PPARγ and the Innate Immune System Mediate the Resolution of Inflammation

The resolution of inflammation is an active and dynamic process, mediated in large part by the innate immune system. Resolution represents not only an increase in anti-inflammatory actions, but also a paradigm shift in immune cell function to restore homeostasis. PPARγ, a ligand activated transcript...

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Main Authors: Amanda Croasdell, Parker F. Duffney, Nina Kim, Shannon H. Lacy, Patricia J. Sime, Richard P. Phipps
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2015/549691
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author Amanda Croasdell
Parker F. Duffney
Nina Kim
Shannon H. Lacy
Patricia J. Sime
Richard P. Phipps
author_facet Amanda Croasdell
Parker F. Duffney
Nina Kim
Shannon H. Lacy
Patricia J. Sime
Richard P. Phipps
author_sort Amanda Croasdell
collection DOAJ
description The resolution of inflammation is an active and dynamic process, mediated in large part by the innate immune system. Resolution represents not only an increase in anti-inflammatory actions, but also a paradigm shift in immune cell function to restore homeostasis. PPARγ, a ligand activated transcription factor, has long been studied for its anti-inflammatory actions, but an emerging body of literature is investigating the role of PPARγ and its ligands (including thiazolidinediones, prostaglandins, and oleanolic acids) in all phases of resolution. PPARγ can shift production from pro- to anti-inflammatory mediators by neutrophils, platelets, and macrophages. PPARγ and its ligands further modulate platelet and neutrophil function, decreasing trafficking, promoting neutrophil apoptosis, and preventing platelet-leukocyte interactions. PPARγ alters macrophage trafficking, increases efferocytosis and phagocytosis, and promotes alternative M2 macrophage activation. There are also roles for this receptor in the adaptive immune response, particularly regarding B cells. These effects contribute towards the attenuation of multiple disease states, including COPD, colitis, Alzheimer’s disease, and obesity in animal models. Finally, novel specialized proresolving mediators—eicosanoids with critical roles in resolution—may act through PPARγ modulation to promote resolution, providing another exciting area of therapeutic potential for this receptor.
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spelling doaj-art-4a86b54c4ea44ea3909b0fa8846da2002025-02-03T07:23:51ZengWileyPPAR Research1687-47571687-47652015-01-01201510.1155/2015/549691549691PPARγ and the Innate Immune System Mediate the Resolution of InflammationAmanda Croasdell0Parker F. Duffney1Nina Kim2Shannon H. Lacy3Patricia J. Sime4Richard P. Phipps5Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USAThe resolution of inflammation is an active and dynamic process, mediated in large part by the innate immune system. Resolution represents not only an increase in anti-inflammatory actions, but also a paradigm shift in immune cell function to restore homeostasis. PPARγ, a ligand activated transcription factor, has long been studied for its anti-inflammatory actions, but an emerging body of literature is investigating the role of PPARγ and its ligands (including thiazolidinediones, prostaglandins, and oleanolic acids) in all phases of resolution. PPARγ can shift production from pro- to anti-inflammatory mediators by neutrophils, platelets, and macrophages. PPARγ and its ligands further modulate platelet and neutrophil function, decreasing trafficking, promoting neutrophil apoptosis, and preventing platelet-leukocyte interactions. PPARγ alters macrophage trafficking, increases efferocytosis and phagocytosis, and promotes alternative M2 macrophage activation. There are also roles for this receptor in the adaptive immune response, particularly regarding B cells. These effects contribute towards the attenuation of multiple disease states, including COPD, colitis, Alzheimer’s disease, and obesity in animal models. Finally, novel specialized proresolving mediators—eicosanoids with critical roles in resolution—may act through PPARγ modulation to promote resolution, providing another exciting area of therapeutic potential for this receptor.http://dx.doi.org/10.1155/2015/549691
spellingShingle Amanda Croasdell
Parker F. Duffney
Nina Kim
Shannon H. Lacy
Patricia J. Sime
Richard P. Phipps
PPARγ and the Innate Immune System Mediate the Resolution of Inflammation
PPAR Research
title PPARγ and the Innate Immune System Mediate the Resolution of Inflammation
title_full PPARγ and the Innate Immune System Mediate the Resolution of Inflammation
title_fullStr PPARγ and the Innate Immune System Mediate the Resolution of Inflammation
title_full_unstemmed PPARγ and the Innate Immune System Mediate the Resolution of Inflammation
title_short PPARγ and the Innate Immune System Mediate the Resolution of Inflammation
title_sort pparγ and the innate immune system mediate the resolution of inflammation
url http://dx.doi.org/10.1155/2015/549691
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