Resolvin D2 is a potent regulator of leukocytes and controls microbial sepsis
Matthew Spite,
Lucy V. Norling,
Lisa Summers,
Rong Yang,
Dianne Cooper,
Nicos A. Petasis,
Roderick J. Flower,
Mauro Perretti and
Charles N. Serhan ()
Additional contact information
Matthew Spite: Center for Experimental Therapeutics and Reperfusion Injury, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
Lucy V. Norling: Center for Experimental Therapeutics and Reperfusion Injury, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
Lisa Summers: Center for Experimental Therapeutics and Reperfusion Injury, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
Rong Yang: Center for Experimental Therapeutics and Reperfusion Injury, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
Dianne Cooper: William Harvey Research Institute, Barts and the London Medical School, Queen Mary University of London
Nicos A. Petasis: University of Southern California, Los Angeles, California 90089, USA
Roderick J. Flower: William Harvey Research Institute, Barts and the London Medical School, Queen Mary University of London
Mauro Perretti: William Harvey Research Institute, Barts and the London Medical School, Queen Mary University of London
Charles N. Serhan: Center for Experimental Therapeutics and Reperfusion Injury, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
Nature, 2009, vol. 461, issue 7268, 1287-1291
Abstract:
Anti-inflammatory activity of resolvin D2 Resolvins, locally acting factors derived from omega-3 fatty acids, have been recognized as inflammation-resolving mediators. Experiments in a mouse abdominal sepsis model now show that resolvin D2 (RvD2) inhibits neutrophil trafficking to inflammatory sites and decreases leukocyte interactions with endothelial cells in a nitric oxide-dependent manner. RvD2's cellular and molecular actions translated to a dramatic increased survival. This work points to RvD2 as a potent anti-inflammatory agent and suggests new therapeutic approaches that do not compromise host defences.
Date: 2009
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:461:y:2009:i:7268:d:10.1038_nature08541
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DOI: 10.1038/nature08541
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