Substance P receptor mediated maintenance of chronic inflammation in EAE
Substance P (SP) is a modulatory, pro-inflammatory neuropeptide. We investigated the role of the SP receptor, neurokinin-1 (NK-1), in EAE. Our data show that in the chronic phase, mice lacking NK-1 have improved mobility and decreased numbers of LFA-1 high CD4+ T cells and MOG-specific, IFN-γ produc...
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| Veröffentlicht in: | Journal of neuroimmunology 2006-11, Vol.180 (1), p.117-125 |
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| container_title | Journal of neuroimmunology |
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| creator | Reinke, Emily K. Johnson, Matthew J. Ling, Changying Karman, Jozsef Lee, JangEun Weinstock, Joel V. Sandor, Matyas Fabry, Zsuzsa |
| description | Substance P (SP) is a modulatory, pro-inflammatory neuropeptide. We investigated the role of the SP receptor, neurokinin-1 (NK-1), in EAE. Our data show that in the chronic phase, mice lacking NK-1 have improved mobility and decreased numbers of LFA-1 high CD4+ T cells and MOG-specific, IFN-γ producing CD4+ T cells. SR140333, an NK-1 antagonist, administered alone during the chronic phase of EAE was not sufficient to ameliorate symptoms. These results indicate that SP, through NK-1, contributes to maintenance of CNS inflammation, and combining NK-1 antagonists with conventional anti-inflammatory treatments may enhance the success of treatments for diseases like multiple sclerosis. |
| doi_str_mv | 10.1016/j.jneuroim.2006.07.010 |
| format | Article |
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We investigated the role of the SP receptor, neurokinin-1 (NK-1), in EAE. Our data show that in the chronic phase, mice lacking NK-1 have improved mobility and decreased numbers of LFA-1 high CD4+ T cells and MOG-specific, IFN-γ producing CD4+ T cells. SR140333, an NK-1 antagonist, administered alone during the chronic phase of EAE was not sufficient to ameliorate symptoms. These results indicate that SP, through NK-1, contributes to maintenance of CNS inflammation, and combining NK-1 antagonists with conventional anti-inflammatory treatments may enhance the success of treatments for diseases like multiple sclerosis.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/j.jneuroim.2006.07.010</identifier><identifier>PMID: 16942803</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; CD4-Positive T-Lymphocytes - immunology ; Chronic Disease - therapy ; Disease Models, Animal ; Drug Synergism ; Drug Therapy, Combination ; EAE ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - physiopathology ; Female ; Immunity, Cellular - drug effects ; Immunity, Cellular - immunology ; Immunosuppression - methods ; Immunosuppression - standards ; Interferon-gamma - immunology ; Interferon-gamma - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity - drug effects ; Motor Activity - immunology ; Myelin Proteins ; Myelin-Associated Glycoprotein - immunology ; Myelin-Oligodendrocyte Glycoprotein ; Neuroimmunomodulation - immunology ; Neurokinin ; Neurokinin-1 Receptor Antagonists ; Neuropeptide ; Piperidines - pharmacology ; Piperidines - therapeutic use ; Quinuclidines - pharmacology ; Quinuclidines - therapeutic use ; Receptors, Neurokinin-1 - genetics ; SR140333 ; Substance P ; Substance P - immunology</subject><ispartof>Journal of neuroimmunology, 2006-11, Vol.180 (1), p.117-125</ispartof><rights>2006 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-2418c4e61d4931717213810a9392d37393156ffd5aa64e96057e74a76c4ea7743</citedby><cites>FETCH-LOGICAL-c463t-2418c4e61d4931717213810a9392d37393156ffd5aa64e96057e74a76c4ea7743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jneuroim.2006.07.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16942803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reinke, Emily K.</creatorcontrib><creatorcontrib>Johnson, Matthew J.