Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease
Adenosine has been implicated as an important regulator of the inflammatory response. Four subtypes of adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) have been described, of which A 2A potentially inhibits inflammation. The aim of this study was to investigate the role of A 2A in mucosal inflamm...
Gespeichert in:
| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2005-07, Vol.129 (1), p.26-33 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 33 |
|---|---|
| container_issue | 1 |
| container_start_page | 26 |
| container_title | Gastroenterology (New York, N.Y. 1943) |
| container_volume | 129 |
| creator | Odashima, Masaru Bamias, Giorgos Rivera-Nieves, Jesus Linden, Joel Nast, Cynthia C Moskaluk, Christopher A Marini, Marco Sugawara, Kazuhiko Kozaiwa, Kosuke Otaka, Michiro Watanabe, Sumio Cominelli, Fabio |
| description | Adenosine has been implicated as an important regulator of the inflammatory response. Four subtypes of adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) have been described, of which A 2A potentially inhibits inflammation. The aim of this study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A agonist (ATL-146e) to experimental models of inflammatory bowel disease.
The anti-inflammatory effects of ATL-146e were studied in the acute and chronic rabbit formalin-immune complex models of colitis and the SAMP1/YitFc mouse model of spontaneous ileitis.
ATL-146e significantly reduced the acute inflammatory index and tissue necrosis compared with vehicle ( P < .01) in the acute model of rabbit immune colitis. In the chronic rabbit immune colitis model, ATL-146e significantly suppressed inflammatory cell infiltration into the colonic mucosa ( P < .05) and prevented mortality. The administration of ATL-146e significantly decreased the chronic inflammatory index ( P < .01) and villus distortion index ( P < .01) in the ileum of SAMP1/YitFc mice, and ameliorated adoptively transferred ileitis in severe combined immunodeficient mice injected with CD4 + T cells from SAMP1/Yit mice ( P < .05). Tumor necrosis factor, interferon gamma, and interleukin 4 concentrations were significantly suppressed by ATL-146e treatment in supernatants from cultures of mesenteric lymph node cells of SAMP1/YitFc mice ( P < .05 vs vehicle-treated mice).
A 2A adenosine receptor activation by ATL-146e significantly reduced inflammation in the intestinal mucosa. This effect was associated with decreased leukocyte infiltration and inhibition of proinflammatory cytokines. Activation of A 2A by selective agonism may therefore serve as a novel therapy for the treatment of inflammatory bowel disease. |
| doi_str_mv | 10.1053/j.gastro.2005.05.032 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68024391</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68024391</sourcerecordid><originalsourceid>FETCH-LOGICAL-c286t-83c04a78e824004d685dcecbc87ccc7a38b18512feff38697eab3cd392c450063</originalsourceid><addsrcrecordid>eNpFUE1LAzEQzUGxtfoPRHLy1jpJ9iN7LMUvKHjRc8hmZyVlN6lJWum_d5ctCo-ZYXjvMfMIuWOwYpCLx93qS8cU_IoD5KsRgl-QOQArljnIfEauY9wBQCUkuyIzVgDjlWBzclybZI86We-ob-mar6lu0PloHdKABvfJB6pTQnfQCSO1bqjJOt0NY9vpvp_E1lHtbD-se99gF0e3P4IPJ1r7H-xoYyPqiDfkstVdxNtzX5DP56ePzety-_7ytllvl4bLIi2lMJDpUqLkGUDWFDJvDJrayNIYU2ohayZzxltsWyGLqkRdC9OIipssByjEgjxMvvvgvw_D4aq30WDXaYf-EFUhgWeiYgMxm4gm-BgDtmofhm_CSTFQY8Zqp6aM1ZixGiH4ILs_-x_qHpt_0Tlg8Qv7uX7F</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68024391</pqid></control><display><type>article</type><title>Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><source>Alma/SFX Local Collection</source><creator>Odashima, Masaru ; Bamias, Giorgos ; Rivera-Nieves, Jesus ; Linden, Joel ; Nast, Cynthia C ; Moskaluk, Christopher A ; Marini, Marco ; Sugawara, Kazuhiko ; Kozaiwa, Kosuke ; Otaka, Michiro ; Watanabe, Sumio ; Cominelli, Fabio</creator><creatorcontrib>Odashima, Masaru ; Bamias, Giorgos ; Rivera-Nieves, Jesus ; Linden, Joel ; Nast, Cynthia C ; Moskaluk, Christopher A ; Marini, Marco ; Sugawara, Kazuhiko ; Kozaiwa, Kosuke ; Otaka, Michiro ; Watanabe, Sumio ; Cominelli, Fabio</creatorcontrib><description><![CDATA[Adenosine has been implicated as an important regulator of the inflammatory response. Four subtypes of adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) have been described, of which A 2A potentially inhibits inflammation. The aim of this study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A agonist (ATL-146e) to experimental models of inflammatory bowel disease.
