Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation
Background Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the ma...
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| Veröffentlicht in: | The Annals of thoracic surgery 2008-12, Vol.86 (6), p.1774-1779 |
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| creator | McCourtie, Anton S., MRCS Farivar, Alexander S., MD Woolley, Steven M., MRCS Merry, Heather E., MD Wolf, Patrick S., MD Mackinnon-Patterson, Brendan, BS Keech, John C., MD FitzSullivan, Elizabeth, MD Mulligan, Michael S., MD |
| description | Background Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown. Utilizing an in vitro model of hypoxia and reoxygenation, we sought to determine if the proinflammatory response of type 2 pneumocytes to oxidative stress would be amplified by alveolar macrophage secretory products. Methods Cultured pneumocytes were exposed to control media or media from cultured macrophages exposed to hypoxia and reoxygenation. Pneumocytes were subsequently subjected to hypoxia and reoxygenation and assessed for both nuclear translocation of nuclear factor kappa B and inflammatory cytokine and chemokine secretion. To examine for any reciprocal interactions, we reversed the experiment, exposing macrophages to conditioned pneumocyte media. Results In the presence of media from stimulated macrophages, production of proinflammatory mediators by type 2 pneumocytes was dramatically enhanced. In contrast, exposure of the macrophage to conditioned pneumocyte media had an inhibitory effect on macrophage responses subsequently exposed to hypoxia and reoxygenation. Conclusions The alveolar macrophage drives the development of lung reperfusion injury in part through amplification of the inflammatory response of type 2 pneumocytes subjected to hypoxia and reoxygenation. |
| doi_str_mv | 10.1016/j.athoracsur.2008.07.071 |
| format | Article |
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Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown. Utilizing an in vitro model of hypoxia and reoxygenation, we sought to determine if the proinflammatory response of type 2 pneumocytes to oxidative stress would be amplified by alveolar macrophage secretory products. Methods Cultured pneumocytes were exposed to control media or media from cultured macrophages exposed to hypoxia and reoxygenation. Pneumocytes were subsequently subjected to hypoxia and reoxygenation and assessed for both nuclear translocation of nuclear factor kappa B and inflammatory cytokine and chemokine secretion. To examine for any reciprocal interactions, we reversed the experiment, exposing macrophages to conditioned pneumocyte media. Results In the presence of media from stimulated macrophages, production of proinflammatory mediators by type 2 pneumocytes was dramatically enhanced. In contrast, exposure of the macrophage to conditioned pneumocyte media had an inhibitory effect on macrophage responses subsequently exposed to hypoxia and reoxygenation. Conclusions The alveolar macrophage drives the development of lung reperfusion injury in part through amplification of the inflammatory response of type 2 pneumocytes subjected to hypoxia and reoxygenation.</description><identifier>ISSN: 0003-4975</identifier><identifier>EISSN: 1552-6259</identifier><identifier>DOI: 10.1016/j.athoracsur.2008.07.071</identifier><identifier>PMID: 19021974</identifier><identifier>CODEN: ATHSAK</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiothoracic Surgery ; Cell Hypoxia - physiology ; Cells, Cultured ; Chemokines - metabolism ; Culture Media, Conditioned ; Cytokines - metabolism ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Inflammation Mediators - metabolism ; Interleukin-1beta - metabolism ; Macrophage Activation - physiology ; Macrophages, Alveolar - secretion ; Male ; Medical sciences ; Oxidative Stress - physiology ; Oxygen - pharmacology ; Pneumology ; Probability ; Rats ; Rats, Long-Evans ; Reference Values ; Reperfusion Injury - physiopathology ; Sensitivity and Specificity ; Surgery ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>The Annals of thoracic surgery, 2008-12, Vol.86 (6), p.1774-1779</ispartof><rights>The Society of Thoracic Surgeons</rights><rights>2008 The Society of Thoracic