Annexin A1 promotes timely resolution of inflammation in murine gout
Gout is a self‐limited inflammatory disease caused by deposition of monosodium urate (MSU) crystals in the joints. Resolution of inflammation is an active process leading to restoration of tissue homeostasis. Here, we studied the role of Annexin A1 (AnxA1), a glucocorticoid‐regulated protein that ha...
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| Veröffentlicht in: | European journal of immunology 2017-03, Vol.47 (3), p.585-596 |
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| creator | Galvão, Izabela Vago, Juliana P. Barroso, Livia C. Tavares, Luciana P. Queiroz‐Junior, Celso M. Costa, Vivian V. Carneiro, Fernanda S. Ferreira, Tatiana P. Silva, Patricia M. R. Amaral, Flávio A. Sousa, Lirlândia P. Teixeira, Mauro M. |
| description | Gout is a self‐limited inflammatory disease caused by deposition of monosodium urate (MSU) crystals in the joints. Resolution of inflammation is an active process leading to restoration of tissue homeostasis. Here, we studied the role of Annexin A1 (AnxA1), a glucocorticoid‐regulated protein that has anti‐inflammatory and proresolving actions, in resolution of acute gouty inflammation. Injection of MSU crystals in the knee joint of mice induced inflammation that was associated with expression of AnxA1 during the resolving phase of inflammation. Neutralization of AnxA1 with antiserum or blockade of its receptor with BOC‐1 (nonselective) or WRW4 (selective) prevented the spontaneous resolution of gout. There was greater neutrophil infiltration after challenge with MSU crystals in AnxA1 knockout mice (AnxA1−/−) and delayed resolution associated to decreased neutrophil apoptosis and efferocytosis. Pretreatment of mice with AnxA1‐active N‐terminal peptide (Ac2–26) decreased neutrophil influx, IL‐1β, and CXCL1 production in periarticular joint. Posttreatment with Ac2–26 decreased neutrophil accumulation, IL‐1β, and hypernociception, and improved the articular histopathological score. Importantly, the therapeutic effects of Ac2–26 were associated with increased neutrophils apoptosis and shortened resolution intervals. In conclusion, AnxA1 plays a crucial role in the context of acute gouty inflammation by promoting timely resolution of inflammation.
Endogenous Annexin A1 regulates the intensity and duration of inflammation induced by MSU crystals. Exogenous Annexin A1 has anti‐inflammatory effects and drives resolution of inflammation. |
| doi_str_mv | 10.1002/eji.201646551 |
| format | Article |
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Endogenous Annexin A1 regulates the intensity and duration of inflammation induced by MSU crystals. Exogenous Annexin A1 has anti‐inflammatory effects and drives resolution of inflammation.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.201646551</identifier><identifier>PMID: 27995621</identifier><identifier>CODEN: EJIMAF</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Animals ; Annexin A1 ; Annexin A1 - genetics ; Annexin A1 - metabolism ; Annexin A1 - therapeutic use ; Anti-Inflammatory Agents - therapeutic use ; Antibodies, Blocking - administration & dosage ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Cell Movement - drug effects ; Disease Models, Animal ; Gout ; Gout - chemically induced ; Gout - drug therapy ; Gout - immunology ; Humans ; Inflammation ; Inflammation - drug therapy ; Inflammation - immunology ; Joints - drug effects ; Joints - immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils ; Neutrophils - drug effects ; Neutrophils - physiology ; Oligopeptides - administration & dosage ; Peptides - therapeutic use ; Phagocytosis - drug effects ; Phagocytosis - genetics ; Resolution of inflammation ; Rheumatism ; Rodents ; Uric Acid</subject><ispartof>European journal of immunology, 2017-03, Vol.47 (3), p.585-596</ispartof><rights>2016 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</rights><rights>2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4369-b40638c41f8704fd2f4e291bdc15b7ca89141f6b01e133461b9e33b2fafd50553</citedby><cites>FETCH-LOGICAL-c4369-b40638c41f8704fd2f4e291bdc15b7ca89141f6b01e133461b9e33b2fafd50553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.201646551$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.201646551$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,1435,27933,27934,45583,45584,46418,46842</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27995621$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galvão, Izabela</creatorcontrib><creatorcontrib>Vago, Juliana P.