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Mouse genetic background influences severity of immune responses following trauma-hemorrhage
Studies have shown that following bacterial infection or endotoxin administration, immune functions are regulated differently in mice of different genetic background. Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine w...
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Published in: | Cytokine (Philadelphia, Pa.) Pa.), 2005-05, Vol.30 (4), p.168-176 |
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container_title | Cytokine (Philadelphia, Pa.) |
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creator | Matsutani, Takeshi Anantha Samy, T.S. Kang, Shih-Ching Bland, Kirby I. Chaudry, Irshad H. |
description | Studies have shown that following bacterial infection or endotoxin administration, immune functions are regulated differently in mice of different genetic background. Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine whether genetic background of the animal influence immune functions after trauma-hemorrhage. The aim of our studies, therefore, was to assess differences in the immune functions in genetically different strains of age-matched C3H/HeN and C57BL/6 male mice following trauma-hemorrhage. The analysis for immune functions included: proliferation of splenocyte and bone-marrow cells, IL-2 and IFN-γ release by splenocytes, and TNF-α and IL-10 release by splenic, peritoneal, liver (Kupffer cell), and bone-marrow macrophages. The results show significant differences in splenocyte and bone-marrow functions, and in the release of the mediators of immune function by immune competent cells: (a) between the two genetic strains, and (b) in each mouse strain following trauma-hemorrhage. Thus, genetic background appears to significantly influence the severity of immune responses in males following trauma-hemorrhage. |
doi_str_mv | 10.1016/j.cyto.2004.12.019 |
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Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine whether genetic background of the animal influence immune functions after trauma-hemorrhage. The aim of our studies, therefore, was to assess differences in the immune functions in genetically different strains of age-matched C3H/HeN and C57BL/6 male mice following trauma-hemorrhage. The analysis for immune functions included: proliferation of splenocyte and bone-marrow cells, IL-2 and IFN-γ release by splenocytes, and TNF-α and IL-10 release by splenic, peritoneal, liver (Kupffer cell), and bone-marrow macrophages. The results show significant differences in splenocyte and bone-marrow functions, and in the release of the mediators of immune function by immune competent cells: (a) between the two genetic strains, and (b) in each mouse strain following trauma-hemorrhage. Thus, genetic background appears to significantly influence the severity of immune responses in males following trauma-hemorrhage.</description><identifier>ISSN: 1043-4666</identifier><identifier>EISSN: 1096-0023</identifier><identifier>DOI: 10.1016/j.cyto.2004.12.019</identifier><identifier>PMID: 15863390</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Bone Marrow Cells ; Bone-marrow proliferation ; Cell Proliferation ; Cytokine release ; Genetic Predisposition to Disease ; Hemorrhage - genetics ; Hemorrhage - immunology ; Immunity, Cellular - genetics ; Interferon-gamma - metabolism ; Interleukin-10 - metabolism ; Interleukin-2 - metabolism ; Macrophages - metabolism ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Spleen - cytology ; Spleen - immunology ; Spleen - metabolism ; Splenocytes ; Tumor Necrosis Factor-alpha - metabolism ; Wounds and Injuries - genetics ; Wounds and Injuries - immunology</subject><ispartof>Cytokine (Philadelphia, Pa.), 2005-05, Vol.30 (4), p.168-176</ispartof><rights>2005 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-2c592a36f8ceb91c2c82a7ebf94e1837571cc5f991a63987596a8d35b06785a03</citedby></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/15863390$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsutani, Takeshi</creatorcontrib><creatorcontrib>Anantha Samy, T.S.</creatorcontrib><creatorcontrib>Kang, Shih-Ching</creatorcontrib><creatorcontrib>Bland, Kirby I.</creatorcontrib><creatorcontrib>Chaudry, Irshad H.</creatorcontrib><title>Mouse genetic background influences severity of immune responses following trauma-hemorrhage</title><title>Cytokine (Philadelphia, Pa.)</title><addtitle>Cytokine</addtitle><description>Studies have shown that following bacterial infection or endotoxin administration, immune functions are regulated differently in mice of different genetic background. Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine whether genetic background of the animal influence immune functions after trauma-hemorrhage. The aim of our studies, therefore, was to assess differences in the immune functions in genetically different strains of age-matched C3H/HeN and C57BL/6 male mice following trauma-hemorrhage. The analysis for immune functions included: proliferation of splenocyte and bone-marrow cells, IL-2 and IFN-γ release by splenocytes, and TNF-α and IL-10 release by splenic, peritoneal, liver (Kupffer cell), and bone-marrow macrophages. The results show significant differences in splenocyte and bone-marrow functions, and in the release of the mediators of immune function by immune competent cells: (a) between the two genetic strains, and (b) in each mouse strain following trauma-hemorrhage. Thus, genetic background appears to significantly influence the severity of immune responses in males following trauma-hemorrhage.