Hypothermia induces interleukin-10 and attenuates injury in the lungs of endotoxemic rats
We recently reported that hypothermia protects against intrapulmonary nitric oxide overproduction and nitric oxide-mediated lung injury in endotoxemic rats. Few studies have been performed to investigate whether hypothermia reduces inflammation by affecting favorable changes in chemokine and pro- an...
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| Veröffentlicht in: | Shock (Augusta, Ga.) Ga.), 2003-07, Vol.20 (1), p.41-45 |
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| creator | SARCIA, Paul J SCUMPIA, Philip O MOLDAWER, Lyle L DEMARCO, Vincent G SKIMMING, Jeffrey W |
| description | We recently reported that hypothermia protects against intrapulmonary nitric oxide overproduction and nitric oxide-mediated lung injury in endotoxemic rats. Few studies have been performed to investigate whether hypothermia reduces inflammation by affecting favorable changes in chemokine and pro- and anti-inflammatory cytokine profiles. In this study, we tested the hypothesis that hypothermia decreases concentrations of growth-related oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1), interleukin (IL)-1beta, IL-6, and myeloperoxidase and increases concentration of IL-10 in the lungs endotoxemic rats. Twelve rats were anesthetized and randomized to treatment with either hypothermia (T = 18-24 degrees C; n = 6) or normothermia (T = 36-38 degrees C, n = 6). Endotoxin (15 mg/kg of Escherichia coli lipopolysaccharide) was administered intravascularly and lung tissue was harvested 150 min later. Three additional rats were sham instrumented and maintained as normothermic but not given endotoxin. Hematoxylin & eosin staining was performed for qualitative inspection of tissues. Quantitative analyses of lung homogenates were performed using enzyme-linked immunosorbent assays for IL-1beta, IL-6, IL-10, and GRO/CINC-1. Myeloperoxidase concentrations were determined using a colorimetric assay. Hypothermia attenuated the induction of intrapulmonary IL-1beta (P < 0.05), IL-6 (P < 0.05), GRO/CINC-1 (P < 0.05), and myeloperoxidase (P < 0.05) caused by endotoxin. Inspection of the lungs revealed that hypothermia similarly attenuated histological signs of injury, such as interstitial edema and neutrophil accumulation. Hypothermia increased the intrapulmonary concentration of IL-10 more than 3-fold over that measured in the normothermia (endotoxin-exposed) group (P < 0.05). Hypothermia inhibits neutrophil recruitment in the lungs of endotoxemic rats in part by decreasing proinflammatory cytokine expression. Additionally, hypothermia induces intrapulmonary IL-10 expression. Further studies are needed to investigate whether IL-10 mediates the anti-inflammatory effects of hypothermia. |
| doi_str_mv | 10.1097/01.shk.0000071080.50028.f2 |
| format | Article |
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Few studies have been performed to investigate whether hypothermia reduces inflammation by affecting favorable changes in chemokine and pro- and anti-inflammatory cytokine profiles. In this study, we tested the hypothesis that hypothermia decreases concentrations of growth-related oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1), interleukin (IL)-1beta, IL-6, and myeloperoxidase and increases concentration of IL-10 in the lungs endotoxemic rats. Twelve rats were anesthetized and randomized to treatment with either hypothermia (T = 18-24 degrees C; n = 6) or normothermia (T = 36-38 degrees C, n = 6). Endotoxin (15 mg/kg of Escherichia coli lipopolysaccharide) was administered intravascularly and lung tissue was harvested 150 min later. Three additional rats were sham instrumented and maintained as normothermic but not given endotoxin. Hematoxylin & eosin staining was performed for qualitative inspection of tissues. Quantitative analyses of lung homogenates were performed using enzyme-linked immunosorbent assays for IL-1beta, IL-6, IL-10, and GRO/CINC-1. Myeloperoxidase