</creatorcontrib><creatorcontrib>Barroso, Livia C.</creatorcontrib><creatorcontrib>Tavares, Luciana P.</creatorcontrib><creatorcontrib>Queiroz‐Junior, Celso M.</creatorcontrib><creatorcontrib>Costa, Vivian V.</creatorcontrib><creatorcontrib>Carneiro, Fernanda S.</creatorcontrib><creatorcontrib>Ferreira, Tatiana P.</creatorcontrib><creatorcontrib>Silva, Patricia M. R.</creatorcontrib><creatorcontrib>Amaral, Flávio A.</creatorcontrib><creatorcontrib>Sousa, Lirlândia P.</creatorcontrib><creatorcontrib>Teixeira, Mauro M.</creatorcontrib><title>Annexin A1 promotes timely resolution of inflammation in murine gout</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>Gout is a self‐limited inflammatory disease caused by deposition of monosodium urate (MSU) crystals in the joints. Resolution of inflammation is an active process leading to restoration of tissue homeostasis. Here, we studied the role of Annexin A1 (AnxA1), a glucocorticoid‐regulated protein that has anti‐inflammatory and proresolving actions, in resolution of acute gouty inflammation. Injection of MSU crystals in the knee joint of mice induced inflammation that was associated with expression of AnxA1 during the resolving phase of inflammation. Neutralization of AnxA1 with antiserum or blockade of its receptor with BOC‐1 (nonselective) or WRW4 (selective) prevented the spontaneous resolution of gout. There was greater neutrophil infiltration after challenge with MSU crystals in AnxA1 knockout mice (AnxA1−/−) and delayed resolution associated to decreased neutrophil apoptosis and efferocytosis. Pretreatment of mice with AnxA1‐active N‐terminal peptide (Ac2–26) decreased neutrophil influx, IL‐1β, and CXCL1 production in periarticular joint. Posttreatment with Ac2–26 decreased neutrophil accumulation, IL‐1β, and hypernociception, and improved the articular histopathological score. Importantly, the therapeutic effects of Ac2–26 were associated with increased neutrophils apoptosis and shortened resolution intervals. In conclusion, AnxA1 plays a crucial role in the context of acute gouty inflammation by promoting timely resolution of inflammation.
Endogenous Annexin A1 regulates the intensity and duration of inflammation induced by MSU crystals. Exogenous Annexin A1 has anti‐inflammatory effects and drives resolution of inflammation.</description><subject>Animals</subject><subject>Annexin A1</subject><subject>Annexin A1 - genetics</subject><subject>Annexin A1 - metabolism</subject><subject>Annexin A1 - therapeutic use</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antibodies, Blocking - administration & dosage</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Cell Movement - drug effects</subject><subject>Disease Models, Animal</subject><subject>Gout</subject><subject>Gout - chemically induced</subject><subject>Gout - drug therapy</subject><subject>Gout - immunology</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - immunology</subject><subject>Joints - drug effects</subject><subject>Joints - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neutrophils</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - physiology</subject><subject>Oligopeptides - administration & dosage</subject><subject>Peptides - therapeutic use</subject><subject>Phagocytosis - drug effects</subject><subject>Phagocytosis - genetics</subject><subject>Resolution of inflammation</subject><subject>Rheumatism</subject><subject>Rodents</subject><subject>Uric Acid</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kD1PwzAQhi0EoqUwsqJILCwpPn8lHqtSoKgSC8xRPmzkKrZLnAj67zG0dGBgudNJz7169SB0CXgKGJNbtTZTgkEwwTkcoTFwAikDBsdojDGwlMgcj9BZCGuMsRRcnqIRyaTkgsAY3c2cU5_GJTNINp23vlch6Y1V7TbpVPDt0BvvEq8T43RbWlv-3PHBDp1xKnnzQ3-OTnTZBnWx3xP0er94mT-mq-eH5Xy2SmtGhUwrhgXNawY6zzDTDdFMEQlVUwOvsrrMZaytRYVBAaVMQCUVpRXRpW445pxO0M0uNzZ9H1ToC2tCrdq2dMoPoYA8h0zEKSJ6_Qdd-6FzsV2ksmiLCSkjle6ouvMhdEoXm87YstsWgItvvUXUWxz0Rv5qnzpUVjUH-tdnBMgO-DCt2v6fViyeljQnkn4B_GODTA</recordid><startdate>201703</startdate><enddate>201703</enddate><creator>Galvão, Izabela</creator><creator>Vago, Juliana P.</creator><creator>Barroso, Livia C.</creator><creator>Tavares, Luciana P.</creator><creator>Queiroz‐Junior, Celso M.</creator><creator>Costa, Vivian V.</creator><creator>Carneiro, Fernanda S.