The anti-inflammatory effects of ATL-146e were studied in the acute and chronic rabbit formalin-immune complex models of colitis and the SAMP1/YitFc mouse model of spontaneous ileitis.
ATL-146e significantly reduced the acute inflammatory index and tissue necrosis compared with vehicle ( P < .01) in the acute model of rabbit immune colitis. In the chronic rabbit immune colitis model, ATL-146e significantly suppressed inflammatory cell infiltration into the colonic mucosa ( P < .05) and prevented mortality. The administration of ATL-146e significantly decreased the chronic inflammatory index ( P < .01) and villus distortion index ( P < .01) in the ileum of SAMP1/YitFc mice, and ameliorated adoptively transferred ileitis in severe combined immunodeficient mice injected with CD4 + T cells from SAMP1/Yit mice ( P < .05). Tumor necrosis factor, interferon gamma, and interleukin 4 concentrations were significantly suppressed by ATL-146e treatment in supernatants from cultures of mesenteric lymph node cells of SAMP1/YitFc mice ( P < .05 vs vehicle-treated mice).
A 2A adenosine receptor activation by ATL-146e significantly reduced inflammation in the intestinal mucosa. This effect was associated with decreased leukocyte infiltration and inhibition of proinflammatory cytokines. Activation of A 2A by selective agonism may therefore serve as a novel therapy for the treatment of inflammatory bowel disease.]]></description><identifier>ISSN: 0016-5085</identifier><identifier>DOI: 10.1053/j.gastro.2005.05.032</identifier><identifier>PMID: 16012931</identifier><language>eng</language><publisher>United States</publisher><subject>Acute Disease ; Adoptive Transfer ; Animals ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Chronic Disease ; Colitis - drug therapy ; Colitis - immunology ; Colitis - metabolism ; Cyclohexanecarboxylic Acids - pharmacology ; Cytokines - metabolism ; Disease Models, Animal ; Formaldehyde ; Ileitis - drug therapy ; Ileitis - immunology ; Ileitis - metabolism ; Inflammatory Bowel Diseases - drug therapy ; Inflammatory Bowel Diseases - immunology ; Inflammatory Bowel Diseases - metabolism ; Male ; Mice ; Mice, SCID ; Purines - pharmacology ; Rabbits ; Receptor, Adenosine A2A - metabolism ; Recurrence</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2005-07, Vol.129 (1), p.26-33</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c286t-83c04a78e824004d685dcecbc87ccc7a38b18512feff38697eab3cd392c450063</citedby><cites>FETCH-LOGICAL-c286t-83c04a78e824004d685dcecbc87ccc7a38b18512feff38697eab3cd392c450063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16012931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Odashima, Masaru</creatorcontrib><creatorcontrib>Bamias, Giorgos</creatorcontrib><creatorcontrib>Rivera-Nieves, Jesus</creatorcontrib><creatorcontrib>Linden, Joel</creatorcontrib><creatorcontrib>Nast, Cynthia C</creatorcontrib><creatorcontrib>Moskaluk, Christopher A</creatorcontrib><creatorcontrib>Marini, Marco</creatorcontrib><creatorcontrib>Sugawara, Kazuhiko</creatorcontrib><creatorcontrib>Kozaiwa, Kosuke</creatorcontrib><creatorcontrib>Otaka, Michiro</creatorcontrib><creatorcontrib>Watanabe, Sumio</creatorcontrib><creatorcontrib>Cominelli, Fabio</creatorcontrib><title>Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description><![CDATA[Adenosine has been implicated as an important regulator of the inflammatory response. Four subtypes of adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) have been described, of which A 2A potentially inhibits inflammation. The aim of this study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A agonist (ATL-146e) to experimental models of inflammatory bowel disease.
The anti-inflammatory effects of ATL-146e were studied in the acute and chronic rabbit formalin-immune complex models of colitis and the SAMP1/YitFc mouse model of spontaneous ileitis.
