| pubmed-article:17256058 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17256058 | lifeskim:mentions | umls-concept:C0007018 | lld:lifeskim |
| pubmed-article:17256058 | lifeskim:mentions | umls-concept:C0538674 | lld:lifeskim |
| pubmed-article:17256058 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:17256058 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:17256058 | pubmed:dateCreated | 2007-2-2 | lld:pubmed |
| pubmed-article:17256058 | pubmed:abstractText | Heme oxygenase-1 (HO-1, encoded by HMOX1) dampens inflammatory reactions via the catabolism of heme into CO, Fe, and biliverdin. We report that expression of HO-1 dictates the pathologic outcome of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). Induction of EAE in Hmox1(-/- )C57BL/6 mice led to enhanced CNS demyelination, paralysis, and mortality, as compared with Hmox1(+/+) mice. Induction of HO-1 by cobalt protoporphyrin IX (CoPPIX) administration after EAE onset reversed paralysis in C57BL/6 and SJL/J mice and disease relapse in SJL/J mice. These effects were not observed using zinc protoporphyrin IX, which does not induce HO-1. CoPPIX protection was abrogated in Hmox1(-/-) C57BL/6 mice, indicating that CoPPIX acts via HO-1 to suppress EAE progression. The protective effect of HO-1 was associated with inhibition of MHC class II expression by APCs and inhibition of Th and CD8 T cell accumulation, proliferation, and effector function within the CNS. Exogenous CO mimicked these effects, suggesting that CO contributes to the protective action of HO-1. In conclusion, HO-1 or exposure to its end product CO counters autoimmune neuroinflammation and thus might be used therapeutically to treat MS. | lld:pubmed |
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| pubmed-article:17256058 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17256058 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17256058 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:17256058 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17256058 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17256058 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:SteinmanLawre... | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:SobelRaymond... | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:SoaresMiguel... | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:FontouraPaulo... | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:HoPeggy PPP | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:PaisTeresa... | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:LeeLowen YLY | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:CunhaAndreiaA | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:ChoraAngelo... | lld:pubmed |
| pubmed-article:17256058 | pubmed:author | pubmed-author:CardosoSílvia... | lld:pubmed |
| pubmed-article:17256058 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17256058 | pubmed:volume | 117 | lld:pubmed |
| pubmed-article:17256058 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17256058 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17256058 | pubmed:pagination | 438-47 | lld:pubmed |
| pubmed-article:17256058 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17256058 | pubmed:year | 2007 | lld:pubmed |
