses and well-choreographed neutrophil migration patterns. However, in animal models, physical access to the molecular signals coordinating neutrophil activities during swarming is limited. Here, we report the development and validation of large microscale arrays of zymosan particle clusters for the study of human neutrophils during swarming ex vivo. We characterized the synchronized swarming of human neutrophils under the guidance of neutrophil-released chemokines, and measured the mediators released at different phases of human-neutrophil swarming against targets simulating infections. We found that the network of mediators coordinating human-neutrophil swarming includes start and stop signals, proteolytic enzymes and enzyme inhibitors, as well as modulators of activation of other immune and non-immune cells. We also show that the swarming behaviour of neutrophils from patients following major trauma is deficient and gives rise to smaller swarms than those of neutrophils from healthy individuals.

中性粒细胞群通过封闭感染部位来保护健康组织。在无群的情况下，微生物入侵周围组织会导致严重感染。动物模型中的最新观察表明，蜂群需要快速的嗜中性粒细胞反应和精心编排的嗜中性粒细胞迁移模式。但是，在动物模型中，在蜂拥而至时，协调分子调节中性粒细胞活动的分子信号的物理通路受到限制。在这里，我们在蜂拥报道的人中性粒细胞的研究酵母多糖颗粒簇大微尺度阵列的开发和验证体外。我们在嗜中性粒细胞释放的趋化因子的指导下表征了人类嗜中性粒细胞的同步群，并针对模拟感染的靶标测量了人类嗜中性粒细胞群不同阶段释放的介体。我们发现，协调人类嗜中性粒细胞聚集的介体网络包括起始和终止信号，蛋白水解酶和酶抑制剂，以及其他免疫和非免疫细胞激活的调节剂。我们还显示，严重创伤后患者的嗜中性粒细胞群聚集不足，并且与健康个体的嗜中性粒细胞群相比，群体较小。