ATL-146e significantly reduced the acute inflammatory index and tissue necrosis compared with vehicle ( P < .01) in the acute model of rabbit immune colitis. In the chronic rabbit immune colitis model, ATL-146e significantly suppressed inflammatory cell infiltration into the colonic mucosa ( P < .05) and prevented mortality. The administration of ATL-146e significantly decreased the chronic inflammatory index ( P < .01) and villus distortion index ( P < .01) in the ileum of SAMP1/YitFc mice, and ameliorated adoptively transferred ileitis in severe combined immunodeficient mice injected with CD4 + T cells from SAMP1/Yit mice ( P < .05). Tumor necrosis factor, interferon gamma, and interleukin 4 concentrations were significantly suppressed by ATL-146e treatment in supernatants from cultures of mesenteric lymph node cells of SAMP1/YitFc mice ( P < .05 vs vehicle-treated mice).
A 2A adenosine receptor activation by ATL-146e significantly reduced inflammation in the intestinal mucosa. This effect was associated with decreased leukocyte infiltration and inhibition of proinflammatory cytokines. Activation of A 2A by selective agonism may therefore serve as a novel therapy for the treatment of inflammatory bowel disease.]]></description><subject>Acute Disease</subject><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Chronic Disease</subject><subject>Colitis - drug therapy</subject><subject>Colitis - immunology</subject><subject>Colitis - metabolism</subject><subject>Cyclohexanecarboxylic Acids - pharmacology</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Formaldehyde</subject><subject>Ileitis - drug therapy</subject><subject>Ileitis - immunology</subject><subject>Ileitis - metabolism</subject><subject>Inflammatory Bowel Diseases - drug therapy</subject><subject>Inflammatory Bowel Diseases - immunology</subject><subject>Inflammatory Bowel Diseases - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Purines - pharmacology</subject><subject>Rabbits</subject><subject>Receptor, Adenosine A2A - metabolism</subject><subject>Recurrence</subject><issn>0016-5085</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUE1LAzEQzUGxtfoPRHLy1jpJ9iN7LMUvKHjRc8hmZyVlN6lJWum_d5ctCo-ZYXjvMfMIuWOwYpCLx93qS8cU_IoD5KsRgl-QOQArljnIfEauY9wBQCUkuyIzVgDjlWBzclybZI86We-ob-mar6lu0PloHdKABvfJB6pTQnfQCSO1bqjJOt0NY9vpvp_E1lHtbD-se99gF0e3P4IPJ1r7H-xoYyPqiDfkstVdxNtzX5DP56ePzety-_7ytllvl4bLIi2lMJDpUqLkGUDWFDJvDJrayNIYU2ohayZzxltsWyGLqkRdC9OIipssByjEgjxMvvvgvw_D4aq30WDXaYf-EFUhgWeiYgMxm4gm-BgDtmofhm_CSTFQY8Zqp6aM1ZixGiH4ILs_-x_qHpt_0Tlg8Qv7uX7F</recordid><startdate>200507</startdate><enddate>200507</enddate><creator>Odashima, Masaru</creator><creator>Bamias, Giorgos</creator><creator>Rivera-Nieves, Jesus</creator><creator>Linden, Joel</creator><creator>Nast, Cynthia C</creator><creator>Moskaluk, Christopher A</creator><creator>Marini, Marco</creator><creator>Sugawara, Kazuhiko</creator><creator>Kozaiwa, Kosuke</creator><creator>Otaka, Michiro</creator><creator>Watanabe, Sumio</creator><creator>Cominelli, Fabio</creator><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>200507</creationdate><title>Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease</title><author>Odashima, Masaru ; Bamias, Giorgos ; Rivera-Nieves, Jesus ; Linden, Joel ; Nast, Cynthia C ; Moskaluk, Christopher A ; Marini, Marco ; Sugawara, Kazuhiko ; Kozaiwa, Kosuke ; Otaka, Michiro ; Watanabe, Sumio ; Cominelli, Fabio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c286t-83c04a78e824004d685dcecbc87ccc7a38b18512feff38697eab3cd392c450063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acute Disease</topic><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Chronic Disease</topic><topic>Colitis - drug therapy</topic><topic>Colitis - immunology</topic><topic>Colitis - metabolism</topic><topic>Cyclohexanecarboxylic Acids - pharmacology</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Formaldehyde</topic><topic>Ileitis - drug therapy</topic><topic>Ileitis - immunology</topic><topic>Ileitis - metabolism</topic><topic>Inflammatory Bowel Diseases - drug therapy</topic><topic>Inflammatory Bowel Diseases - immunology</topic><topic>Inflammatory Bowel Diseases - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Purines - pharmacology</topic><topic>Rabbits</topic><topic>Receptor, Adenosine A2A - metabolism</topic><topic>Recurrence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Odashima, Masaru</creatorcontrib><creatorcontrib>Bamias, Giorgos</creatorcontrib><creatorcontrib>Rivera-Nieves, Jesus</creatorcontrib><creatorcontrib>Linden, Joel</creatorcontrib><creatorcontrib>Nast, Cynthia