Surgeons</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c664t-927853cfefaa189881212861c807a76ca80e1867dd59606c7aa929a300287e623</citedby><cites>FETCH-LOGICAL-c664t-927853cfefaa189881212861c807a76ca80e1867dd59606c7aa929a300287e623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20939341$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19021974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McCourtie, Anton S., MRCS</creatorcontrib><creatorcontrib>Farivar, Alexander S., MD</creatorcontrib><creatorcontrib>Woolley, Steven M., MRCS</creatorcontrib><creatorcontrib>Merry, Heather E., MD</creatorcontrib><creatorcontrib>Wolf, Patrick S., MD</creatorcontrib><creatorcontrib>Mackinnon-Patterson, Brendan, BS</creatorcontrib><creatorcontrib>Keech, John C., MD</creatorcontrib><creatorcontrib>FitzSullivan, Elizabeth, MD</creatorcontrib><creatorcontrib>Mulligan, Michael S., MD</creatorcontrib><title>Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation</title><title>The Annals of thoracic surgery</title><addtitle>Ann Thorac Surg</addtitle><description>Background Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown. Utilizing an in vitro model of hypoxia and reoxygenation, we sought to determine if the proinflammatory response of type 2 pneumocytes to oxidative stress would be amplified by alveolar macrophage secretory products. Methods Cultured pneumocytes were exposed to control media or media from cultured macrophages exposed to hypoxia and reoxygenation. Pneumocytes were subsequently subjected to hypoxia and reoxygenation and assessed for both nuclear translocation of nuclear factor kappa B and inflammatory cytokine and chemokine secretion. To examine for any reciprocal interactions, we reversed the experiment, exposing macrophages to conditioned pneumocyte media. Results In the presence of media from stimulated macrophages, production of proinflammatory mediators by type 2 pneumocytes was dramatically enhanced. In contrast, exposure of the macrophage to conditioned pneumocyte media had an inhibitory effect on macrophage responses subsequently exposed to hypoxia and reoxygenation. Conclusions The alveolar macrophage drives the development of lung reperfusion injury in part through amplification of the inflammatory response of type 2 pneumocytes subjected to hypoxia and reoxygenation.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiothoracic Surgery</subject><subject>Cell Hypoxia - physiology</subject><subject>Cells, Cultured</subject><subject>Chemokines - metabolism</subject><subject>Culture Media, Conditioned</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>Macrophage Activation - physiology</subject><subject>Macrophages, Alveolar - secretion</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Oxidative Stress - physiology</subject><subject>Oxygen - pharmacology</subject><subject>Pneumology</subject><subject>Probability</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Reference Values</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Sensitivity and Specificity</subject><subject>Surgery</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0003-4975</issn><issn>1552-6259</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUk1v1DAQjRCILoW_gHKBW7a2s_HHpVKpCq1UREVbiZs1OJOsl6yd2smq-fc42lULnJBGsq158-Z53mRZTsmSEspPNksY1j6AiWNYMkLkkogU9EW2oFXFCs4q9TJbEELKYqVEdZS9iXGTniylX2dHVKWbEqtFBmfdDn0HIf8KJvh-DS3mt2gCDj5M-U3w9WiGmF80DZohv5t6zFl-43DcejMNGPN7V2NovXVtfjn1_tFC8R3949Sig8F69zZ71UAX8d3hPM7uP1_cnV8W19--XJ2fXReG89VQKCZkVZoGGwAqlZSUUSY5NZIIENyAJEglF3VdKU64EQCKKSjTn6RAzsrj7HTP248_t1gbdEOATvfBbiFM2oPVf2ecXevW7zTjlaoYTwQfDwTBP4wYB7210WDXgUM_Rs1V0iQrmoByD0wDizFg89SEEj37ozf62R89-6OJSDGXvv9T5HPhwZAE-HAAQDTQNQGcsfEJx4gqVbmaiT7tcZhGurMYdDQWncHahmSUrr39HzWn_5CYzjqb-v7CCePGj8ElyzTVkWmib-d9mteJSEIrJX6UvwHBrMq0</recordid><startdate>20081201</startdate><enddate>20081201</enddate><creator>McCourtie, Anton S., MRCS</creator><creator>Farivar, Alexander S., MD</creator><creator>Woolley, Steven M., MRCS</creator><creator>Merry, Heather E., MD</creator><creator>Wolf, Patrick S., MD</creator><creator>Mackinnon-Patterson, Brendan, BS</creator><creator>Keech, John C., MD</creator><creator>FitzSullivan, Elizabeth, MD</creator><creator>Mulligan, Michael S., MD</creator><general>Elsevier Inc</general><general>Elsevier</general><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><scope>5PM</scope></search><sort><creationdate>20081201</creationdate><title>Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation</title><author>McCourtie, Anton S., MRCS ; Farivar, Alexander S., MD ; Woolley, Steven M., MRCS ; Merry, Heather E., MD ; Wolf, Patrick