Interleukin 8 and acute lung injury
Acute lung injury is a complex clinical syndrome involving acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure culminating in often-fatal acute respiratory distress syndrome. Interleukin 8 (IL-8), a...
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| Veröffentlicht in: | Archives of pathology & laboratory medicine (1976) 2014-02, Vol.138 (2), p.266-269 |
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| container_title | Archives of pathology & laboratory medicine (1976) |
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| creator | Allen, Timothy Craig Kurdowska, Anna |
| description | Acute lung injury is a complex clinical syndrome involving acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure culminating in often-fatal acute respiratory distress syndrome. Interleukin 8 (IL-8), a potent neutrophil attractant and activator, plays a significant role in acute lung injury via the formation of anti-IL-8 autoantibody:IL-8 complexes and those complexes' interaction with FcγRIIa receptors, leading to the development of acute lung injury by, among other possible mechanisms, effecting neutrophil apoptosis. These complexes may also interact with lung endothelial cells in patients with acute respiratory distress syndrome. Continuing research of the role of neutrophils, IL-8, anti-IL-8 autoantibody:IL-8 complexes, and FcγRIIa receptors may ultimately provide molecular therapies that could lower acute respiratory distress syndrome mortality, as well as reduce or even prevent the development of acute lung injury altogether. |
| doi_str_mv | 10.5858/arpa.2013-0182-ra |
| format | Article |
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Interleukin 8 (IL-8), a potent neutrophil attractant and activator, plays a significant role in acute lung injury via the formation of anti-IL-8 autoantibody:IL-8 complexes and those complexes' interaction with FcγRIIa receptors, leading to the development of acute lung injury by, among other possible mechanisms, effecting neutrophil apoptosis. These complexes may also interact with lung endothelial cells in patients with acute respiratory distress syndrome. Continuing research of the role of neutrophils, IL-8, anti-IL-8 autoantibody:IL-8 complexes, and FcγRIIa receptors may ultimately provide molecular therapies that could lower acute respiratory distress syndrome mortality, as well as reduce or even prevent the development of acute lung injury altogether.</description><identifier>ISSN: 0003-9985</identifier><identifier>ISSN: 1543-2165</identifier><identifier>EISSN: 1543-2165</identifier><identifier>DOI: 10.5858/arpa.2013-0182-ra</identifier><identifier>PMID: 23782136</identifier><identifier>CODEN: APLMAS</identifier><language>eng</language><publisher>United States: College of American Pathologists</publisher><subject>Acute Lung Injury - blood ; Acute Lung Injury - immunology ; Acute Lung Injury - metabolism ; Acute Lung Injury - pathology ; Acute respiratory distress syndrome ; Animals ; Apoptosis ; Autoantibodies ; Autoantibodies - analysis ; Autoimmunity ; Biomarkers ; Biomarkers - blood ; Biomarkers - metabolism ; Biopsy ; Cytokines ; Edema ; Endothelium ; Endothelium, Vascular - immunology ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Humans ; Inflammation ; Interleukin-8 - blood ; Interleukin-8 - metabolism ; Interleukins ; Kinases ; Lavage ; Lung - blood supply ; Lung - immunology ; Lung - metabolism ; Lung - pathology ; Medical research ; Medicine, Experimental ; Mortality ; Neutrophil Activation ; Neutrophils ; Neutrophils - immunology ; Neutrophils - metabolism ; Neutrophils - pathology ; Patients ; Permeability ; Receptors, IgG - blood ; Receptors, IgG - metabolism ; Respiratory distress syndrome ; Respiratory failure ; Ventilators</subject><ispartof>Archives of pathology & laboratory medicine (1976), 2014-02, Vol.138 (2), p.266-269</ispartof><rights>COPYRIGHT 2014 College of American Pathologists</rights><rights>Copyright College of American Pathologists Feb 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c579t-a6afd2944ccb26ebaa3e786ea2dfcab5206a5f50888e353936a8d8c3a8c2b7273</citedby><cites>FETCH-LOGICAL-c579t-a6afd2944ccb26ebaa3e786ea2dfcab5206a5f50888e353936a8d8c3a8c2b7273</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/23782136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Allen, Timothy