PGE 2 production at sites of tissue injury promotes an anti-inflammatory neutrophil phenotype and determines the outcome of inflammation resolution in vivo

Author:

Loynes Catherine A.1ORCID,Lee Jou A.1,Robertson Anne L.12,Steel Michael JG.1ORCID,Ellett Felix13ORCID,Feng Yi4ORCID,Levy Bruce D.5ORCID,Whyte Moira K.B.4ORCID,Renshaw Stephen A.1ORCID

Affiliation:

1. The Bateson Centre, Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield Medical School, Beech Hill Road, Sheffield S10 2RX, UK.

2. Division of Hematology/Oncology, Boston Children’s Hospital and Harvard Medical School, Boston, MA 02115, USA.

3. BioMEMS Resource Center, Department of Surgery, Massachusetts General Hospital, Shriners Burns Hospital, Harvard Medical School, Boston, MA 02129, USA.

4. Medical Research Council Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK.

5. Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA.

Abstract

Neutrophil removal from inflammatory sites is regulated by lipid mediator signals between macrophages and neutrophils.

Funder

NIH Grant

MRC Centre Grant

Wellcome trust Sir Henry Dale Grant

MRC Senior Clinical Fellowship

MRC Programme Grant

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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