concentrations were determined using a colorimetric assay. Hypothermia attenuated the induction of intrapulmonary IL-1beta (P < 0.05), IL-6 (P < 0.05), GRO/CINC-1 (P < 0.05), and myeloperoxidase (P < 0.05) caused by endotoxin. Inspection of the lungs revealed that hypothermia similarly attenuated histological signs of injury, such as interstitial edema and neutrophil accumulation. Hypothermia increased the intrapulmonary concentration of IL-10 more than 3-fold over that measured in the normothermia (endotoxin-exposed) group (P < 0.05). Hypothermia inhibits neutrophil recruitment in the lungs of endotoxemic rats in part by decreasing proinflammatory cytokine expression. Additionally, hypothermia induces intrapulmonary IL-10 expression. Further studies are needed to investigate whether IL-10 mediates the anti-inflammatory effects of hypothermia.]]></description><identifier>ISSN: 1073-2322</identifier><identifier>EISSN: 1540-0514</identifier><identifier>DOI: 10.1097/01.shk.0000071080.50028.f2</identifier><identifier>PMID: 12813367</identifier><language>eng</language><publisher>Augusta, GA: BioMedical Press</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Bacterial diseases ; Bacterial sepsis ; Biological and medical sciences ; Blood Pressure ; Chemokine CXCL1 ; Chemokines - metabolism ; Chemokines, CXC ; Chemotactic Factors - metabolism ; Disease Models, Animal ; Emergency and intensive care: infection, septic shock ; Endotoxemia - metabolism ; Endotoxemia - physiopathology ; Endotoxemia - therapy ; Heart Rate ; Human bacterial diseases ; Hypothermia, Induced - adverse effects ; Infectious diseases ; Intensive care medicine ; Intercellular Signaling Peptides and Proteins - metabolism ; Interleukin-1 - metabolism ; Interleukin-10 - metabolism ; Interleukin-6 - metabolism ; Lung - metabolism ; Lung - pathology ; Lung Injury ; Male ; Medical sciences ; Peroxidase - metabolism ; Rats ; Rats, Sprague-Dawley</subject><ispartof>Shock (Augusta, Ga.), 2003-07, Vol.20 (1), p.41-45</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-2ee0524c8514d5e4dc99cbbeca9296ffe11081222632ebe311ef0069edbdae5c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14917764$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12813367$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SARCIA, Paul J</creatorcontrib><creatorcontrib>SCUMPIA, Philip O</creatorcontrib><creatorcontrib>MOLDAWER, Lyle L</creatorcontrib><creatorcontrib>DEMARCO, Vincent G</creatorcontrib><creatorcontrib>SKIMMING, Jeffrey W</creatorcontrib><title>Hypothermia induces interleukin-10 and attenuates injury in the lungs of endotoxemic rats</title><title>Shock (Augusta, Ga.)</title><addtitle>Shock</addtitle><description><![CDATA[We recently reported that hypothermia protects against intrapulmonary nitric oxide overproduction and nitric oxide-mediated lung injury in endotoxemic rats. Few studies have been performed to investigate whether hypothermia reduces inflammation by affecting favorable changes in chemokine and pro- and anti-inflammatory cytokine profiles. In this study, we tested the hypothesis that hypothermia decreases concentrations of growth-related oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1), interleukin (IL)-1beta, IL-6, and myeloperoxidase and increases concentration of IL-10 in the lungs endotoxemic rats. Twelve rats were anesthetized and randomized to treatment with either hypothermia (T = 18-24 degrees C; n = 6) or normothermia (T = 36-38 degrees C, n = 6). Endotoxin (15 mg/kg of Escherichia coli lipopolysaccharide) was administered intravascularly and lung tissue was harvested 150 min later. Three additional rats were sham instrumented and maintained as normothermic but not given endotoxin. Hematoxylin & eosin staining was performed for qualitative inspection of tissues. Quantitative analyses of lung homogenates were performed using enzyme-linked immunosorbent assays for IL-1beta, IL-6, IL-10, and GRO/CINC-1. Myeloperoxidase concentrations were determined using a colorimetric