</description><subject>Animals</subject><subject>Bone Marrow Cells</subject><subject>Bone-marrow proliferation</subject><subject>Cell Proliferation</subject><subject>Cytokine release</subject><subject>Genetic Predisposition to Disease</subject><subject>Hemorrhage - genetics</subject><subject>Hemorrhage - immunology</subject><subject>Immunity, Cellular - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-2 - metabolism</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Spleen - cytology</subject><subject>Spleen - immunology</subject><subject>Spleen - metabolism</subject><subject>Splenocytes</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Wounds and Injuries - genetics</subject><subject>Wounds and Injuries - immunology</subject><issn>1043-4666</issn><issn>1096-0023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkE1Lw0AQhhdRbK3-AQ-Sk7fE_Ug2WfAixS-oeNGbsGw2k3Zrkq27SaX_3g0teNPTDMzzvjAPQpcEJwQTfrNO9K63CcU4TQhNMBFHaEqw4DHGlB2Pe8rilHM-QWferzHGguX5KZqQrOCMCTxFHy928BAtoYPe6KhU-nPp7NBVkenqZoBOg488bMGZfhfZOjJtO3QQOfAb2_lwrG3T2G_TLaPeqaFV8Qpa69xKLeEcndSq8XBxmDP0_nD_Nn-KF6-Pz_O7RaxZkfUx1ZmgivG60FAKoqkuqMqhrEUKpGB5lhOts1oIojgTRZ4JroqKZSXmeZEpzGboet-7cfZrAN_L1ngNTaM6CO_JgGER4v-CJGecEMEDSPegdtZ7B7XcONMqt5MEy1G-XMtRvhzlS0JlkB9CV4f2oWyh-o0cbAfgdg9AkLE14KTXZlRcGQe6l5U1f_X_AAVFl0E</recordid><startdate>20050521</startdate><enddate>20050521</enddate><creator>Matsutani, Takeshi</creator><creator>Anantha Samy, T.S.</creator><creator>Kang, Shih-Ching</creator><creator>Bland, Kirby I.</creator><creator>Chaudry, Irshad H.</creator><general>Elsevier Ltd</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>7QL</scope><scope>7T5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050521</creationdate><title>Mouse genetic background influences severity of immune responses following trauma-hemorrhage</title><author>Matsutani, Takeshi ; Anantha Samy, T.S. ; Kang, Shih-Ching ; Bland, Kirby I. ; Chaudry, Irshad H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-2c592a36f8ceb91c2c82a7ebf94e1837571cc5f991a63987596a8d35b06785a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Bone Marrow Cells</topic><topic>Bone-marrow proliferation</topic><topic>Cell Proliferation</topic><topic>Cytokine release</topic><topic>Genetic Predisposition to Disease</topic><topic>Hemorrhage - genetics</topic><topic>Hemorrhage - immunology</topic><topic>Immunity, Cellular - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-10 - metabolism</topic><topic>Interleukin-2 - metabolism</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred C57BL</topic><topic>Spleen - cytology</topic><topic>Spleen - immunology</topic><topic>Spleen - metabolism</topic><topic>Splenocytes</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Wounds and Injuries - genetics</topic><topic>Wounds and Injuries - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsutani, Takeshi</creatorcontrib><creatorcontrib>Anantha Samy, T.S.</creatorcontrib><creatorcontrib>Kang, Shih-Ching</creatorcontrib><creatorcontrib>Bland, Kirby I.</creatorcontrib><creatorcontrib>Chaudry, Irshad H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</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><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cytokine (Philadelphia, Pa.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsutani, Takeshi</au><au>Anantha Samy, T.S.</au><au>Kang, Shih-Ching</au><au>Bland, Kirby I.</au><au>Chaudry, Irshad H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mouse genetic background influences severity of immune responses following trauma-hemorrhage</atitle><jtitle>Cytokine (Philadelphia, Pa.)</jtitle><addtitle>Cytokine</addtitle><date>2005-05-21</date><risdate>2005</risdate><volume>30</volume><issue>4</issue><spage>168</spage><epage>176</epage><pages>168-176</pages><issn>1043-4666</issn><eissn>1096-0023</eissn><abstract>Studies have shown that following bacterial infection or endotoxin administration, immune functions are regulated differently in mice of different genetic background. Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine whether genetic background of the animal influence immune functions after trauma-hemorrhage. The aim of our studies, therefore, was to assess differences in the immune functions in genetically different strains of age-matched C3H/HeN and C57BL/6 male mice following trauma-hemorrhage. The analysis for immune functions included: proliferation of splenocyte and bone-marrow cells, IL-2 and IFN-γ release by splenocytes, and TNF-α and IL-10 release by splenic, peritoneal, liver (Kupffer cell), and bone-marrow macrophages. The results show significant differences in splenocyte and bone-marrow functions, and in the release of the mediators of immune function by immune competent cells: (a) between the two genetic strains, and (b) in each mouse strain following trauma-hemorrhage. 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subjects | Animals Bone Marrow Cells Bone-marrow proliferation Cell Proliferation Cytokine release Genetic Predisposition to Disease Hemorrhage - genetics Hemorrhage - immunology Immunity, Cellular - genetics Interferon-gamma - metabolism Interleukin-10 - metabolism Interleukin-2 - metabolism Macrophages - metabolism Mice Mice, Inbred C3H Mice, Inbred C57BL Spleen - cytology Spleen - immunology Spleen - metabolism Splenocytes Tumor Necrosis Factor-alpha - metabolism Wounds and Injuries - genetics Wounds and Injuries - immunology |
title | Mouse genetic background influences severity of immune responses following trauma-hemorrhage |
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