Immunoregulatory mechanisms of macrophage PPAR-γ in mice with experimental inflammatory bowel disease.
Identifieur interne : 000047 ( PubMed/Curation ); précédent : 000046; suivant : 000048Immunoregulatory mechanisms of macrophage PPAR-γ in mice with experimental inflammatory bowel disease.
Auteurs : R. Hontecillas [États-Unis] ; W T Horne ; M. Climent ; A J Guri ; C. Evans ; Y. Zhang ; B W Sobral ; J. Bassaganya-RieraSource :
- Mucosal immunology [ 1935-3456 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents (pharmacology), Anti-Inflammatory Agents (therapeutic use), Cells, Cultured, Colitis (chemically induced), Colitis (drug therapy), Colitis (immunology), Colon (pathology), Computational Biology, Dextran Sulfate (administration & dosage), Disease Models, Animal, Gene Expression Regulation (immunology), Humans, Immunomodulation, Inflammatory Bowel Diseases (drug therapy), Inflammatory Bowel Diseases (immunology), Macrophages (drug effects), Macrophages (immunology), Macrophages (metabolism), Macrophages (pathology), Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Microarray Analysis, Mucous Membrane (pathology), PPAR gamma (antagonists & inhibitors), PPAR gamma (genetics), PPAR gamma (immunology), PPAR gamma (metabolism), T-Lymphocyte Subsets (drug effects), T-Lymphocyte Subsets (immunology), T-Lymphocyte Subsets (metabolism), T-Lymphocyte Subsets (pathology), T-Lymphocytes, Regulatory (drug effects), T-Lymphocytes, Regulatory (immunology), T-Lymphocytes, Regulatory (metabolism), T-Lymphocytes, Regulatory (pathology), Thiazolidinediones (pharmacology), Thiazolidinediones (therapeutic use).
- MESH :
- chemical , administration & dosage : Dextran Sulfate.
- chemical , antagonists & inhibitors : PPAR gamma.
- chemical , genetics : PPAR gamma.
- chemical , immunology : PPAR gamma.
- chemical , metabolism : PPAR gamma.
- chemical , pharmacology : Anti-Inflammatory Agents, Thiazolidinediones.
- chemical , therapeutic use : Anti-Inflammatory Agents, Thiazolidinediones.
- chemically induced : Colitis.
- drug effects : Macrophages, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory.
- drug therapy : Colitis, Inflammatory Bowel Diseases.
- immunology : Colitis, Gene Expression Regulation, Inflammatory Bowel Diseases, Macrophages, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory.
- metabolism : Macrophages, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory.
- pathology : Colon, Macrophages, Mucous Membrane, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory.
- Animals, Cells, Cultured, Computational Biology, Disease Models, Animal, Humans, Immunomodulation, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Microarray Analysis.
Abstract
Peroxisome proliferator-activated receptor-γ (PPAR-γ) is widely expressed in macrophages and has been identified as a putative target for the development of novel therapies against inflammatory bowel disease (IBD). Computational simulations identified macrophages as key targets for therapeutic interventions against IBD. This study aimed to characterize the mechanisms underlying the beneficial effects of macrophage PPAR-γ in IBD. Macrophage-specific PPAR-γ deletion significantly exacerbated clinical activity and colonic pathology, impaired the splenic and mesenteric lymph node regulatory T-cell compartment, increased percentages of lamina propria (LP) CD8+ T cells, increased surface expression of CD40, Ly6C, and Toll-like receptor 4 (TLR-4) in LP macrophages, and upregulated expression of colonic IFN-γ, CXCL9, CXCL10, IL-22, IL1RL1, CCR1, suppressor of cytokine signaling 3, and MHC class II in mice with IBD. Moreover, macrophage PPAR-γ was required for accelerating pioglitazone-mediated recovery from dextran sodium sulfate (DSS) colitis, providing a cellular target for the anti-inflammatory effects of PPAR-γ agonists in IBD.
