Activation of PPARγ and δ by dietary punicic acid ameliorates intestinal inflammation in mice
The goal of the present study was to elucidate the mechanisms of immunoregulation by which dietary punicic acid (PUA) prevents or ameliorates experimental inflammatory bowel disease (IBD). The expression of PPARγ and δ, their responsive genes and pro-inflammatory cytokines was assayed in the colonic...
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| Veröffentlicht in: | British journal of nutrition 2011-09, Vol.106 (6), p.878-886 |
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| creator | Bassaganya-Riera, Josep DiGuardo, Margaret Climent, Montse Vives, Cristina Carbo, Adria Jouni, Zeina E. Einerhand, Alexandra W. C. O'Shea, Marianne Hontecillas, Raquel |
| description | The goal of the present study was to elucidate the mechanisms of immunoregulation by which dietary punicic acid (PUA) prevents or ameliorates experimental inflammatory bowel disease (IBD). The expression of PPARγ and δ, their responsive genes and pro-inflammatory cytokines was assayed in the colonic mucosa. Immune cell-specific PPARγ null, PPARδ knockout and wild-type mice were treated with PUA and challenged with 2·5 % dextran sodium sulphate (DSS). The prophylactic efficacy of PUA was examined in an IL-10− / − model of IBD. The effect of PUA on the regulatory T-cell (Treg) compartment was also examined in mice with experimental IBD. PUA ameliorated spontaneous pan-enteritis in IL-10− / − mice and DSS colitis, up-regulated Foxp3 expression in Treg and suppressed TNF-α, but the loss of functional PPARγ or δ impaired these anti-inflammatory effects. At the cellular level, the macrophage-specific deletion of PPARγ caused a complete abrogation of the protective effect of PUA, whereas the deletion of PPARδ or intestinal epithelial cell-specific PPARγ decreased its anti-inflammatory efficacy. We provide in vivo molecular evidence demonstrating that PUA ameliorates experimental IBD by regulating macrophage and T-cell function through PPARγ- and δ-dependent mechanisms. |
| doi_str_mv | 10.1017/S0007114511001188 |
| format | Article |
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C. ; O'Shea, Marianne ; Hontecillas, Raquel</creator><creatorcontrib>Bassaganya-Riera, Josep ; DiGuardo, Margaret ; Climent, Montse ; Vives, Cristina ; Carbo, Adria ; Jouni, Zeina E. ; Einerhand, Alexandra W. C. ; O'Shea, Marianne ; Hontecillas, Raquel</creatorcontrib><description>The goal of the present study was to elucidate the mechanisms of immunoregulation by which dietary punicic acid (PUA) prevents or ameliorates experimental inflammatory bowel disease (IBD). The expression of PPARγ and δ, their responsive genes and pro-inflammatory cytokines was assayed in the colonic mucosa. Immune cell-specific PPARγ null, PPARδ knockout and wild-type mice were treated with PUA and challenged with 2·5 % dextran sodium sulphate (DSS). The prophylactic efficacy of PUA was examined in an IL-10− / − model of IBD. The effect of PUA on the regulatory T-cell (Treg) compartment was also examined in mice with experimental IBD. PUA ameliorated spontaneous pan-enteritis in IL-10− / − mice and DSS colitis, up-regulated Foxp3 expression in Treg and suppressed TNF-α, but the loss of functional PPARγ or δ impaired these anti-inflammatory effects. At the cellular level, the macrophage-specific deletion of PPARγ caused a complete abrogation of the protective effect of PUA, whereas the deletion of PPARδ or intestinal epithelial cell-specific PPARγ decreased its anti-inflammatory efficacy. We provide in vivo molecular evidence demonstrating that PUA ameliorates experimental IBD by regulating macrophage and T-cell function through PPARγ- and δ-dependent mechanisms.</description><identifier>ISSN: 0007-1145</identifier><identifier>EISSN: 1475-2662</identifier><identifier>DOI: 10.1017/S0007114511001188</identifier><identifier>PMID: 21736821</identifier><identifier>CODEN: BJNUAV</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Animal Feed ; Animals ; anti-inflammatory activity ; Anti-Inflammatory Agents - pharmacology ; Biological and medical sciences ; colitis ; dextran ; Feeding. Feeding behavior ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; genes ; immunomodulation ; Inflammation ; Inflammatory Bowel Diseases - drug therapy ; Interleukin-10 - genetics ; Intestinal Mucosa - microbiology ; Intestines - metabolism ; Linolenic Acids - pharmacology ; macrophages ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; mucosa ; Nutritional Immunology ; PPAR delta - metabolism ; PPAR gamma - metabolism ; protective effect ; sodium sulfate ; T-Lymphocytes - cytology ; T-Lymphocytes, Regulatory - cytology ; tumor necrosis factor-alpha ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>British