S., MD ; Mackinnon-Patterson, Brendan, BS ; Keech, John C., MD ; FitzSullivan, Elizabeth, MD ; Mulligan, Michael S., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c664t-927853cfefaa189881212861c807a76ca80e1867dd59606c7aa929a300287e623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiothoracic Surgery</topic><topic>Cell Hypoxia - physiology</topic><topic>Cells, Cultured</topic><topic>Chemokines - metabolism</topic><topic>Culture Media, Conditioned</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-1beta - metabolism</topic><topic>Macrophage Activation - physiology</topic><topic>Macrophages, Alveolar - secretion</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Oxidative Stress - physiology</topic><topic>Oxygen - pharmacology</topic><topic>Pneumology</topic><topic>Probability</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Reference Values</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Sensitivity and Specificity</topic><topic>Surgery</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McCourtie, Anton S., MRCS</creatorcontrib><creatorcontrib>Farivar, Alexander S., MD</creatorcontrib><creatorcontrib>Woolley, Steven M., MRCS</creatorcontrib><creatorcontrib>Merry, Heather E., MD</creatorcontrib><creatorcontrib>Wolf, Patrick S., MD</creatorcontrib><creatorcontrib>Mackinnon-Patterson, Brendan, BS</creatorcontrib><creatorcontrib>Keech, John C., MD</creatorcontrib><creatorcontrib>FitzSullivan, Elizabeth, MD</creatorcontrib><creatorcontrib>Mulligan, Michael S., MD</creatorcontrib><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Annals of thoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McCourtie, Anton S., MRCS</au><au>Farivar, Alexander S., MD</au><au>Woolley, Steven M., MRCS</au><au>Merry, Heather E., MD</au><au>Wolf, Patrick S., MD</au><au>Mackinnon-Patterson, Brendan, BS</au><au>Keech, John C., MD</au><au>FitzSullivan, Elizabeth, MD</au><au>Mulligan, Michael S., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation</atitle><jtitle>The Annals of thoracic surgery</jtitle><addtitle>Ann Thorac Surg</addtitle><date>2008-12-01</date><risdate>2008</risdate><volume>86</volume><issue>6</issue><spage>1774</spage><epage>1779</epage><pages>1774-1779</pages><issn>0003-4975</issn><eissn>1552-6259</eissn><coden>ATHSAK</coden><abstract>Background Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown. Utilizing an in vitro model of hypoxia and reoxygenation, we sought to determine if the proinflammatory response of type 2 pneumocytes to oxidative stress would be amplified by alveolar macrophage secretory products. Methods Cultured pneumocytes were exposed to control media or media from cultured macrophages exposed to hypoxia and reoxygenation. Pneumocytes were subsequently subjected to hypoxia and reoxygenation and assessed for both nuclear translocation of nuclear factor kappa B and inflammatory cytokine and chemokine secretion. To examine for any reciprocal interactions, we reversed the experiment, exposing macrophages to conditioned pneumocyte media. Results In the presence of media from stimulated macrophages, production of proinflammatory mediators by type 2 pneumocytes was dramatically enhanced. In contrast, exposure of the macrophage to conditioned pneumocyte media had an inhibitory effect on macrophage responses subsequently exposed to hypoxia and reoxygenation. Conclusions The alveolar macrophage drives the development of lung reperfusion injury in part through amplification of the inflammatory response of type 2 pneumocytes subjected to hypoxia and reoxygenation.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>19021974</pmid><doi>10.1016/j.athoracsur.2008.07.071</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Cardiology. Vascular system Cardiothoracic Surgery Cell Hypoxia - physiology Cells, Cultured Chemokines - metabolism Culture Media, Conditioned Cytokines - metabolism Disease Models, Animal Enzyme-Linked Immunosorbent Assay Inflammation Mediators - metabolism Interleukin-1beta - metabolism Macrophage Activation - physiology Macrophages, Alveolar - secretion Male Medical sciences Oxidative Stress - physiology Oxygen - pharmacology Pneumology Probability Rats Rats, Long-Evans Reference Values Reperfusion Injury - physiopathology Sensitivity and Specificity Surgery Tumor Necrosis Factor-alpha - metabolism |
| title | Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation |
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