DOI: 10.1038/mi.2010.75
PubMed: 21068720
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pubmed:21068720Le document en format XML
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<author><name sortKey="Bassaganya Riera, J" sort="Bassaganya Riera, J" uniqKey="Bassaganya Riera J" first="J" last="Bassaganya-Riera">J. Bassaganya-Riera</name>
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<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Anti-Inflammatory Agents (therapeutic use)</term>
<term>Cells, Cultured</term>
<term>Colitis (chemically induced)</term>
<term>Colitis (drug therapy)</term>
<term>Colitis (immunology)</term>
<term>Colon (pathology)</term>
<term>Computational Biology</term>
<term>Dextran Sulfate (administration & dosage)</term>
<term>Disease Models, Animal</term>
<term>Gene Expression Regulation (immunology)</term>
<term>Humans</term>
<term>Immunomodulation</term>
<term>Inflammatory Bowel Diseases (drug therapy)</term>
<term>Inflammatory Bowel Diseases (immunology)</term>
<term>Macrophages (drug effects)</term>
<term>Macrophages (immunology)</term>
<term>Macrophages (metabolism)</term>
<term>Macrophages (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Mutant Strains</term>
<term>Microarray Analysis</term>
<term>Mucous Membrane (pathology)</term>
<term>PPAR gamma (antagonists & inhibitors)</term>
<term>PPAR gamma (genetics)</term>
<term>PPAR gamma (immunology)</term>
<term>PPAR gamma (metabolism)</term>
<term>T-Lymphocyte Subsets (drug effects)</term>
<term>T-Lymphocyte Subsets (immunology)</term>
<term>T-Lymphocyte Subsets (metabolism)</term>
<term>T-Lymphocyte Subsets (pathology)</term>
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<term>T-Lymphocytes, Regulatory (immunology)</term>
<term>T-Lymphocytes, Regulatory (metabolism)</term>
<term>T-Lymphocytes, Regulatory (pathology)</term>
<term>Thiazolidinediones (pharmacology)</term>
<term>Thiazolidinediones (therapeutic use)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>PPAR gamma</term>
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<term>Thiazolidinediones</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Thiazolidinediones</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Colitis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages</term>
<term>T-Lymphocyte Subsets</term>
<term>T-Lymphocytes, Regulatory</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Colitis</term>
<term>Inflammatory Bowel Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Colitis</term>
<term>Gene Expression Regulation</term>
<term>Inflammatory Bowel Diseases</term>
<term>Macrophages</term>
<term>T-Lymphocyte Subsets</term>
<term>T-Lymphocytes, Regulatory</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term>
<term>T-Lymphocyte Subsets</term>
<term>T-Lymphocytes, Regulatory</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Colon</term>
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<term>Mucous Membrane</term>
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<term>T-Lymphocytes, Regulatory</term>
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<term>Immunomodulation</term>
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<front><div type="abstract" xml:lang="en">Peroxisome proliferator-activated receptor-γ (PPAR-γ) is widely expressed in macrophages and has been identified as a putative target for the development of novel therapies against inflammatory bowel disease (IBD). Computational simulations identified macrophages as key targets for therapeutic interventions against IBD. This study aimed to characterize the mechanisms underlying the beneficial effects of macrophage PPAR-γ in IBD. Macrophage-specific PPAR-γ deletion significantly exacerbated clinical activity and colonic pathology, impaired the splenic and mesenteric lymph node regulatory T-cell compartment, increased percentages of lamina propria (LP) CD8+ T cells, increased surface expression of CD40, Ly6C, and Toll-like receptor 4 (TLR-4) in LP macrophages, and upregulated expression of colonic IFN-γ, CXCL9, CXCL10, IL-22, IL1RL1, CCR1, suppressor of cytokine signaling 3, and MHC class II in mice with IBD. Moreover, macrophage PPAR-γ was required for accelerating pioglitazone-mediated recovery from dextran sodium sulfate (DSS) colitis, providing a cellular target for the anti-inflammatory effects of PPAR-γ agonists in IBD.</div>
</front>
</TEI>
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<Abstract><AbstractText>Peroxisome proliferator-activated receptor-γ (PPAR-γ) is widely expressed in macrophages and has been identified as a putative target for the development of novel therapies against inflammatory bowel disease (IBD). Computational simulations identified macrophages as key targets for therapeutic interventions against IBD. This study aimed to characterize the mechanisms underlying the beneficial effects of macrophage PPAR-γ in IBD. Macrophage-specific PPAR-γ deletion significantly exacerbated clinical activity and colonic pathology, impaired the splenic and mesenteric lymph node regulatory T-cell compartment, increased percentages of lamina propria (LP) CD8+ T cells, increased surface expression of CD40, Ly6C, and Toll-like receptor 4 (TLR-4) in LP macrophages, and upregulated expression of colonic IFN-γ, CXCL9, CXCL10, IL-22, IL1RL1, CCR1, suppressor of cytokine signaling 3, and MHC class II in mice with IBD. Moreover, macrophage PPAR-γ was required for accelerating pioglitazone-mediated recovery from dextran sodium sulfate (DSS) colitis, providing a cellular target for the anti-inflammatory effects of PPAR-γ agonists in IBD.</AbstractText>
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<CommentsCorrections RefType="Cites"><RefSource>Am J Nephrol. 2006;26(4):356-62</RefSource>
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<CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2010 Apr;176(4):1816-27</RefSource>
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