</creatorcontrib><creatorcontrib>Ling, Changying</creatorcontrib><creatorcontrib>Karman, Jozsef</creatorcontrib><creatorcontrib>Lee, JangEun</creatorcontrib><creatorcontrib>Weinstock, Joel V.</creatorcontrib><creatorcontrib>Sandor, Matyas</creatorcontrib><creatorcontrib>Fabry, Zsuzsa</creatorcontrib><title>Substance P receptor mediated maintenance of chronic inflammation in EAE</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>Substance P (SP) is a modulatory, pro-inflammatory neuropeptide. We investigated the role of the SP receptor, neurokinin-1 (NK-1), in EAE. Our data show that in the chronic phase, mice lacking NK-1 have improved mobility and decreased numbers of LFA-1 high CD4+ T cells and MOG-specific, IFN-γ producing CD4+ T cells. SR140333, an NK-1 antagonist, administered alone during the chronic phase of EAE was not sufficient to ameliorate symptoms. These results indicate that SP, through NK-1, contributes to maintenance of CNS inflammation, and combining NK-1 antagonists with conventional anti-inflammatory treatments may enhance the success of treatments for diseases like multiple sclerosis.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Chronic Disease - therapy</subject><subject>Disease Models, Animal</subject><subject>Drug Synergism</subject><subject>Drug Therapy, Combination</subject><subject>EAE</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - physiopathology</subject><subject>Female</subject><subject>Immunity, Cellular - drug effects</subject><subject>Immunity, Cellular - immunology</subject><subject>Immunosuppression - methods</subject><subject>Immunosuppression - standards</subject><subject>Interferon-gamma - immunology</subject><subject>Interferon-gamma - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Motor Activity - drug effects</subject><subject>Motor Activity - immunology</subject><subject>Myelin Proteins</subject><subject>Myelin-Associated Glycoprotein - immunology</subject><subject>Myelin-Oligodendrocyte Glycoprotein</subject><subject>Neuroimmunomodulation - immunology</subject><subject>Neurokinin</subject><subject>Neurokinin-1 Receptor Antagonists</subject><subject>Neuropeptide</subject><subject>Piperidines - pharmacology</subject><subject>Piperidines - therapeutic use</subject><subject>Quinuclidines - pharmacology</subject><subject>Quinuclidines - therapeutic use</subject><subject>Receptors, Neurokinin-1 - genetics</subject><subject>SR140333</subject><subject>Substance P</subject><subject>Substance P - immunology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkF1LwzAUhoMobk7_wuiVd61J89XeOWQ6YaCgXocsPcWUNZlJK_jvzdzES68OOXnevORBaE5wQTARN13RORiDt31RYiwKLAtM8AmakkqWecVKcoqmCeQ5l2U1QRcxdhgTTll9jiZE1KysMJ2i1cu4iYN2BrLnLICB3eBD1kNj9QBN1mvrBnA_977NzHvwzprMunar-14P1rt0yJaL5SU6a_U2wtVxztDb_fL1bpWvnx4e7xbr3DBBh7xkpDIMBGlYTYkksiS0IljXtC4bKmlactG2DddaMKgF5hIk01KkkJaS0Rm6Pry7C_5jhDio3kYD26124MeoSM2xlBwnUBxAE3yMAVq1C7bX4UsRrPYOVad-Haq9Q4WlSg5TcH5sGDdJxF_sKC0BtwcA0j8_LQQVjYWkqLHJ4KAab__r-AZuhYSt</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Reinke, Emily K.</creator><creator>Johnson, Matthew J.</creator><creator>Ling, Changying</creator><creator>Karman, Jozsef</creator><creator>Lee, JangEun</creator><creator>Weinstock, Joel V.</creator><creator>Sandor, Matyas</creator><creator>Fabry, Zsuzsa</creator><general>Elsevier B.V</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>7T5</scope><scope>7TK</scope><scope>H94</scope></search><sort><creationdate>20061101</creationdate><title>Substance P receptor mediated maintenance of chronic inflammation in EAE</title><author>Reinke, Emily K. ; Johnson, Matthew J. ; Ling, Changying ; Karman, Jozsef ; Lee, JangEun ; Weinstock, Joel V. ; Sandor, Matyas ; Fabry, Zsuzsa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-2418c4e61d4931717213810a9392d37393156ffd5aa64e96057e74a76c4ea7743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Chronic Disease - therapy</topic><topic>Disease Models, Animal</topic><topic>Drug