德国马克斯·普朗克免疫生物学和表观遗传学研究所Tim Lmmermann课题组发现，中性粒细胞通过自我限性聚集来抑制体内细菌生长。这一研究成果于2021年6月18日发表在国际学术期刊《科学》上。

使用转基因小鼠，研究人员发现中性粒细胞已经进化出一种内在机制来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）脱敏作为一种负反馈控制，当中性粒细胞感觉到高浓度的自我分泌引诱剂时，它们会阻止中性粒细胞的迁移，这些引诱剂最初会放大聚集。对这一过程的干扰能够使得中性粒细胞扫描更大的组织区域来寻找微生物。

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会受阻。这些数据揭示了自动信号如何阻止自组织的聚集行为，以及中性粒细胞趋化性和捕获的微调平衡如何抵抗细菌逃逸。

据悉，中性粒细胞相互交流，从而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。

附：英文原文

Title: Neutrophils self-limit swarming to contain bacterial growth in vivo

Author: Korbinian Kienle, Katharina M. Glaser, Sarah Eickhoff, Michael Mihlan, Konrad Knpper, Eduardo Reátegui, Maximilian W. Epple, Matthias Gunzer, Ralf Baumeister, Teresa K. Tarrant, Ronald N. Germain, Daniel Irimia, Wolfgang Kastenmüller, Tim Lmmermann

Issue&Volume: 2021/06/18

Abstract: 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.

DOI: 10.1126/science.abe7729

Source: https://science.sciencemag.org/content/372/6548/eabe7729