Neutrophils communicate with each other to form swarms in infected organs. Coordination of this population response is critical for the elimination of bacteria and fungi. Using transgenic mice, we found that neutrophils have evolved an intrinsic mechanism to self-limit swarming and avoid uncontrolled aggregation during inflammation. G protein–coupled receptor (GPCR) desensitization acts as a negative feedback control to stop migration of neutrophils when they sense high concentrations of self-secreted attractants that initially amplify swarming. Interference with this process allows neutrophils to scan larger tissue areas for microbes. Unexpectedly, this does not benefit bacterial clearance as containment of proliferating bacteria by neutrophil clusters becomes impeded. Our data reveal how autosignaling stops self-organized swarming behavior and how the finely tuned balance of neutrophil chemotaxis and arrest counteracts bacterial escape.

中性粒细胞相互交流，在受感染的器官中形成群。这种群体反应的协调对于消除细菌和真菌至关重要。使用转基因小鼠，我们发现中性粒细胞已经进化出一种内在机制，可以自我限制聚集并避免炎症期间不受控制的聚集。G 蛋白偶联受体 (GPCR) 脱敏作为负反馈控制，在中性粒细胞感觉到高浓度的自分泌引诱剂最初会放大蜂群时停止迁移。对这一过程的干扰允许中性粒细胞扫描更大的组织区域以寻找微生物。出乎意料的是，这不利于细菌清除，因为中性粒细胞簇对增殖细菌的遏制受到阻碍。