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Neutrophils self-limit swarming to contain bacterial growth in vivo.
Kienle, Korbinian; Glaser, Katharina M; Eickhoff, Sarah; Mihlan, Michael; Knöpper, Konrad; Reátegui, Eduardo; Epple, Maximilian W; Gunzer, Matthias; Baumeister, Ralf; Tarrant, Teresa K; Germain, Ronald N; Irimia, Daniel; Kastenmüller, Wolfgang; Lämmermann, Tim.
  • Kienle K; Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
  • Glaser KM; International Max Planck Research School for Immunobiology, Epigenetics and Metabolism (IMPRS-IEM), Freiburg, Germany.
  • Eickhoff S; Faculty of Biology, University of Freiburg, Freiburg, Germany.
  • Mihlan M; Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
  • Knöpper K; International Max Planck Research School for Immunobiology, Epigenetics and Metabolism (IMPRS-IEM), Freiburg, Germany.
  • Reátegui E; Faculty of Biology, University of Freiburg, Freiburg, Germany.
  • Epple MW; Institute of Systems Immunology, University of Würzburg, Max Planck Research Group, Würzburg, Germany.
  • Gunzer M; Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
  • Baumeister R; Institute of Systems Immunology, University of Würzburg, Max Planck Research Group, Würzburg, Germany.
  • Tarrant TK; Center for Engineering in Medicine, Massachusetts General Hospital, Harvard Medical School, Shriners Hospital for Children, Boston, MA, USA.
  • Germain RN; William G. Lowrie Department of Chemical and Biomolecular Engineering, The Ohio State University, Columbus, OH, USA.
  • Irimia D; Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
  • Kastenmüller W; International Max Planck Research School for Immunobiology, Epigenetics and Metabolism (IMPRS-IEM), Freiburg, Germany.
  • Lämmermann T; Faculty of Biology, University of Freiburg, Freiburg, Germany.
Science ; 372(6548)2021 06 18.
Article en En | MEDLINE | ID: mdl-34140358
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.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Pseudomonas aeruginosa / Infecciones por Pseudomonas / Quimiotaxis de Leucocito / Quinasa 2 del Receptor Acoplado a Proteína-G / Ganglios Linfáticos / Neutrófilos Límite: Animals Idioma: En Año: 2021 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Pseudomonas aeruginosa / Infecciones por Pseudomonas / Quimiotaxis de Leucocito / Quinasa 2 del Receptor Acoplado a Proteína-G / Ganglios Linfáticos / Neutrófilos Límite: Animals Idioma: En Año: 2021 Tipo del documento: Article