Ingested (oral) alpha-MSH inhibits acute EAE
Abstract Ingested type I IFN and SIRS peptide administered orally inhibit EAE. We examined whether another immunoactive protein, tridecapeptide alpha-MSH, would have similar anti-inflammatory effects in EAE after oral administration. B6 mice were immunized with MOG peptide 35–55 and gavaged with 0.1...
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Veröffentlicht in: | Journal of neuroimmunology 2008-01, Vol.193 (1), p.106-112 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Ingested type I IFN and SIRS peptide administered orally inhibit EAE. We examined whether another immunoactive protein, tridecapeptide alpha-MSH, would have similar anti-inflammatory effects in EAE after oral administration. B6 mice were immunized with MOG peptide 35–55 and gavaged with 0.1 ml of control saline or alpha-MSH peptide starting on day − 7 preceding active immunization, and continuing through day +14 post-immunization. Alpha-MSH peptide delayed disease onset and decreased inflammatory foci. CNS lymphocytes showed decreases in Th1-like encephalitogenic cytokines IL-2 and IL12p70 in the alpha-MSH fed group compared to the mock fed group. For Th2-like counter-regulatory cytokines, there were increases in peripheral SDF-1 levels comparing alpha-MSH fed vs mock fed groups. There were decreases of chemokines MIP-1-α and MIP-1-γ in the CNS comparing alpha-MSH fed mice vs mock fed mice. Ingested (orally administered) alpha-MSH peptide can reduce clinical disease and inhibit CNS inflammation by decreasing migration of antigen driven CNS Th1 cells into the target organ. |
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ISSN: | 0165-5728 1872-8421 |
DOI: | 10.1016/j.jneuroim.2007.10.026 |