Document Detail


PPARγ activation normalizes resolution of acute sterile inflammation in murine chronic granulomatous disease.
MedLine Citation:
PMID:  20693431     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Absence of a functional nicotinamide adenine dinucleotide phosphate (NADPH) oxidase predisposes chronic granulomatous disease (CGD) patients to infection, and also to unexplained, exaggerated inflammation. The impaired recognition and removal (efferocytosis) of apoptotic neutrophils by CGD macrophages may contribute to this effect. We hypothesized that peroxisome proliferator-activated receptor γ (PPARγ) activation during CGD inflammation is deficient, leading to altered macrophage programming and decreased efferocytosis, and that PPARγ agonism would enhance resolution. using the gp91(phox-/-) murine model of X-linked CGD in a well-characterized model of sterile, zymosan-induced peritonitis, it was demonstrated that PPARγ expression and activation in CGD macrophages were significantly deficient at baseline, and acquisition was delayed over the course of inflammation relative to that of wild-type. Efferocytosis by macrophages reflected PPARγ activation during peritonitis and was impaired in CGD mice (versus wild-type), leading to accumulation of apoptotic neutrophils. Importantly, provision of the PPARγ agonist, pioglitazone, either prophylactically or during inflammation, significantly enhanced macrophage PPARγ-mediated programming and efferocytosis, reduced accumulation of apoptotic neutrophils, and normalized the course of peritonitis in CGD mice. As such, PPARγ may be a therapeutic target for CGD, and possibly other inflammatory conditions where aberrant macrophage programming and impaired efferocytosis delay resolution of inflammation.
Authors:
Ruby Fernandez-Boyanapalli; S Courtney Frasch; David W H Riches; R William Vandivier; Peter M Henson; Donna L Bratton
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-08-06
Journal Detail:
Title:  Blood     Volume:  116     ISSN:  1528-0020     ISO Abbreviation:  Blood     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-26     Completed Date:  2011-01-13     Revised Date:  2012-04-04    
Medline Journal Info:
Nlm Unique ID:  7603509     Medline TA:  Blood     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4512-22     Citation Subset:  AIM; IM    
Affiliation:
Department of Pediatrics, National Jewish Health, Denver, CO, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cytokines / immunology
Gene Deletion
Gene Expression Regulation / drug effects
Granulomatous Disease, Chronic / complications*,  drug therapy*,  immunology
Humans
Inflammation / chemically induced,  complications,  drug therapy,  immunology
Macrophages / drug effects,  immunology,  metabolism
Male
Membrane Glycoproteins / genetics
Mice
Mice, Inbred C57BL
NADPH Oxidase / genetics
Neutrophils / drug effects
PPAR gamma / agonists*,  genetics,  immunology*
Peritonitis / chemically induced,  complications*,  drug therapy*,  immunology
Thiazolidinediones / therapeutic use*
Zymosan
Grant Support
ID/Acronym/Agency:
A1058228//PHS HHS; GM61031/GM/NIGMS NIH HHS; HL34303/HL/NHLBI NIH HHS; HL68864/HL/NHLBI NIH HHS; HL81151/HL/NHLBI NIH HHS; R01 HL068864-09/HL/NHLBI NIH HHS; R01 HL081151-07/HL/NHLBI NIH HHS; R01 HL081151-08/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Membrane Glycoproteins; 0/PPAR gamma; 0/Thiazolidinediones; 111025-46-8/pioglitazone; 9010-72-4/Zymosan; EC 1.6.3.1/Cybb protein, mouse; EC 1.6.3.1/NADPH Oxidase

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