Cardiac dysfunction induced by experimental myocardial infarction impairs the host defense response to bacterial infection in mice because of reduced phagocytosis of Kupffer cells
Objective This study was undertaken to investigate the effects of cardiac dysfunction induced by experimental myocardial infarction on the host defense response to bacterial infection and the role of Kupffer cells in mediating this response. Methods Myocardial infarction was induced in C57BL/6 mice...
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| Veröffentlicht in: | The Journal of thoracic and cardiovascular surgery 2010-09, Vol.140 (3), p.624-632.e3 |
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| creator | Nogami, Yashiro, MD Kinoshita, Manabu, MD Takase, Bonpei, MD Inatsu, Akihito, MD Ishihara, Masayuki, PhD Seki, Shuhji, MD Maehara, Tadaaki, MD |
| description | Objective This study was undertaken to investigate the effects of cardiac dysfunction induced by experimental myocardial infarction on the host defense response to bacterial infection and the role of Kupffer cells in mediating this response. Methods Myocardial infarction was induced in C57BL/6 mice by ligation of the left anterior descending coronary artery. Mice were challenged with Escherichia coli intravenously 1, 5, and 14 days after myocardial infarction or sham operation. Thereafter, the cytokine production and the function of their Kupffer cells were assessed. Results Mice with myocardial infarction showed remarkable cardiac dysfunction and had a significantly lower survival than sham mice after bacterial challenge at 5 days after surgery; bacterial challenge at 1 or 14 days after surgery resulted in no difference in survival between myocardial infarction and sham mice. The phagocytic activity of Kupffer cells, assessed by fluorescein isothiocyanate microspheres, remarkably decreased in mice with myocardial infarction 5 days after surgery. Serum peaks of tumor necrosis factor and interferon-γ after bacterial challenge were also suppressed in mice with myocardial infarction at 5 days. Production of these cytokines and immunoglobulin-M from liver mononuclear cells was also impaired in mice with myocardial infarction. Enhancement of the phagocytic activity of Kupffer cells by C-reactive protein significantly improved survival after infection in mice with myocardial infarction, although neither interleukin-18 nor immunoglobulin-M treatment improved survival. Conclusions Cardiac dysfunction induced by myocardial infarction renders mice susceptible to bacterial infection and increases mortality because of a reduced ability of Kupffer cells to clear infectious bacteria. C-reactive protein-enhanced phagocytic activity of Kupffer cells may improve the poor prognosis after bacterial infection in mice with myocardial infarction. |
| doi_str_mv | 10.1016/j.jtcvs.2009.11.005 |
| format | Article |
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Methods Myocardial infarction was induced in C57BL/6 mice by ligation of the left anterior descending coronary artery. Mice were challenged with Escherichia coli intravenously 1, 5, and 14 days after myocardial infarction or sham operation. Thereafter, the cytokine production and the function of their Kupffer cells were assessed. Results Mice with myocardial infarction showed remarkable cardiac dysfunction and had a significantly lower survival than sham mice after bacterial challenge at 5 days after surgery; bacterial challenge at 1 or 14 days after surgery resulted in no difference in survival between myocardial infarction and sham mice. The phagocytic activity of Kupffer cells, assessed by fluorescein isothiocyanate microspheres, remarkably decreased in mice with myocardial infarction 5 days after surgery. Serum peaks of tumor necrosis factor and interferon-γ after bacterial challenge were also suppressed in mice with myocardial infarction at 5 days. Production of these cytokines and immunoglobulin-M from liver mononuclear cells was also impaired in mice with myocardial infarction. Enhancement of the phagocytic activity of Kupffer cells by C-reactive protein significantly improved survival after infection in mice with myocardial infarction, although neither interleukin-18 nor immunoglobulin-M treatment improved survival. Conclusions Cardiac dysfunction induced by myocardial infarction renders mice susceptible to bacterial infection and increases mortality because of a reduced ability of Kupffer cells to clear infectious bacteria. C-reactive protein-enhanced phagocytic activity of Kupffer cells may improve the poor prognosis after bacterial infection in mice with myocardial infarction.