journal of nutrition, 2011-09, Vol.106 (6), p.878-886</ispartof><rights>Copyright © The Authors 2011</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-4e0e42335d1b55828923403ee7ca9b463d887d96e13189fb447e26870ae642e43</citedby><cites>FETCH-LOGICAL-c441t-4e0e42335d1b55828923403ee7ca9b463d887d96e13189fb447e26870ae642e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0007114511001188/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>164,314,780,784,27924,27925,55628</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24545563$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21736821$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bassaganya-Riera, Josep</creatorcontrib><creatorcontrib>DiGuardo, Margaret</creatorcontrib><creatorcontrib>Climent, Montse</creatorcontrib><creatorcontrib>Vives, Cristina</creatorcontrib><creatorcontrib>Carbo, Adria</creatorcontrib><creatorcontrib>Jouni, Zeina E.</creatorcontrib><creatorcontrib>Einerhand, Alexandra W. C.</creatorcontrib><creatorcontrib>O'Shea, Marianne</creatorcontrib><creatorcontrib>Hontecillas, Raquel</creatorcontrib><title>Activation of PPARγ and δ by dietary punicic acid ameliorates intestinal inflammation in mice</title><title>British journal of nutrition</title><addtitle>Br J Nutr</addtitle><description>The goal of the present study was to elucidate the mechanisms of immunoregulation by which dietary punicic acid (PUA) prevents or ameliorates experimental inflammatory bowel disease (IBD). The expression of PPARγ and δ, their responsive genes and pro-inflammatory cytokines was assayed in the colonic mucosa. Immune cell-specific PPARγ null, PPARδ knockout and wild-type mice were treated with PUA and challenged with 2·5 % dextran sodium sulphate (DSS). The prophylactic efficacy of PUA was examined in an IL-10− / − model of IBD. The effect of PUA on the regulatory T-cell (Treg) compartment was also examined in mice with experimental IBD. PUA ameliorated spontaneous pan-enteritis in IL-10− / − mice and DSS colitis, up-regulated Foxp3 expression in Treg and suppressed TNF-α, but the loss of functional PPARγ or δ impaired these anti-inflammatory effects. At the cellular level, the macrophage-specific deletion of PPARγ caused a complete abrogation of the protective effect of PUA, whereas the deletion of PPARδ or intestinal epithelial cell-specific PPARγ decreased its anti-inflammatory efficacy. We provide in vivo molecular evidence demonstrating that PUA ameliorates experimental IBD by regulating macrophage and T-cell function through PPARγ- and δ-dependent mechanisms.</description><subject>Animal Feed</subject><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>colitis</subject><subject>dextran</subject><subject>Feeding. Feeding behavior</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Deletion</subject><subject>genes</subject><subject>immunomodulation</subject><subject>Inflammation</subject><subject>Inflammatory Bowel Diseases - drug therapy</subject><subject>Interleukin-10 - genetics</subject><subject>Intestinal Mucosa - microbiology</subject><subject>Intestines - metabolism</subject><subject>Linolenic Acids - pharmacology</subject><subject>macrophages</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>mucosa</subject><subject>Nutritional Immunology</subject><subject>PPAR delta - metabolism</subject><subject>PPAR gamma - metabolism</subject><subject>protective effect</subject><subject>sodium sulfate</subject><subject>T-Lymphocytes - cytology</subject><subject>T-Lymphocytes, Regulatory - cytology</subject><subject>tumor necrosis factor-alpha</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0007-1145</issn><issn>1475-2662</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtuFDEQRS0URIbAB7Ah3kSsGlx-dLuXo4iESJGICFlb1e7qyFE_JnY3Ur6LfEe-CY9mAotIbPxQnbp16zL2AcRnEFB9uRZCVADaAAgBYO0rtgJdmUKWpTxgq2252NYP2duU7vLXgqjfsEMJlSqthBVzaz-HXziHaeRTx6-u1j-efnMcW_70yJsH3gaaMT7wzTIGHzxHH1qOA_VhijhT4mHM5xxG7POz63EYdmJh5EPw9I697rBP9H5_H7Gbs68_T78Vl9_PL07Xl4XXGuZCkyAtlTItNMZYaWuptFBElce60aVqra3auiRQYOuu0boiWdpKIJVaklZH7NNOdxOn-yU7ckNInvoeR5qW5GwthFJSmEzCjvRxSilS5zYxDHlHB8JtY3UvYs09H_fqSzNQ-7fjOccMnOwBTB77LuLoQ_rHaaONKVXmjndch5PD25iZm2spQOdBRuVVMqH29nBoYmhvyd1NS8z5pv8Y_AOStJeF</recordid><startdate>20110928</startdate><enddate>20110928</enddate><creator>Bassaganya-Riera, Josep</creator><creator>DiGuardo, Margaret</creator><creator>Climent, Montse</creator><creator>Vives, Cristina</creator><creator>Carbo, Adria</creator><creator>Jouni, Zeina E.</creator><creator>Einerhand, Alexandra W. C.