Synergism</topic><topic>Drug Therapy, Combination</topic><topic>EAE</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - physiopathology</topic><topic>Female</topic><topic>Immunity, Cellular - drug effects</topic><topic>Immunity, Cellular - immunology</topic><topic>Immunosuppression - methods</topic><topic>Immunosuppression - standards</topic><topic>Interferon-gamma - immunology</topic><topic>Interferon-gamma - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Motor Activity - drug effects</topic><topic>Motor Activity - immunology</topic><topic>Myelin Proteins</topic><topic>Myelin-Associated Glycoprotein - immunology</topic><topic>Myelin-Oligodendrocyte Glycoprotein</topic><topic>Neuroimmunomodulation - immunology</topic><topic>Neurokinin</topic><topic>Neurokinin-1 Receptor Antagonists</topic><topic>Neuropeptide</topic><topic>Piperidines - pharmacology</topic><topic>Piperidines - therapeutic use</topic><topic>Quinuclidines - pharmacology</topic><topic>Quinuclidines - therapeutic use</topic><topic>Receptors, Neurokinin-1 - genetics</topic><topic>SR140333</topic><topic>Substance P</topic><topic>Substance P - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reinke, Emily K.</creatorcontrib><creatorcontrib>Johnson, Matthew J.</creatorcontrib><creatorcontrib>Ling, Changying</creatorcontrib><creatorcontrib>Karman, Jozsef</creatorcontrib><creatorcontrib>Lee, JangEun</creatorcontrib><creatorcontrib>Weinstock, Joel V.</creatorcontrib><creatorcontrib>Sandor, Matyas</creatorcontrib><creatorcontrib>Fabry, Zsuzsa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reinke, Emily K.</au><au>Johnson, Matthew J.</au><au>Ling, Changying</au><au>Karman, Jozsef</au><au>Lee, JangEun</au><au>Weinstock, Joel V.</au><au>Sandor, Matyas</au><au>Fabry, Zsuzsa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Substance P receptor mediated maintenance of chronic inflammation in EAE</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>180</volume><issue>1</issue><spage>117</spage><epage>125</epage><pages>117-125</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>Substance P (SP) is a modulatory, pro-inflammatory neuropeptide. We investigated the role of the SP receptor, neurokinin-1 (NK-1), in EAE. Our data show that in the chronic phase, mice lacking NK-1 have improved mobility and decreased numbers of LFA-1 high CD4+ T cells and MOG-specific, IFN-γ producing CD4+ T cells. SR140333, an NK-1 antagonist, administered alone during the chronic phase of EAE was not sufficient to ameliorate symptoms. These results indicate that SP, through NK-1, contributes to maintenance of CNS inflammation, and combining NK-1 antagonists with conventional anti-inflammatory treatments may enhance the success of treatments for diseases like multiple sclerosis.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>16942803</pmid><doi>10.1016/j.jneuroim.2006.07.010</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use CD4-Positive T-Lymphocytes - immunology Chronic Disease - therapy Disease Models, Animal Drug Synergism Drug Therapy, Combination EAE Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - physiopathology Female Immunity, Cellular - drug effects Immunity, Cellular - immunology Immunosuppression - methods Immunosuppression - standards Interferon-gamma - immunology Interferon-gamma - metabolism Mice Mice, Inbred C57BL Mice, Knockout Motor Activity - drug effects Motor Activity - immunology Myelin Proteins Myelin-Associated Glycoprotein - immunology Myelin-Oligodendrocyte Glycoprotein Neuroimmunomodulation - immunology Neurokinin Neurokinin-1 Receptor Antagonists Neuropeptide Piperidines - pharmacology Piperidines - therapeutic use Quinuclidines - pharmacology Quinuclidines - therapeutic use Receptors, Neurokinin-1 - genetics SR140333 Substance P Substance P - immunology |
| title | Substance P receptor mediated maintenance of chronic inflammation in EAE |
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