</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1016/j.jtcvs.2009.11.005</identifier><identifier>PMID: 20138636</identifier><identifier>CODEN: JTCSAQ</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; C-reactive protein ; C-Reactive Protein - administration & dosage ; Cardiology. Vascular system ; Cardiothoracic Surgery ; Cells, Cultured ; Coronary heart disease ; Disease Models, Animal ; Escherichia coli ; Escherichia coli Infections - immunology ; Heart ; Immunity, Innate ; Immunoglobulin M - administration & dosage ; Immunoglobulin M - metabolism ; Inflammation Mediators - blood ; Injections, Intraperitoneal ; Interferon-gamma - blood ; Interleukin-18 - administration & dosage ; Kupffer Cells - immunology ; Kupffer Cells - microbiology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction - diagnostic imaging ; Myocardial Infarction - immunology ; Myocardial Infarction - physiopathology ; Myocarditis. Cardiomyopathies ; Phagocytosis ; Pneumology ; Time Factors ; Tumor Necrosis Factor-alpha - blood ; Ultrasonography ; Ventricular Dysfunction, Left - diagnostic imaging ; Ventricular Dysfunction, Left - immunology ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Function, Left</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 2010-09, Vol.140 (3), p.624-632.e3</ispartof><rights>The American Association for Thoracic Surgery</rights><rights>2010 The American Association for Thoracic Surgery</rights><rights>2015 INIST-CNRS</rights><rights>2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c586t-e326cf6fa7b42975c947f21f12628063a0864964e426dcdf2c76396e05247fed3</citedby><cites>FETCH-LOGICAL-c586t-e326cf6fa7b42975c947f21f12628063a0864964e426dcdf2c76396e05247fed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022522309014329$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23175983$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20138636$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nogami, Yashiro, MD</creatorcontrib><creatorcontrib>Kinoshita, Manabu, MD</creatorcontrib><creatorcontrib>Takase, Bonpei, MD</creatorcontrib><creatorcontrib>Inatsu, Akihito, MD</creatorcontrib><creatorcontrib>Ishihara, Masayuki, PhD</creatorcontrib><creatorcontrib>Seki, Shuhji, MD</creatorcontrib><creatorcontrib>Maehara, Tadaaki, MD</creatorcontrib><title>Cardiac dysfunction induced by experimental myocardial infarction impairs the host defense response to bacterial infection in mice because of reduced phagocytosis of Kupffer cells</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>Objective This study was undertaken to investigate the effects of cardiac dysfunction induced by experimental myocardial infarction on the host defense response to bacterial infection and the role of Kupffer cells in mediating this response. Methods Myocardial infarction was induced in C57BL/6 mice by ligation of the left anterior descending coronary artery. Mice were challenged with Escherichia coli intravenously 1, 5, and 14 days after myocardial infarction or sham operation. Thereafter, the cytokine production and the function of their Kupffer cells were assessed. Results Mice with myocardial infarction showed remarkable cardiac dysfunction and had a significantly lower survival than sham mice after bacterial challenge at 5 days after surgery; bacterial challenge at 1 or 14 days after surgery resulted in no difference in survival between myocardial infarction and sham mice. The phagocytic activity of Kupffer cells, assessed by fluorescein isothiocyanate microspheres, remarkably decreased in mice with myocardial infarction 5 days after surgery. Serum peaks of tumor necrosis factor and interferon-γ after bacterial challenge were also suppressed in mice with myocardial infarction at 5 days. Production of these cytokines and immunoglobulin-M from liver mononuclear cells was also impaired in mice with myocardial infarction. Enhancement of the phagocytic activity of Kupffer cells by C-reactive protein significantly improved survival after infection in mice with myocardial infarction, although neither interleukin-18 nor immunoglobulin-M treatment improved survival. Conclusions Cardiac dysfunction induced by myocardial infarction renders mice susceptible to bacterial infection and increases mortality because of a reduced ability of Kupffer cells to clear infectious bacteria. C-reactive protein-enhanced phagocytic activity of Kupffer cells may improve the poor prognosis after bacterial infection in mice with myocardial infarction.