</creator><creator>O'Shea, Marianne</creator><creator>Hontecillas, Raquel</creator><general>Cambridge University Press</general><general>CABI Pub</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20110928</creationdate><title>Activation of PPARγ and δ by dietary punicic acid ameliorates intestinal inflammation in mice</title><author>Bassaganya-Riera, Josep ; DiGuardo, Margaret ; Climent, Montse ; Vives, Cristina ; Carbo, Adria ; Jouni, Zeina E. ; Einerhand, Alexandra W. C. ; O'Shea, Marianne ; Hontecillas, Raquel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-4e0e42335d1b55828923403ee7ca9b463d887d96e13189fb447e26870ae642e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animal Feed</topic><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>colitis</topic><topic>dextran</topic><topic>Feeding. Feeding behavior</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Deletion</topic><topic>genes</topic><topic>immunomodulation</topic><topic>Inflammation</topic><topic>Inflammatory Bowel Diseases - drug therapy</topic><topic>Interleukin-10 - genetics</topic><topic>Intestinal Mucosa - microbiology</topic><topic>Intestines - metabolism</topic><topic>Linolenic Acids - pharmacology</topic><topic>macrophages</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>mucosa</topic><topic>Nutritional Immunology</topic><topic>PPAR delta - metabolism</topic><topic>PPAR gamma - metabolism</topic><topic>protective effect</topic><topic>sodium sulfate</topic><topic>T-Lymphocytes - cytology</topic><topic>T-Lymphocytes, Regulatory - cytology</topic><topic>tumor necrosis factor-alpha</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bassaganya-Riera, Josep</creatorcontrib><creatorcontrib>DiGuardo, Margaret</creatorcontrib><creatorcontrib>Climent, Montse</creatorcontrib><creatorcontrib>Vives, Cristina</creatorcontrib><creatorcontrib>Carbo, Adria</creatorcontrib><creatorcontrib>Jouni, Zeina E.</creatorcontrib><creatorcontrib>Einerhand, Alexandra W. C.</creatorcontrib><creatorcontrib>O'Shea, Marianne</creatorcontrib><creatorcontrib>Hontecillas, Raquel</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bassaganya-Riera, Josep</au><au>DiGuardo, Margaret</au><au>Climent, Montse</au><au>Vives, Cristina</au><au>Carbo, Adria</au><au>Jouni, Zeina E.</au><au>Einerhand, Alexandra W. C.</au><au>O'Shea, Marianne</au><au>Hontecillas, Raquel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of PPARγ and δ by dietary punicic acid ameliorates intestinal inflammation in mice</atitle><jtitle>British journal of nutrition</jtitle><addtitle>Br J Nutr</addtitle><date>2011-09-28</date><risdate>2011</risdate><volume>106</volume><issue>6</issue><spage>878</spage><epage>886</epage><pages>878-886</pages><issn>0007-1145</issn><eissn>1475-2662</eissn><coden>BJNUAV</coden><abstract>The goal of the present study was to elucidate the mechanisms of immunoregulation by which dietary punicic acid (PUA) prevents or ameliorates experimental inflammatory bowel disease (IBD). The expression of PPARγ and δ, their responsive genes and pro-inflammatory cytokines was assayed in the colonic mucosa. Immune cell-specific PPARγ null, PPARδ knockout and wild-type mice were treated with PUA and challenged with 2·5 % dextran sodium sulphate (DSS). The prophylactic efficacy of PUA was examined in an IL-10− / − model of IBD. The effect of PUA on the regulatory T-cell (Treg) compartment was also examined in mice with experimental IBD. PUA ameliorated spontaneous pan-enteritis in IL-10− / − mice and DSS colitis, up-regulated Foxp3 expression in Treg and suppressed TNF-α, but the loss of functional PPARγ or δ impaired these anti-inflammatory effects. At the cellular level, the macrophage-specific deletion of PPARγ caused a complete abrogation of the protective effect of PUA, whereas the deletion of PPARδ or intestinal epithelial cell-specific PPARγ decreased its anti-inflammatory efficacy. We provide in vivo molecular evidence demonstrating that PUA ameliorates experimental IBD by regulating macrophage and T-cell function through PPARγ- and δ-dependent mechanisms.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>21736821</pmid><doi>10.1017/S0007114511001188</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animal Feed Animals anti-inflammatory activity Anti-Inflammatory Agents - pharmacology Biological and medical sciences colitis dextran Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology Gene Deletion genes immunomodulation Inflammation Inflammatory Bowel Diseases - drug therapy Interleukin-10 - genetics Intestinal Mucosa - microbiology Intestines - metabolism Linolenic Acids - pharmacology macrophages Mice Mice, Inbred C57BL Mice, Transgenic mucosa Nutritional Immunology PPAR delta - metabolism PPAR gamma - metabolism protective effect sodium sulfate T-Lymphocytes - cytology T-Lymphocytes, Regulatory - cytology tumor necrosis factor-alpha Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Activation of PPARγ and δ by dietary punicic acid ameliorates intestinal inflammation in mice |
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