assay. Hypothermia attenuated the induction of intrapulmonary IL-1beta (P < 0.05), IL-6 (P < 0.05), GRO/CINC-1 (P < 0.05), and myeloperoxidase (P < 0.05) caused by endotoxin. Inspection of the lungs revealed that hypothermia similarly attenuated histological signs of injury, such as interstitial edema and neutrophil accumulation. Hypothermia increased the intrapulmonary concentration of IL-10 more than 3-fold over that measured in the normothermia (endotoxin-exposed) group (P < 0.05). Hypothermia inhibits neutrophil recruitment in the lungs of endotoxemic rats in part by decreasing proinflammatory cytokine expression. Additionally, hypothermia induces intrapulmonary IL-10 expression. Further studies are needed to investigate whether IL-10 mediates the anti-inflammatory effects of hypothermia.]]></description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Bacterial diseases</subject><subject>Bacterial sepsis</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Chemokine CXCL1</subject><subject>Chemokines - metabolism</subject><subject>Chemokines, CXC</subject><subject>Chemotactic Factors - metabolism</subject><subject>Disease Models, Animal</subject><subject>Emergency and intensive care: infection, septic shock</subject><subject>Endotoxemia - metabolism</subject><subject>Endotoxemia - physiopathology</subject><subject>Endotoxemia - therapy</subject><subject>Heart Rate</subject><subject>Human bacterial diseases</subject><subject>Hypothermia, Induced - adverse effects</subject><subject>Infectious diseases</subject><subject>Intensive care medicine</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Interleukin-1 - metabolism</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung Injury</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Peroxidase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>1073-2322</issn><issn>1540-0514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LAzEURYMotlb_ggyC7mZ8SebTnRS1QsGNLlyFTObFTjsfNcmA_fem7UCzuYGcm7wcQu4oRBSK7BFoZFebCPYro5BDlACwPNLsjExpEkMICY3P_R4yHjLO2IRcWbv2UMyL7JJMKMsp52k2Jd-L3bZ3KzRtLYO6qwaF1qdD0-CwqbuQQiC7KpDOYTdIdzhdD2bnI_C9oBm6Hxv0OsCu6l3_h22tAiOdvSYXWjYWb8acka_Xl8_5Ilx-vL3Pn5eh8rO4kCFCwmKV-5GrBONKFYUqS1SyYEWqNVL_Q8oYSznDEjmlqAHSAquykpgoPiMPx3u3pv8d0DrR1lZh08gO-8GKjPOc5Tnz4NMRVKa31qAWW1O30uwEBbEXK4AKL1acxIqDWKH35dvxlaFssTpVR5MeuB8BaZVstJGdqu2JiwuaZWnM_wEW54O8</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>SARCIA, Paul J</creator><creator>SCUMPIA, Philip O</creator><creator>MOLDAWER, Lyle L</creator><creator>DEMARCO, Vincent G</creator><creator>SKIMMING, Jeffrey W</creator><general>BioMedical Press</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></search><sort><creationdate>20030701</creationdate><title>Hypothermia induces interleukin-10 and attenuates injury in the lungs of endotoxemic rats</title><author>SARCIA, Paul J ; SCUMPIA, Philip O ; MOLDAWER, Lyle L ; DEMARCO, Vincent G ; SKIMMING, Jeffrey W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-2ee0524c8514d5e4dc99cbbeca9296ffe11081222632ebe311ef0069edbdae5c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Bacterial diseases</topic><topic>Bacterial sepsis</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Chemokine CXCL1</topic><topic>Chemokines - metabolism</topic><topic>Chemokines, CXC</topic><topic>Chemotactic Factors - metabolism</topic><topic>Disease Models, Animal</topic><topic>Emergency and intensive care: infection, septic shock</topic><topic>Endotoxemia - metabolism</topic><topic>Endotoxemia - physiopathology</topic><topic>Endotoxemia - therapy</topic><topic>Heart Rate</topic><topic>Human bacterial diseases</topic><topic>Hypothermia, Induced - adverse effects</topic><topic>Infectious diseases</topic><topic>Intensive care medicine</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Interleukin-1 - metabolism</topic><topic>Interleukin-10 - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung Injury</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Peroxidase - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SARCIA, Paul J</creatorcontrib><creatorcontrib>SCUMPIA, Philip O</creatorcontrib><creatorcontrib>MOLDAWER, Lyle L</creatorcontrib><creatorcontrib>DEMARCO, Vincent G</creatorcontrib><creatorcontrib>SKIMMING, Jeffrey W</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><jtitle>Shock (Augusta, Ga.