Craig</creatorcontrib><creatorcontrib>Kurdowska, Anna</creatorcontrib><title>Interleukin 8 and acute lung injury</title><title>Archives of pathology & laboratory medicine (1976)</title><addtitle>Arch Pathol Lab Med</addtitle><description>Acute lung injury is a complex clinical syndrome involving acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure culminating in often-fatal acute respiratory distress syndrome. Interleukin 8 (IL-8), a potent neutrophil attractant and activator, plays a significant role in acute lung injury via the formation of anti-IL-8 autoantibody:IL-8 complexes and those complexes' interaction with FcγRIIa receptors, leading to the development of acute lung injury by, among other possible mechanisms, effecting neutrophil apoptosis. These complexes may also interact with lung endothelial cells in patients with acute respiratory distress syndrome. Continuing research of the role of neutrophils, IL-8, anti-IL-8 autoantibody:IL-8 complexes, and FcγRIIa receptors may ultimately provide molecular therapies that could lower acute respiratory distress syndrome mortality, as well as reduce or even prevent the development of acute lung injury altogether.</description><subject>Acute Lung Injury - blood</subject><subject>Acute Lung Injury - immunology</subject><subject>Acute Lung Injury - metabolism</subject><subject>Acute Lung Injury - pathology</subject><subject>Acute respiratory distress syndrome</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autoantibodies</subject><subject>Autoantibodies - analysis</subject><subject>Autoimmunity</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Biomarkers - metabolism</subject><subject>Biopsy</subject><subject>Cytokines</subject><subject>Edema</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - immunology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin-8 - blood</subject><subject>Interleukin-8 - metabolism</subject><subject>Interleukins</subject><subject>Kinases</subject><subject>Lavage</subject><subject>Lung - blood supply</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Mortality</subject><subject>Neutrophil Activation</subject><subject>Neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Neutrophils - pathology</subject><subject>Patients</subject><subject>Permeability</subject><subject>Receptors, IgG - blood</subject><subject>Receptors, IgG - metabolism</subject><subject>Respiratory distress syndrome</subject><subject>Respiratory failure</subject><subject>Ventilators</subject><issn>0003-9985</issn><issn>1543-2165</issn><issn>1543-2165</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNptkd9L5DAQx4N46Lr6B_hyFATxpWt-NG3yuIh6gnBwnM9hmk7X7mXTNWke_O9t1fP0WPIwZPh8h2E-hJwyupBKqksIW1hwykROmeJ5gD0yY7IQOWel3CczSqnItVbykBzFuB6_mnN2QA65qBRnopyRszs_YHCY_nQ-Uxn4JgObBsxc8qus8-sUno_JtxZcxJP3OicPN9e_r37k9z9v766W97mVlR5yKKFtuC4Ka2teYg0gsFIlAm9aC7XktATZSqqUQiGFFiWoRlkByvK64pWYk4u3udvQPyWMg9l00aJz4LFP0bBCi0oXWokRPfsPXfcp-HE7Mx5gBFjFy3_UChyazrf9EMBOQ81SMlbIV3RO8h3UCj0GcL3HthvbX_jFDn58DW46uzNw_inwiOCGx9i7NHS9j19B9gba0McYsDXb0G0gPBtGzWTcTMbNZNxMxs2v5Zj5_n6JVG-w-Uj8VSxeACpDouI</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Allen, Timothy Craig</creator><creator>Kurdowska, Anna</creator><general>College of American Pathologists</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>3V.</scope><scope>4T-</scope><scope>4U-</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</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>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20140201</creationdate><title>Interleukin 8 and acute lung injury</title><author>Allen, Timothy Craig ; Kurdowska, Anna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c579t-a6afd2944ccb26ebaa3e786ea2dfcab5206a5f50888e353936a8d8c3a8c2b7273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acute Lung Injury - blood</topic><topic>Acute Lung Injury - immunology</topic><topic>Acute Lung Injury - metabolism</topic><topic>Acute Lung Injury - pathology</topic><topic>Acute respiratory distress syndrome</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autoantibodies</topic><topic>Autoantibodies - analysis</topic><topic>Autoimmunity</topic><topic>Biomarkers</topic><topic>Biomarkers - blood</topic><topic>Biomarkers - metabolism</topic><topic>Biopsy</topic><topic>Cytokines</topic><topic>Edema</topic><topic>Endothelium</topic><topic>Endothelium, Vascular - immunology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin-8 - blood</topic><topic>Interleukin-8 - metabolism</topic><topic>Interleukins</topic><topic>Kinases</topic><topic>Lavage</topic><topic>Lung - blood supply</topic><topic>Lung - immunology</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Mortality</topic><topic>Neutrophil Activation</topic><topic>Neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - metabolism</topic><topic>Neutrophils - pathology</topic><topic>Patients</topic><topic>Permeability</topic><topic>Receptors, IgG - blood</topic><topic>Receptors, IgG - metabolism</topic><topic>Respiratory distress syndrome</topic><topic>Respiratory failure</topic><topic>Ventilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Allen, Timothy Craig</creatorcontrib><creatorcontrib>Kurdowska, Anna</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Docstoc</collection><collection>University Readers</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of pathology & laboratory medicine (1976)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Allen, Timothy Craig</au><au>Kurdowska, Anna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin 8 and acute lung injury</atitle><jtitle>Archives of pathology & laboratory medicine (1976)</jtitle><addtitle>Arch Pathol Lab Med</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>138</volume><issue>2</issue><spage>266</spage><epage>269</epage><pages>266-269</pages><issn>0003-9985</issn><issn>1543-2165</issn><eissn>1543-2165</eissn><coden>APLMAS</coden><abstract>Acute lung injury is a complex clinical syndrome involving acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure culminating in often-fatal acute respiratory distress syndrome. Interleukin 8 (IL-8), a potent neutrophil attractant and activator, plays a significant role in acute lung injury via the formation of anti-IL-8 autoantibody:IL-8 complexes and those complexes' interaction with FcγRIIa receptors, leading to the development of acute lung injury by, among other possible mechanisms, effecting neutrophil apoptosis. These complexes may also interact with lung endothelial cells in patients with acute respiratory distress syndrome. Continuing research of the role of neutrophils, IL-8, anti-IL-8 autoantibody:IL-8 complexes, and FcγRIIa receptors may ultimately provide molecular therapies that could lower acute respiratory distress syndrome mortality, as well as reduce or even prevent the development of acute lung injury altogether.</abstract><cop>United States</cop><pub>College of American Pathologists</pub><pmid>23782136</pmid><doi>10.5858/arpa.2013-0182-ra</doi><tpages>4</tpages></addata></record> |
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| ispartof | Archives of pathology & laboratory medicine (1976), 2014-02, Vol.138 (2), p.266-269 |
| issn | 0003-9985 1543-2165 1543-2165 |
| language | eng |
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| source | MEDLINE; Allen Press Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Acute Lung Injury - blood Acute Lung Injury - immunology Acute Lung Injury - metabolism Acute Lung Injury - pathology Acute respiratory distress syndrome Animals Apoptosis Autoantibodies Autoantibodies - analysis Autoimmunity Biomarkers Biomarkers - blood Biomarkers - metabolism Biopsy Cytokines Edema Endothelium Endothelium, Vascular - immunology Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Humans Inflammation Interleukin-8 - blood Interleukin-8 - metabolism Interleukins Kinases Lavage Lung - blood supply Lung - immunology Lung - metabolism Lung - pathology Medical research Medicine, Experimental Mortality Neutrophil Activation Neutrophils Neutrophils - immunology Neutrophils - metabolism Neutrophils - pathology Patients Permeability Receptors, IgG - blood Receptors, IgG - metabolism Respiratory distress syndrome Respiratory failure Ventilators |
| title | Interleukin 8 and acute lung injury |
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