Neutrophils self-limit swarming to contain bacterial growth in vivo-Reference-Cited by-同舟云学术

Neutrophils self-limit swarming to contain bacterial growth in vivo

Published:2021-06-18 Issue:6548 Volume:372 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Kienle Korbinian¹²³^ORCID,Glaser Katharina M.¹²³^ORCID,Eickhoff Sarah⁴^ORCID,Mihlan Michael¹^ORCID,Knöpper Konrad⁴^ORCID,Reátegui Eduardo⁵⁶,Epple Maximilian W.¹²³,Gunzer Matthias⁷⁸^ORCID,Baumeister Ralf⁹^ORCID,Tarrant Teresa K.¹⁰^ORCID,Germain Ronald N.¹¹^ORCID,Irimia Daniel⁵^ORCID,Kastenmüller Wolfgang⁴^ORCID,Lämmermann Tim¹^ORCID

Affiliation:

1. Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.

2. International Max Planck Research School for Immunobiology, Epigenetics and Metabolism (IMPRS-IEM), Freiburg, Germany.

3. Faculty of Biology, University of Freiburg, Freiburg, Germany.

4. Institute of Systems Immunology, University of Würzburg, Max Planck Research Group, Würzburg, Germany.

5. Center for Engineering in Medicine, Massachusetts General Hospital, Harvard Medical School, Shriners Hospital for Children, Boston, MA, USA.

6. William G. Lowrie Department of Chemical and Biomolecular Engineering, The Ohio State University, Columbus, OH, USA.

7. Institute for Experimental Immunology and Imaging, University Hospital, University Duisburg-Essen, Essen, Germany.

8. Leibniz-Institut für Analytische Wissenschaften–ISAS–e.V., Dortmund, Germany.

9. Bioinformatics and Molecular Genetics, Faculty of Biology, Centre for Biochemistry and Molecular Cell Research, Faculty of Medicine, Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany.

10. Division of Rheumatology and Immunology, Department of Medicine, Duke University School of Medicine, Durham, NC, USA.

11. Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA.

Abstract

Stopping the swarm Neutrophils play a major role in the early immune response and are recruited in large numbers into inflamed and infected tissues. By secreting chemoattractants that bind G protein–coupled receptors (GPCRs) on neighboring cells, neutrophils coordinate their behavior as a swarm. Less clear is how this auto-amplifying swarming activity is ultimately turned off. Kienle et al. show that desensitization of these GPCRs by the same chemoattractants by GPCR-kinase 2 (GRK2) is one way in which these swarms are shut down (see the Perspective by Rocha-Gregg and Huttenlocher). Unexpectedly, mice with GRK2-deficient neutrophils showed impaired rather than enhanced bacterial clearance. The heightened scanning ability of GRK2-deficient neutrophils may come at the cost of suboptimal phagocytosis and containment of bacteria. Science , abe7729, this issue p. eabe7729 ; see also abj3065, p. 1262

Funder

Division of Intramural Research, National Institute of Allergy and Infectious Diseases

H2020 European Research Council

European Research Council

Deutsche Forschungsgemeinschaft

Max-Planck-Gesellschaft

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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