A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-Deficient Mice
Histamine can modulate the cytokine network and influence Th1 and Th2 balance and Ab-isotype switching. Thus, pharmacological blockade or genetic deletion of specific histamine receptors has been shown to reduce the severity of experimental autoimmune encephalomyelitis (EAE), a prototypic Th1-mediat...
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Veröffentlicht in: | Journal of Immunology 2006-01, Vol.176 (1), p.17-26 |
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creator | Musio, Silvia Gallo, Barbara Scabeni, Stefano Lapilla, Marilena Poliani, Pietro L Matarese, Giuseppe Ohtsu, Hiroshi Galli, Stephen J Mantegazza, Renato Steinman, Lawrence Pedotti, Rosetta |
description | Histamine can modulate the cytokine network and influence Th1 and Th2 balance and Ab-isotype switching. Thus, pharmacological blockade or genetic deletion of specific histamine receptors has been shown to reduce the severity of experimental autoimmune encephalomyelitis (EAE), a prototypic Th1-mediated disease with similarities to human multiple sclerosis. To study the comprehensive contribution of endogenous histamine to the expression of EAE, we attempted to induce EAE in histidine decarboxylase-deficient mice, which are genetically unable to make histamine. In this study, we show that EAE is significantly more severe in HDC-/-, histamine-deficient mice, with diffuse inflammatory infiltrates, including a prevalent granulocytic component, in the brain and cerebellum. Unlike splenocytes from wild-type mice, splenocytes from HDC-/- mice do not produce histamine in response to the myelin Ag, whereas production of IFN-gamma, TNF, and leptin are increased in HDC-/- splenocytes in comparison to those from wild-type mice. Endogenous histamine thus appears to regulate importantly the autoimmune response against myelin and the expression of EAE, in this model, and to limit immune damage to the CNS. Understanding which receptor(s) for histamine is/are involved in regulating autoimmunity against the CNS might help in the development of new strategies of treatment for EAE and multiple sclerosis. |
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Thus, pharmacological blockade or genetic deletion of specific histamine receptors has been shown to reduce the severity of experimental autoimmune encephalomyelitis (EAE), a prototypic Th1-mediated disease with similarities to human multiple sclerosis. To study the comprehensive contribution of endogenous histamine to the expression of EAE, we attempted to induce EAE in histidine decarboxylase-deficient mice, which are genetically unable to make histamine. In this study, we show that EAE is significantly more severe in HDC-/-, histamine-deficient mice, with diffuse inflammatory infiltrates, including a prevalent granulocytic component, in the brain and cerebellum. Unlike splenocytes from wild-type mice, splenocytes from HDC-/- mice do not produce histamine in response to the myelin Ag, whereas production of IFN-gamma, TNF, and leptin are increased in HDC-/- splenocytes in comparison to those from wild-type mice. Endogenous histamine thus appears to regulate importantly the autoimmune response against myelin and the expression of EAE, in this model, and to limit immune damage to the CNS. Understanding which receptor(s) for histamine is/are involved in regulating autoimmunity against the CNS might help in the development of new strategies of treatment for EAE and multiple sclerosis.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.4049/jimmunol.176.1.17</identifier><identifier>PMID: 16365391</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Animals ; Brain - immunology ; Brain - pathology ; Chemokine CCL2 - biosynthesis ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Glycoproteins - immunology ; Histamine ; Histidine Decarboxylase - deficiency ; Interferon-gamma - biosynthesis ; Leptin - biosynthesis ; Mice ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments - immunology ; T-Lymphocytes - immunology ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Journal of Immunology, 2006-01, Vol.176 (1), p.17-26</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-a1d4c86ea0380908accafe672b6d81099e814e9577e3a32cd1a221d67d45f8303</citedby><cites>FETCH-LOGICAL-c469t-a1d4c86ea0380908accafe672b6d81099e814e9577e3a32cd1a221d67d45f8303</cites></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/16365391$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Musio, Silvia</creatorcontrib><creatorcontrib>Gallo, Barbara</creatorcontrib><creatorcontrib>Scabeni, Stefano</creatorcontrib><creatorcontrib>Lapilla, Marilena</creatorcontrib><creatorcontrib>Poliani, Pietro L</creatorcontrib><creatorcontrib>Matarese, Giuseppe</creatorcontrib><creatorcontrib>Ohtsu, Hiroshi</creatorcontrib><creatorcontrib>Galli, Stephen J</creatorcontrib><creatorcontrib>Mantegazza, Renato</creatorcontrib><creatorcontrib>Steinman, Lawrence</creatorcontrib><creatorcontrib>Pedotti, Rosetta</creatorcontrib><title>A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-Deficient Mice</title><title>Journal of Immunology</title><addtitle>J Immunol</addtitle><description>Histamine can modulate the cytokine network and influence Th1 and Th2 balance and Ab-isotype switching. Thus, pharmacological blockade or genetic deletion of specific histamine receptors has been shown to reduce the severity of experimental autoimmune encephalomyelitis (EAE), a prototypic Th1-mediated disease with similarities to human multiple sclerosis. To study the comprehensive contribution of endogenous histamine to the expression of EAE, we attempted to induce EAE in histidine decarboxylase-deficient mice, which are genetically unable to make histamine. In this study, we show that EAE is significantly more severe in HDC-/-, histamine-deficient mice, with diffuse inflammatory infiltrates, including a prevalent granulocytic component, in the brain and cerebellum. Unlike splenocytes from wild-type mice, splenocytes from HDC-/- mice do not produce histamine in response to the myelin Ag, whereas production of IFN-gamma, TNF, and leptin are increased in HDC-/- splenocytes in comparison to those from wild-type mice. Endogenous histamine thus appears to regulate importantly the autoimmune response against myelin and the expression of EAE, in this model, and to limit immune damage to the CNS. Understanding which receptor(s) for histamine is/are involved in regulating autoimmunity against the CNS might help in the development of new strategies of treatment for EAE and multiple sclerosis.</description><subject>Animals</subject><subject>Brain - immunology</subject><subject>Brain - pathology</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Glycoproteins - immunology</subject><subject>Histamine</subject><subject>Histidine Decarboxylase - deficiency</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Leptin - biosynthesis</subject><subject>Mice</subject><subject>Myelin-Oligodendrocyte Glycoprotein</subject><subject>Peptide Fragments - immunology</subject><subject>T-Lymphocytes - immunology</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9uEzEQhy0EomnhAbggX-htg2f_2Lvcoia0iCIkBGdr4p1tXHnXwd5VkrfgkXGaAEcuHkvzzTfS_Bh7A2JeirJ5_2j7fhq8m4OSc0jvMzaDqhKZlEI-ZzMh8jxLPXXBLmN8FEJIkZcv2QXIQlZFAzP2a8E_04F_o4fJ4ehD-npHvPOB39k4Ym8H4nbgq_2Wgu1pGNHxxTT6p9XEV4Oh7Qad7w_k7GjjB760kTCm1h4NhTWO1g9HxdFn26NvSQbD2u8PLnHZkjprbDLzL9bQK_aiQxfp9blesR8fV99v7rL7r7efbhb3mSllM2YIbWlqSSiKWjSiRmOwI6nytWxrEE1DNZTUVEpRgUVuWsA8h1aqtqy6uhDFFbs-ebfB_5wojrq30ZBzOJCfopaqqqEC9V8QVAkqwQmEE2iCjzFQp7fpYhgOGoQ-5qX_5JVmpAb9JH97lk_rntp_E-eAEvDuBGzsw2ZnA-nYo3MJB73b7f6KfgNGxqMD</recordid><startdate>20060101</startdate><enddate>20060101</enddate><creator>Musio, Silvia</creator><creator>Gallo, Barbara</creator><creator>Scabeni, Stefano</creator><creator>Lapilla, Marilena</creator><creator>Poliani, Pietro L</creator><creator>Matarese, Giuseppe</creator><creator>Ohtsu, Hiroshi</creator><creator>Galli, Stephen J</creator><creator>Mantegazza, Renato</creator><creator>Steinman, Lawrence</creator><creator>Pedotti, Rosetta</creator><general>Am Assoc Immnol</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>H94</scope><scope>7X8</scope></search><sort><creationdate>20060101</creationdate><title>A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-Deficient