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SARCIA, Paul J</au><au>SCUMPIA, Philip O</au><au>MOLDAWER, Lyle L</au><au>DEMARCO, Vincent G</au><au>SKIMMING, Jeffrey W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypothermia induces interleukin-10 and attenuates injury in the lungs of endotoxemic rats</atitle><jtitle>Shock (Augusta, Ga.)</jtitle><addtitle>Shock</addtitle><date>2003-07-01</date><risdate>2003</risdate><volume>20</volume><issue>1</issue><spage>41</spage><epage>45</epage><pages>41-45</pages><issn>1073-2322</issn><eissn>1540-0514</eissn><abstract><![CDATA[We recently reported that hypothermia protects against intrapulmonary nitric oxide overproduction and nitric oxide-mediated lung injury in endotoxemic rats. Few studies have been performed to investigate whether hypothermia reduces inflammation by affecting favorable changes in chemokine and pro- and anti-inflammatory cytokine profiles. In this study, we tested the hypothesis that hypothermia decreases concentrations of growth-related oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1), interleukin (IL)-1beta, IL-6, and myeloperoxidase and increases concentration of IL-10 in the lungs endotoxemic rats. Twelve rats were anesthetized and randomized to treatment with either hypothermia (T = 18-24 degrees C; n = 6) or normothermia (T = 36-38 degrees C, n = 6). Endotoxin (15 mg/kg of Escherichia coli lipopolysaccharide) was administered intravascularly and lung tissue was harvested 150 min later. Three additional rats were sham instrumented and maintained as normothermic but not given endotoxin. Hematoxylin & eosin staining was performed for qualitative inspection of tissues. Quantitative analyses of lung homogenates were performed using enzyme-linked immunosorbent assays for IL-1beta, IL-6, IL-10, and GRO/CINC-1. Myeloperoxidase concentrations were determined using a colorimetric assay. Hypothermia attenuated the induction of intrapulmonary IL-1beta (P < 0.05), IL-6 (P < 0.05), GRO/CINC-1 (P < 0.05), and myeloperoxidase (P < 0.05) caused by endotoxin. Inspection of the lungs revealed that hypothermia similarly attenuated histological signs of injury, such as interstitial edema and neutrophil accumulation. Hypothermia increased the intrapulmonary concentration of IL-10 more than 3-fold over that measured in the normothermia (endotoxin-exposed) group (P < 0.05). Hypothermia inhibits neutrophil recruitment in the lungs of endotoxemic rats in part by decreasing proinflammatory cytokine expression. Additionally, hypothermia induces intrapulmonary IL-10 expression. Further studies are needed to investigate whether IL-10 mediates the anti-inflammatory effects of hypothermia.]]></abstract><cop>Augusta, GA</cop><pub>BioMedical Press</pub><pmid>12813367</pmid><doi>10.1097/01.shk.0000071080.50028.f2</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Bacterial diseases Bacterial sepsis Biological and medical sciences Blood Pressure Chemokine CXCL1 Chemokines - metabolism Chemokines, CXC Chemotactic Factors - metabolism Disease Models, Animal Emergency and intensive care: infection, septic shock Endotoxemia - metabolism Endotoxemia - physiopathology Endotoxemia - therapy Heart Rate Human bacterial diseases Hypothermia, Induced - adverse effects Infectious diseases Intensive care medicine Intercellular Signaling Peptides and Proteins - metabolism Interleukin-1 - metabolism Interleukin-10 - metabolism Interleukin-6 - metabolism Lung - metabolism Lung - pathology Lung Injury Male Medical sciences Peroxidase - metabolism Rats Rats, Sprague-Dawley |
| title | Hypothermia induces interleukin-10 and attenuates injury in the lungs of endotoxemic rats |
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