Enhancement of 1,25-dihydroxyvitamin D₃-mediated suppression of experimental autoimmune encephalomyelitis by calcitonin
The active form of vitamin D, 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], suppresses disease development in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). However, complete disease prevention only occurs with doses that dramatically elevate serum calcium levels, t...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2009-03, Vol.106 (13), p.5276-5281 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Becklund, Bryan R Hansen, Donald W. Jr DeLuca, Hector F |
| description | The active form of vitamin D, 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], suppresses disease development in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). However, complete disease prevention only occurs with doses that dramatically elevate serum calcium levels, thus limiting the usefulness of 1,25(OH)₂D₃ as a potential MS therapeutic agent. Because calcitonin (CT) is believed to be released by hypercalcemia and has been shown to be anti-inflammatory, we examined whether suppression of EAE by 1,25(OH)₂D₃ could be mediated either in part or entirely by CT. Continuous administration of pharmacological doses of CT did not prevent EAE. However, a combination of CT and a subtherapeutic dose of 1,25(OH)₂D₃ additively suppressed EAE without causing hypercalcemia. Moreover, CT decreased the dose of 1,25(OH)₂D₃ required for disease suppression. Our results suggest that CT may be a significant factor but cannot account entirely for 1,25(OH)₂D₃-mediated suppression of EAE. |
| doi_str_mv | 10.1073/pnas.0813312106 |
| format | Article |
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Moreover, CT decreased the dose of 1,25(OH)₂D₃ required for disease suppression. 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Jr</creatorcontrib><creatorcontrib>DeLuca, Hector F</creatorcontrib><title>Enhancement of 1,25-dihydroxyvitamin D₃-mediated suppression of experimental autoimmune encephalomyelitis by calcitonin</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The active form of vitamin D, 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], suppresses disease development in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). However, complete disease prevention only occurs with doses that dramatically elevate serum calcium levels, thus limiting the usefulness of 1,25(OH)₂D₃ as a potential MS therapeutic agent. Because calcitonin (CT) is believed to be released by hypercalcemia and has been shown to be anti-inflammatory, we examined whether suppression of EAE by 1,25(OH)₂D₃ could be mediated either in part or entirely by CT. Continuous administration of pharmacological doses of CT did not prevent EAE. However, a combination of CT and a subtherapeutic dose of 1,25(OH)₂D₃ additively suppressed EAE without causing hypercalcemia. Moreover, CT decreased the dose of 1,25(OH)₂D₃ required for disease suppression. Our results suggest that CT may be a significant factor but cannot account entirely for 1,25(OH)₂D₃-mediated suppression of EAE.</description><subject>Animals</subject><subject>Biological Sciences</subject><subject>Calcitonin - pharmacology</subject><subject>Calcitonin - therapeutic use</subject><subject>Calcium</subject><subject>Calcium - analysis</subject><subject>Diet</subject><subject>Dietary calcium</subject><subject>Dosage</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Synergism</subject><subject>Drug Therapy, Combination</subject><subject>Encephalomyelitis, Autoimmune, Experimental - drug therapy</subject><subject>Encephalomyelitis, Autoimmune, Experimental - prevention & control</subject><subject>Hypercalcemia</subject><subject>Immunization</subject><subject>Mice</subject><subject>Pumps</subject><subject>Vehicles</subject><subject>Vitamin D</subject><subject>Vitamin D - analogs & derivatives</subject><subject>Vitamin D - pharmacology</subject><subject>Vitamin D - therapeutic use</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kTtv1jAUhi1ERT8KMxOQkaEpPr5nQUKlQKVKHaCz5ThOP1eJHcVO9WWFf8ovwVVvsHQ6w_ucR-eC0BvAR4Al_TgFk46wAkqBABbP0AZwA7VgDX6ONhgTWStG2D56mdIVxrjhCr9A-9AQRZhUG7SehK0J1o0u5Cr2FRwSXnd-u3Zz3K3XPpvRh-rLn1-_69F13mTXVWmZptml5GO4aXG7yc3-RmCGyiw5-nFcgqtc0U5bM8RxdYPPPlXtWlkzWJ9j8OEV2uvNkNzru3qALr6e_Dz-Xp-dfzs9_nxW94RTURsHqjGipZxbpiRYapmQ0Da2a6HltGGUqq4VynaKCIGBEmWlJExQJbGl9AB9uvVOS1tWsGXO2Qx6KiObedXReP1_EvxWX8ZrXWwMAyuCd_8KHjrvj1iAD3dA-cZjjIUGqjmRQvfLMGS3ywV9_zRaiLe3xFXKcX5AGGacgxKPht5EbS5nn_TFD1LWxiCASqHoX-ChovA</recordid><startdate>20090331</startdate><enddate>20090331</enddate><creator>Becklund, Bryan R</creator><creator>Hansen, Donald W. 