| Literature DB >> 34140358 |
Korbinian Kienle1,2,3, Katharina M Glaser1,2,3, Sarah Eickhoff4, Michael Mihlan1, Konrad Knöpper4, Eduardo Reátegui5,6, Maximilian W Epple1,2,3, Matthias Gunzer7,8, Ralf Baumeister9, Teresa K Tarrant10, Ronald N Germain11, Daniel Irimia5, Wolfgang Kastenmüller4, Tim Lämmermann12.
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.Entities:
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Year: 2021 PMID: 34140358 PMCID: PMC8926156 DOI: 10.1126/science.abe7729
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 63.714