Ingested (oral) alpha-MSH inhibits acute EAE. J Neuroimmunol 2008 Jan;193(1-2):106-12
Date
11/27/2007Pubmed ID
18037504DOI
10.1016/j.jneuroim.2007.10.026Scopus ID
2-s2.0-37749026839 (requires institutional sign-in at Scopus site) 19 CitationsAbstract
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-alpha and MIP-1-gamma 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.
Author List
Brod SA, Hood ZMMESH terms used to index this publication - Major topics in bold
Acute DiseaseAdministration, Oral
Animals
Anti-Inflammatory Agents
Chemokines
Encephalomyelitis, Autoimmune, Experimental
Female
Glycoproteins
Interferon-gamma
Interleukin-12
Interleukin-2
Mice
Mice, Inbred C57BL
Myelin-Oligodendrocyte Glycoprotein
Peptide Fragments
alpha-MSH