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Jr ; DeLuca, Hector F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-f2536-ae189a6b355c4871c3c4671b9cdb1b5394338db68cd826601328c772463870c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Biological Sciences</topic><topic>Calcitonin - pharmacology</topic><topic>Calcitonin - therapeutic use</topic><topic>Calcium</topic><topic>Calcium - analysis</topic><topic>Diet</topic><topic>Dietary calcium</topic><topic>Dosage</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Synergism</topic><topic>Drug Therapy, Combination</topic><topic>Encephalomyelitis, Autoimmune, Experimental - drug therapy</topic><topic>Encephalomyelitis, Autoimmune, Experimental - prevention & control</topic><topic>Hypercalcemia</topic><topic>Immunization</topic><topic>Mice</topic><topic>Pumps</topic><topic>Vehicles</topic><topic>Vitamin D</topic><topic>Vitamin D - analogs & derivatives</topic><topic>Vitamin D - pharmacology</topic><topic>Vitamin D - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Becklund, Bryan R</creatorcontrib><creatorcontrib>Hansen, Donald W. Jr</creatorcontrib><creatorcontrib>DeLuca, Hector F</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Becklund, Bryan R</au><au>Hansen, Donald W. Jr</au><au>DeLuca, Hector F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhancement of 1,25-dihydroxyvitamin D₃-mediated suppression of experimental autoimmune encephalomyelitis by calcitonin</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2009-03-31</date><risdate>2009</risdate><volume>106</volume><issue>13</issue><spage>5276</spage><epage>5281</epage><pages>5276-5281</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>The active form of vitamin D, 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], suppresses disease development in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). However, complete disease prevention only occurs with doses that dramatically elevate serum calcium levels, thus limiting the usefulness of 1,25(OH)₂D₃ as a potential MS therapeutic agent. Because calcitonin (CT) is believed to be released by hypercalcemia and has been shown to be anti-inflammatory, we examined whether suppression of EAE by 1,25(OH)₂D₃ could be mediated either in part or entirely by CT. Continuous administration of pharmacological doses of CT did not prevent EAE. However, a combination of CT and a subtherapeutic dose of 1,25(OH)₂D₃ additively suppressed EAE without causing hypercalcemia. Moreover, CT decreased the dose of 1,25(OH)₂D₃ required for disease suppression. Our results suggest that CT may be a significant factor but cannot account entirely for 1,25(OH)₂D₃-mediated suppression of EAE.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>19282478</pmid><doi>10.1073/pnas.0813312106</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological Sciences Calcitonin - pharmacology Calcitonin - therapeutic use Calcium Calcium - analysis Diet Dietary calcium Dosage Dose-Response Relationship, Drug Drug Synergism Drug Therapy, Combination Encephalomyelitis, Autoimmune, Experimental - drug therapy Encephalomyelitis, Autoimmune, Experimental - prevention & control Hypercalcemia Immunization Mice Pumps Vehicles Vitamin D Vitamin D - analogs & derivatives Vitamin D - pharmacology Vitamin D - therapeutic use |
| title | Enhancement of 1,25-dihydroxyvitamin D₃-mediated suppression of experimental autoimmune encephalomyelitis by calcitonin |
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