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - administration & dosage</subject><subject>Cardiology. Vascular system</subject><subject>Cardiothoracic Surgery</subject><subject>Cells, Cultured</subject><subject>Coronary heart disease</subject><subject>Disease Models, Animal</subject><subject>Escherichia coli</subject><subject>Escherichia coli Infections - immunology</subject><subject>Heart</subject><subject>Immunity, Innate</subject><subject>Immunoglobulin M - administration & dosage</subject><subject>Immunoglobulin M - metabolism</subject><subject>Inflammation Mediators - blood</subject><subject>Injections, Intraperitoneal</subject><subject>Interferon-gamma - blood</subject><subject>Interleukin-18 - administration & dosage</subject><subject>Kupffer Cells - immunology</subject><subject>Kupffer Cells - microbiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - immunology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Phagocytosis</subject><subject>Pneumology</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Ultrasonography</subject><subject>Ventricular Dysfunction, Left - diagnostic imaging</subject><subject>Ventricular Dysfunction, Left - immunology</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Function, Left</subject><issn>0022-5223</issn><issn>1097-685X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks9u1DAQhyMEotvCEyAhXxCnXfwnceIDSNUKCqISB0DiZjnOmPWSxMGTVOS5eEGcZgsSl55sWd9vZjSfs-wZoztGmXx13B1He4M7TqnaMbajtHiQbRhV5VZWxbeH2YZSzrcF5-IsO0c8UkpLytTj7IxTJiop5Cb7vTex8caSZkY39Xb0oSe-byYLDalnAr8GiL6DfjQt6eZgb_E2Ic7EE90Nxkck4wHIIeBIGnDQI5AIOITlMgZSGzumQmsS7tqQzlsgNVgzJSy4FFk7DwfzPdh5DOhxef84Dc5BJBbaFp9kj5xpEZ6ezovs67u3X_bvt9efrj7sL6-3tqjkuAXBpXXSmbLOuSoLq_LSceYYl7yiUhhayVzJHHIuG9s4bksplARa8ARCIy6yl2vdIYafE-CoO4_LBKaHMKGuSs54KVV-L1nmlVKSsyKRYiVtDIgRnB7Sek2cNaN60aqP-larXrRqxnTSmlLPT_WnuoPmb-bOYwJenACD1rQumt56_McJVhaqEol7vXKQ9nbjIWq0Hvq0ch-TFd0Ef88gb_7L29b3PrX8ATPgMUyxT0o008g11Z-XH7h8QKooywVX4g-4mNp5</recordid><startdate>20100901</startdate><enddate>20100901</enddate><creator>Nogami, Yashiro, MD</creator><creator>Kinoshita, Manabu, MD</creator><creator>Takase, Bonpei, MD</creator><creator>Inatsu, Akihito, MD</creator><creator>Ishihara, Masayuki, PhD</creator><creator>Seki, Shuhji, MD</creator><creator>Maehara, Tadaaki, MD</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>20100901</creationdate><title>Cardiac dysfunction induced by experimental myocardial infarction impairs the host defense response to bacterial infection in mice because of reduced phagocytosis of Kupffer cells</title><author>Nogami, Yashiro, MD ; Kinoshita, Manabu, MD ; Takase, Bonpei, MD ; Inatsu, Akihito, MD ; Ishihara, Masayuki, PhD ; Seki, Shuhji, MD ; Maehara, Tadaaki, MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c586t-e326cf6fa7b42975c947f21f12628063a0864964e426dcdf2c76396e05247fed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>C-reactive protein</topic><topic>C-Reactive Protein - administration & dosage</topic><topic>Cardiology. Vascular system</topic><topic>Cardiothoracic Surgery</topic><topic>Cells, Cultured</topic><topic>Coronary heart disease</topic><topic>Disease Models, Animal</topic><topic>Escherichia coli</topic><topic>Escherichia coli Infections - immunology</topic><topic>Heart</topic><topic>Immunity, Innate</topic><topic>Immunoglobulin M - administration & dosage</topic><topic>Immunoglobulin M - metabolism</topic><topic>Inflammation Mediators - blood</topic><topic>Injections, Intraperitoneal</topic><topic>Interferon-gamma - blood</topic><topic>Interleukin-18 - administration & dosage</topic><topic>Kupffer Cells - immunology</topic><topic>Kupffer Cells - microbiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - immunology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Phagocytosis</topic><topic>Pneumology</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Ultrasonography</topic><topic>Ventricular Dysfunction, Left - diagnostic imaging</topic><topic>Ventricular Dysfunction, Left - immunology</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nogami, Yashiro, MD</creatorcontrib><creatorcontrib>Kinoshita, Manabu, MD</creatorcontrib><creatorcontrib>Takase, Bonpei, MD</creatorcontrib><creatorcontrib>Inatsu, Akihito, MD</creatorcontrib><creatorcontrib>Ishihara, Masayuki, PhD</creatorcontrib><creatorcontrib>Seki, Shuhji, MD</creatorcontrib><creatorcontrib>Maehara, Tadaaki, MD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nogami, Yashiro, MD</au><au>Kinoshita, Manabu, MD</au><au>Takase, Bonpei, MD</au><au>Inatsu, Akihito, MD</au><au>Ishihara, Masayuki, PhD</au><au>Seki, Shuhji, MD</au><au>Maehara, Tadaaki, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac dysfunction induced by experimental myocardial infarction impairs the host defense response to bacterial infection in mice because of reduced phagocytosis of Kupffer cells</atitle><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle><addtitle>J Thorac Cardiovasc Surg</addtitle><date>2010-09-01</date><risdate>2010</risdate><volume>140</volume><issue>3</issue><spage>624</spage><epage>632.e3</epage><pages>624-632.e3</pages><issn>0022-5223</issn><eissn>1097-685X</eissn><coden>JTCSAQ</coden><abstract>Objective This study was undertaken to investigate the effects of cardiac dysfunction induced by experimental myocardial infarction on the host defense response to bacterial infection and the role of Kupffer cells in mediating this response. Methods Myocardial infarction was induced in C57BL/6 mice by ligation of the left anterior descending coronary artery. Mice were challenged with Escherichia coli intravenously 1, 5, and 14 days after myocardial infarction or sham operation. Thereafter, the cytokine production and the function of their Kupffer cells were assessed. Results Mice with myocardial infarction showed remarkable cardiac dysfunction and had a significantly lower survival than sham mice after bacterial challenge at 5 days after surgery; bacterial challenge at 1 or 14 days after surgery resulted in no difference in survival between myocardial infarction and sham mice. The phagocytic activity of Kupffer cells, assessed by fluorescein isothiocyanate microspheres, remarkably decreased in mice with myocardial infarction 5 days after surgery. Serum peaks of tumor necrosis factor and interferon-γ after bacterial challenge were also suppressed in mice with myocardial infarction at 5 days. Production of these cytokines and immunoglobulin-M from liver mononuclear cells was also impaired in mice with myocardial infarction. Enhancement of the phagocytic activity of Kupffer cells by C-reactive protein significantly improved survival after infection in mice with myocardial infarction, although neither interleukin-18 nor immunoglobulin-M treatment improved survival. Conclusions Cardiac dysfunction induced by myocardial infarction renders mice susceptible to bacterial infection and increases mortality because of a reduced ability of Kupffer cells to clear infectious bacteria. C-reactive protein-enhanced phagocytic activity of Kupffer cells may improve the poor prognosis after bacterial infection in mice with myocardial infarction.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>20138636</pmid><doi>10.1016/j.jtcvs.2009.11.005</doi><tpages>9</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 C-reactive protein C-Reactive Protein - administration & dosage Cardiology. Vascular system Cardiothoracic Surgery Cells, Cultured Coronary heart disease Disease Models, Animal Escherichia coli Escherichia coli Infections - immunology Heart Immunity, Innate Immunoglobulin M - administration & dosage Immunoglobulin M - metabolism Inflammation Mediators - blood Injections, Intraperitoneal Interferon-gamma - blood Interleukin-18 - administration & dosage Kupffer Cells - immunology Kupffer Cells - microbiology Male Medical sciences Mice Mice, Inbred C57BL Myocardial Infarction - diagnostic imaging Myocardial Infarction - immunology Myocardial Infarction - physiopathology Myocarditis. Cardiomyopathies Phagocytosis Pneumology Time Factors Tumor Necrosis Factor-alpha - blood Ultrasonography Ventricular Dysfunction, Left - diagnostic imaging Ventricular Dysfunction, Left - immunology Ventricular Dysfunction, Left - physiopathology Ventricular Function, Left |
| title | Cardiac dysfunction induced by experimental myocardial infarction impairs the host defense response to bacterial infection in mice because of reduced phagocytosis of Kupffer cells |
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