Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury
Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid-derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the...
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| Veröffentlicht in: | Mucosal immunology 2013-03, Vol.6 (2), p.256-266 |
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| creator | Eickmeier, O Seki, H Haworth, O Hilberath, J N Gao, F Uddin, M Croze, R H Carlo, T Pfeffer, M A Levy, B D |
| description | Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid-derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the effects of aspirin-triggered resolvin D1 (AT-RvD1; 7
S
,8
R
,17
R
-trihydroxy-4
Z
,9
E
,11
E
,13
Z
,15
E
,19
Z
-docosahexaenoic acid) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (∼0.5–5 μg kg
−1
) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ∼75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil–platelet heterotypic interactions by downregulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, Kupffer cells, and tumor necrosis factor-α, and decreased nuclear factor-κB-phosphorylated p65 nuclear translocation. Taken together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI. |
| doi_str_mv | 10.1038/mi.2012.66 |
| format | Article |
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S
,8
R
,17
R
-trihydroxy-4
Z
,9
E
,11
E
,13
Z
,15
E
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-docosahexaenoic acid) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (∼0.5–5 μg kg
−1
) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ∼75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil–platelet heterotypic interactions by downregulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, Kupffer cells, and tumor necrosis factor-α, and decreased nuclear factor-κB-phosphorylated p65 nuclear translocation. Taken together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI.</description><identifier>ISSN: 1933-0219</identifier><identifier>EISSN: 1935-3456</identifier><identifier>DOI: 10.1038/mi.2012.66</identifier><identifier>PMID: 22785226</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250/347 ; 631/250/516/1909 ; 692/699/1785 ; Acute Lung Injury - metabolism ; Acute Lung Injury - pathology ; Adaptor Proteins, Signal Transducing - metabolism ; Airway Resistance ; Allergology ; Animals ; Anti-Inflammatory Agents, Non-Steroidal - administration & dosage ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Antibodies ; Aspirin - administration & dosage ; Aspirin - pharmacology ; Biomedical and Life Sciences ; Biomedicine ; Blood Platelets - metabolism ; Blood-Air Barrier - physiopathology ; Disease Models, Animal ; Docosahexaenoic Acids - biosynthesis ; Docosahexaenoic Acids - metabolism ; Epinephrine - metabolism ; Gastroenterology ; Immunology ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation Mediators - metabolism ; Leukocytes - immunology ; Macrophages, Alveolar - metabolism ; Male ; Mice ; Neutrophils - immunology ; Pulmonary Edema - immunology ; Pulmonary Edema - metabolism ; Pulmonary Edema - pathology ; Receptors, Formyl Peptide - metabolism ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; Transcription Factor RelA - metabolism</subject><ispartof>Mucosal immunology, 2013-03, Vol.6 (2), p.256-266</ispartof><rights>Society for Mucosal Immunology 2013</rights><rights>Copyright Nature Publishing Group Mar 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-p172t-68399e8f25998bb0cd21e30e6b85b58e05e958df8db8eb435816fccad81f73193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1783037729?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>315,782,786,27933,27934,64394,64398,72478</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22785226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eickmeier, O</creatorcontrib><creatorcontrib>Seki, H</creatorcontrib><creatorcontrib>Haworth, O</creatorcontrib><creatorcontrib>Hilberath, J N</creatorcontrib><creatorcontrib>Gao, F</creatorcontrib><creatorcontrib>Uddin, M</creatorcontrib><creatorcontrib>Croze, R H</creatorcontrib><creatorcontrib>Carlo, T</creatorcontrib><creatorcontrib>Pfeffer, M A</creatorcontrib><creatorcontrib>Levy, B D</creatorcontrib><title>Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury</title><title>Mucosal immunology</title><addtitle>Mucosal Immunol</addtitle><addtitle>Mucosal Immunol</addtitle><description>Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid-derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the effects of aspirin-triggered resolvin D1 (AT-RvD1; 7
S
,8
R
,17
R
-trihydroxy-4
Z
,9
E
,11
E
,13
Z
,15
E
,19
Z
-docosahexaenoic acid) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (∼0.5–5 μg kg
−1
) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ∼75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil–platelet heterotypic interactions by downregulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, Kupffer cells, and tumor necrosis factor-α, and decreased nuclear factor-κB-phosphorylated p65 nuclear translocation. Taken together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI.</description><subject>631/250/347</subject><subject>631/250/516/1909</subject><subject>692/699/1785</subject><subject>Acute Lung Injury - metabolism</subject><subject>Acute Lung Injury - pathology</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Airway Resistance</subject><subject>Allergology</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - administration & dosage</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Antibodies</subject><subject>Aspirin - administration & dosage</subject><subject>Aspirin - pharmacology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood Platelets - metabolism</subject><subject>Blood-Air Barrier - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Docosahexaenoic Acids - biosynthesis</subject><subject>Docosahexaenoic Acids - metabolism</subject><subject>Epinephrine - metabolism</subject><subject>Gastroenterology</subject><subject>Immunology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation Mediators - metabolism</subject><subject>Leukocytes - immunology</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Neutrophils - immunology</subject><subject>Pulmonary Edema - immunology</subject><subject>Pulmonary Edema - metabolism</subject><subject>Pulmonary Edema - pathology</subject><subject>Receptors, Formyl Peptide - metabolism</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory Mucosa - pathology</subject><subject>Transcription Factor RelA - metabolism</subject><issn>1933-0219</issn><issn>1935-3456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpNkUtLAzEUhYMotlY3_gAJuJSpeTSZzLLUJxTc6DpkJpmSMpmMyUTovzd9CK5yyf3OuZdzAbjFaI4RFY_OzgnCZM75GZjiirKCLhg_P9S0QARXE3AV4xYhjhCjl2BCSCkYIXwKdss42GD7Ygx2szHBaBhM9N2P7eETzrVOjYnQpcZH1UHbt51yTo3W91D1Gg7BOz9m4qBKh_8sVVmRXQ10XpsO-haqJo0Gdqnf5P42hd01uGhVF83N6Z2Br5fnz9Vbsf54fV8t18WASzIWXNCqMqIlrKpEXaNGE2woMrwWrGbCIGYqJnQrdC1MvaBMYN42jdICtyXNCczA_dE3r_qdTBzl1qfQ55ESl4IiWpZkT92dqFQ7o-UQrFNhJ_-SysDDEYi51eek_tkgub-DdFbu7yA5p7-JKnn4</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Eickmeier, O</creator><creator>Seki, H</creator><creator>Haworth, O</creator><creator>Hilberath, J N</creator><creator>Gao, F</creator><creator>Uddin, M</creator><creator>Croze, R H</creator><creator>Carlo, T</creator><creator>Pfeffer, M A</creator><creator>Levy, B D</creator><general>Nature Publishing Group US</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20130301</creationdate><title>Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury</title><author>Eickmeier, O ; Seki, H ; Haworth, O ; Hilberath, J N ; Gao, F ; Uddin, M ; Croze, R H ; Carlo, T ; Pfeffer, M A ; Levy, B D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p172t-68399e8f25998bb0cd21e30e6b85b58e05e958df8db8eb435816fccad81f73193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>631/250/347</topic><topic>631/250/516/1909</topic><topic>692/699/1785</topic><topic>Acute Lung Injury - metabolism</topic><topic>Acute Lung Injury - pathology</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Airway Resistance</topic><topic>Allergology</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - administration & dosage</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Antibodies</topic><topic>Aspirin - administration & dosage</topic><topic>Aspirin - pharmacology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood Platelets - metabolism</topic><topic>Blood-Air Barrier - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Docosahexaenoic Acids - biosynthesis</topic><topic>Docosahexaenoic Acids - metabolism</topic><topic>Epinephrine - metabolism</topic><topic>Gastroenterology</topic><topic>Immunology</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation Mediators - metabolism</topic><topic>Leukocytes - immunology</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Neutrophils - immunology</topic><topic>Pulmonary Edema - immunology</topic><topic>Pulmonary Edema - metabolism</topic><topic>Pulmonary Edema - pathology</topic><topic>Receptors, Formyl Peptide - metabolism</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Respiratory Mucosa - pathology</topic><topic>Transcription Factor RelA - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eickmeier, O</creatorcontrib><creatorcontrib>Seki, H</creatorcontrib><creatorcontrib>Haworth, O</creatorcontrib><creatorcontrib>Hilberath, J N</creatorcontrib><creatorcontrib>Gao, F</creatorcontrib><creatorcontrib>Uddin, M</creatorcontrib><creatorcontrib>Croze, R H</creatorcontrib><creatorcontrib>Carlo, T</creatorcontrib><creatorcontrib>Pfeffer, M A</creatorcontrib><creatorcontrib>Levy, B D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>Proquest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Mucosal immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eickmeier, O</au><au>Seki, H</au><au>Haworth, O</au><au>Hilberath, J N</au><au>Gao, F</au><au>Uddin, M</au><au>Croze, R H</au><au>Carlo, T</au><au>Pfeffer, M A</au><au>Levy, B D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury</atitle><jtitle>Mucosal immunology</jtitle><stitle>Mucosal Immunol</stitle><addtitle>Mucosal Immunol</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>6</volume><issue>2</issue><spage>256</spage><epage>266</epage><pages>256-266</pages><issn>1933-0219</issn><eissn>1935-3456</eissn><abstract>Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid-derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the effects of aspirin-triggered resolvin D1 (AT-RvD1; 7
S
,8
R
,17
R
-trihydroxy-4
Z
,9
E
,11
E
,13
Z
,15
E
,19
Z
-docosahexaenoic acid) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (∼0.5–5 μg kg
−1
) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ∼75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil–platelet heterotypic interactions by downregulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, Kupffer cells, and tumor necrosis factor-α, and decreased nuclear factor-κB-phosphorylated p65 nuclear translocation. Taken together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>22785226</pmid><doi>10.1038/mi.2012.66</doi><tpages>11</tpages></addata></record> |
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| ispartof | Mucosal immunology, 2013-03, Vol.6 (2), p.256-266 |
| issn | 1933-0219 1935-3456 |
| language | eng |
| recordid | cdi_proquest_journals_1783037729 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection |
| subjects | 631/250/347 631/250/516/1909 692/699/1785 Acute Lung Injury - metabolism Acute Lung Injury - pathology Adaptor Proteins, Signal Transducing - metabolism Airway Resistance Allergology Animals Anti-Inflammatory Agents, Non-Steroidal - administration & dosage Anti-Inflammatory Agents, Non-Steroidal - pharmacology Antibodies Aspirin - administration & dosage Aspirin - pharmacology Biomedical and Life Sciences Biomedicine Blood Platelets - metabolism Blood-Air Barrier - physiopathology Disease Models, Animal Docosahexaenoic Acids - biosynthesis Docosahexaenoic Acids - metabolism Epinephrine - metabolism Gastroenterology Immunology Inflammation - immunology Inflammation - metabolism Inflammation Mediators - metabolism Leukocytes - immunology Macrophages, Alveolar - metabolism Male Mice Neutrophils - immunology Pulmonary Edema - immunology Pulmonary Edema - metabolism Pulmonary Edema - pathology Receptors, Formyl Peptide - metabolism Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Transcription Factor RelA - metabolism |
| title | Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury |
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