C</creatorcontrib><creatorcontrib>Moskaluk, Christopher A</creatorcontrib><creatorcontrib>Marini, Marco</creatorcontrib><creatorcontrib>Sugawara, Kazuhiko</creatorcontrib><creatorcontrib>Kozaiwa, Kosuke</creatorcontrib><creatorcontrib>Otaka, Michiro</creatorcontrib><creatorcontrib>Watanabe, Sumio</creatorcontrib><creatorcontrib>Cominelli, Fabio</creatorcontrib><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>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Odashima, Masaru</au><au>Bamias, Giorgos</au><au>Rivera-Nieves, Jesus</au><au>Linden, Joel</au><au>Nast, Cynthia C</au><au>Moskaluk, Christopher A</au><au>Marini, Marco</au><au>Sugawara, Kazuhiko</au><au>Kozaiwa, Kosuke</au><au>Otaka, Michiro</au><au>Watanabe, Sumio</au><au>Cominelli, Fabio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2005-07</date><risdate>2005</risdate><volume>129</volume><issue>1</issue><spage>26</spage><epage>33</epage><pages>26-33</pages><issn>0016-5085</issn><abstract><![CDATA[Adenosine has been implicated as an important regulator of the inflammatory response. Four subtypes of adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) have been described, of which A 2A potentially inhibits inflammation. The aim of this study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A agonist (ATL-146e) to experimental models of inflammatory bowel disease.
The anti-inflammatory effects of ATL-146e were studied in the acute and chronic rabbit formalin-immune complex models of colitis and the SAMP1/YitFc mouse model of spontaneous ileitis.
ATL-146e significantly reduced the acute inflammatory index and tissue necrosis compared with vehicle ( P < .01) in the acute model of rabbit immune colitis. In the chronic rabbit immune colitis model, ATL-146e significantly suppressed inflammatory cell infiltration into the colonic mucosa ( P < .05) and prevented mortality. The administration of ATL-146e significantly decreased the chronic inflammatory index ( P < .01) and villus distortion index ( P < .01) in the ileum of SAMP1/YitFc mice, and ameliorated adoptively transferred ileitis in severe combined immunodeficient mice injected with CD4 + T cells from SAMP1/Yit mice ( P < .05). Tumor necrosis factor, interferon gamma, and interleukin 4 concentrations were significantly suppressed by ATL-146e treatment in supernatants from cultures of mesenteric lymph node cells of SAMP1/YitFc mice ( P < .05 vs vehicle-treated mice).
A 2A adenosine receptor activation by ATL-146e significantly reduced inflammation in the intestinal mucosa. This effect was associated with decreased leukocyte infiltration and inhibition of proinflammatory cytokines. Activation of A 2A by selective agonism may therefore serve as a novel therapy for the treatment of inflammatory bowel disease.]]></abstract><cop>United States</cop><pmid>16012931</pmid><doi>10.1053/j.gastro.2005.05.032</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0016-5085 |
| ispartof | Gastroenterology (New York, N.Y. 1943), 2005-07, Vol.129 (1), p.26-33 |
| issn | 0016-5085 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_68024391 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present); Alma/SFX Local Collection |
| subjects | Acute Disease Adoptive Transfer Animals CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Chronic Disease Colitis - drug therapy Colitis - immunology Colitis - metabolism Cyclohexanecarboxylic Acids - pharmacology Cytokines - metabolism Disease Models, Animal Formaldehyde Ileitis - drug therapy Ileitis - immunology Ileitis - metabolism Inflammatory Bowel Diseases - drug therapy Inflammatory Bowel Diseases - immunology Inflammatory Bowel Diseases - metabolism Male Mice Mice, SCID Purines - pharmacology Rabbits Receptor, Adenosine A2A - metabolism Recurrence |
| title | Activation of A2A adenosine receptor attenuates intestinal inflammation in animal models of inflammatory bowel disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T09%3A24%3A30IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Activation%20of%20A2A%20adenosine%20receptor%20attenuates%20intestinal%20inflammation%20in%20animal%20models%20of%20inflammatory%20bowel%20disease&rft.jtitle=Gastroenterology%20(New%20York,%20N.Y.%201943)&rft.au=Odashima,%20Masaru&rft.date=2005-07&rft.volume=129&rft.issue=1&rft.spage=26&rft.epage=33&rft.pages=26-33&rft.issn=0016-5085&rft_id=info:doi/10.1053/j.gastro.2005.05.032&rft_dat=%3Cproquest_cross%3E68024391%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=68024391&rft_id=info:pmid/16012931&rfr_iscdi=true |