</creator><creator>Ferreira, Tatiana P.</creator><creator>Silva, Patricia M. R.</creator><creator>Amaral, Flávio A.</creator><creator>Sousa, Lirlândia P.</creator><creator>Teixeira, Mauro M.</creator><general>Wiley Subscription Services, Inc</general><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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>201703</creationdate><title>Annexin A1 promotes timely resolution of inflammation in murine gout</title><author>Galvão, Izabela ; Vago, Juliana P. ; Barroso, Livia C. ; Tavares, Luciana P. ; Queiroz‐Junior, Celso M. ; Costa, Vivian V. ; Carneiro, Fernanda S. ; Ferreira, Tatiana P. ; Silva, Patricia M. 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R.</creatorcontrib><creatorcontrib>Amaral, Flávio A.</creatorcontrib><creatorcontrib>Sousa, Lirlândia P.</creatorcontrib><creatorcontrib>Teixeira, Mauro M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>European journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galvão, Izabela</au><au>Vago, Juliana P.</au><au>Barroso, Livia C.</au><au>Tavares, Luciana P.</au><au>Queiroz‐Junior, Celso M.</au><au>Costa, Vivian V.</au><au>Carneiro, Fernanda S.</au><au>Ferreira, Tatiana P.</au><au>Silva, Patricia M. R.</au><au>Amaral, Flávio A.</au><au>Sousa, Lirlândia P.</au><au>Teixeira, Mauro M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Annexin A1 promotes timely resolution of inflammation in murine gout</atitle><jtitle>European journal of immunology</jtitle><addtitle>Eur J Immunol</addtitle><date>2017-03</date><risdate>2017</risdate><volume>47</volume><issue>3</issue><spage>585</spage><epage>596</epage><pages>585-596</pages><issn>0014-2980</issn><eissn>1521-4141</eissn><coden>EJIMAF</coden><abstract>Gout is a self‐limited inflammatory disease caused by deposition of monosodium urate (MSU) crystals in the joints. Resolution of inflammation is an active process leading to restoration of tissue homeostasis. Here, we studied the role of Annexin A1 (AnxA1), a glucocorticoid‐regulated protein that has anti‐inflammatory and proresolving actions, in resolution of acute gouty inflammation. Injection of MSU crystals in the knee joint of mice induced inflammation that was associated with expression of AnxA1 during the resolving phase of inflammation. Neutralization of AnxA1 with antiserum or blockade of its receptor with BOC‐1 (nonselective) or WRW4 (selective) prevented the spontaneous resolution of gout. There was greater neutrophil infiltration after challenge with MSU crystals in AnxA1 knockout mice (AnxA1−/−) and delayed resolution associated to decreased neutrophil apoptosis and efferocytosis. Pretreatment of mice with AnxA1‐active N‐terminal peptide (Ac2–26) decreased neutrophil influx, IL‐1β, and CXCL1 production in periarticular joint. Posttreatment with Ac2–26 decreased neutrophil accumulation, IL‐1β, and hypernociception, and improved the articular histopathological score. Importantly, the therapeutic effects of Ac2–26 were associated with increased neutrophils apoptosis and shortened resolution intervals. In conclusion, AnxA1 plays a crucial role in the context of acute gouty inflammation by promoting timely resolution of inflammation.
Endogenous Annexin A1 regulates the intensity and duration of inflammation induced by MSU crystals. Exogenous Annexin A1 has anti‐inflammatory effects and drives resolution of inflammation.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>27995621</pmid><doi>10.1002/eji.201646551</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Annexin A1 Annexin A1 - genetics Annexin A1 - metabolism Annexin A1 - therapeutic use Anti-Inflammatory Agents - therapeutic use Antibodies, Blocking - administration & dosage Apoptosis Apoptosis - drug effects Apoptosis - genetics Cell Movement - drug effects Disease Models, Animal Gout Gout - chemically induced Gout - drug therapy Gout - immunology Humans Inflammation Inflammation - drug therapy Inflammation - immunology Joints - drug effects Joints - immunology Mice Mice, Inbred C57BL Mice, Knockout Neutrophils Neutrophils - drug effects Neutrophils - physiology Oligopeptides - administration & dosage Peptides - therapeutic use Phagocytosis - drug effects Phagocytosis - genetics Resolution of inflammation Rheumatism Rodents Uric Acid |
| title | Annexin A1 promotes timely resolution of inflammation in murine gout |
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