Mice</title><author>Musio, Silvia ; Gallo, Barbara ; Scabeni, Stefano ; Lapilla, Marilena ; Poliani, Pietro L ; Matarese, Giuseppe ; Ohtsu, Hiroshi ; Galli, Stephen J ; Mantegazza, Renato ; Steinman, Lawrence ; Pedotti, Rosetta</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-a1d4c86ea0380908accafe672b6d81099e814e9577e3a32cd1a221d67d45f8303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Brain - immunology</topic><topic>Brain - pathology</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Glycoproteins - immunology</topic><topic>Histamine</topic><topic>Histidine Decarboxylase - deficiency</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Leptin - biosynthesis</topic><topic>Mice</topic><topic>Myelin-Oligodendrocyte Glycoprotein</topic><topic>Peptide Fragments - immunology</topic><topic>T-Lymphocytes - immunology</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Musio, Silvia</creatorcontrib><creatorcontrib>Gallo, Barbara</creatorcontrib><creatorcontrib>Scabeni, Stefano</creatorcontrib><creatorcontrib>Lapilla, Marilena</creatorcontrib><creatorcontrib>Poliani, Pietro L</creatorcontrib><creatorcontrib>Matarese, Giuseppe</creatorcontrib><creatorcontrib>Ohtsu, Hiroshi</creatorcontrib><creatorcontrib>Galli, Stephen J</creatorcontrib><creatorcontrib>Mantegazza, Renato</creatorcontrib><creatorcontrib>Steinman, Lawrence</creatorcontrib><creatorcontrib>Pedotti, Rosetta</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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Musio, Silvia</au><au>Gallo, Barbara</au><au>Scabeni, Stefano</au><au>Lapilla, Marilena</au><au>Poliani, Pietro L</au><au>Matarese, Giuseppe</au><au>Ohtsu, Hiroshi</au><au>Galli, Stephen J</au><au>Mantegazza, Renato</au><au>Steinman, Lawrence</au><au>Pedotti, Rosetta</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-Deficient Mice</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2006-01-01</date><risdate>2006</risdate><volume>176</volume><issue>1</issue><spage>17</spage><epage>26</epage><pages>17-26</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><abstract>Histamine can modulate the cytokine network and influence Th1 and Th2 balance and Ab-isotype switching. Thus, pharmacological blockade or genetic deletion of specific histamine receptors has been shown to reduce the severity of experimental autoimmune encephalomyelitis (EAE), a prototypic Th1-mediated disease with similarities to human multiple sclerosis. To study the comprehensive contribution of endogenous histamine to the expression of EAE, we attempted to induce EAE in histidine decarboxylase-deficient mice, which are genetically unable to make histamine. In this study, we show that EAE is significantly more severe in HDC-/-, histamine-deficient mice, with diffuse inflammatory infiltrates, including a prevalent granulocytic component, in the brain and cerebellum. Unlike splenocytes from wild-type mice, splenocytes from HDC-/- mice do not produce histamine in response to the myelin Ag, whereas production of IFN-gamma, TNF, and leptin are increased in HDC-/- splenocytes in comparison to those from wild-type mice. Endogenous histamine thus appears to regulate importantly the autoimmune response against myelin and the expression of EAE, in this model, and to limit immune damage to the CNS. Understanding which receptor(s) for histamine is/are involved in regulating autoimmunity against the CNS might help in the development of new strategies of treatment for EAE and multiple sclerosis.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>16365391</pmid><doi>10.4049/jimmunol.176.1.17</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Brain - immunology Brain - pathology Chemokine CCL2 - biosynthesis Encephalomyelitis, Autoimmune, Experimental - immunology Glycoproteins - immunology Histamine Histidine Decarboxylase - deficiency Interferon-gamma - biosynthesis Leptin - biosynthesis Mice Myelin-Oligodendrocyte Glycoprotein Peptide Fragments - immunology T-Lymphocytes - immunology Tumor Necrosis Factor-alpha - biosynthesis |
title | A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-Deficient Mice |
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