Suppression of experimental autoimmune encephalomyelitis by ghrelin.

Authors: Theil, Michael-Mark  Miyake, Sachiko  Mizuno, Miho  Tomi, Chiharu  Croxford, J Ludovic  Hosoda, Hiroshi  Theil, Julia  von Hörsten, Stephan  Yokote, Hiroaki  Chiba, Asako  Lin, Youwei  Oki, Shinji  Akamizu, Takashi  Kangawa, Kenji  Yamamura, Takashi 
Citation: Theil MM, etal., J Immunol. 2009 Aug 15;183(4):2859-66. doi: 10.4049/jimmunol.0803362. Epub 2009 Jul 20.
Pubmed: (View Article at PubMed) PMID:19620309
DOI: Full-text: DOI:10.4049/jimmunol.0803362

Ghrelin is a recently identified gastric hormone that displays strong growth hormone-releasing activity mediated by the growth hormone secretagogue receptor. While this unique endogenous peptide participates in the regulation of energy homeostasis, increases food intake, and decreases energy expenditure, its ability to inhibit the production of proinflammatory cytokines in vitro indicates its role in the regulation of inflammatory process in vivo. Here we examine the effect of exogenous ghrelin on the development of experimental autoimmune encephalomyelitis (EAE), a representative model of multiple sclerosis. In the C57BL/6 mouse model of EAE induced by sensitization to myelin oligodendrocyte glycoprotein 35-55 peptide, we found that alternate-day s.c. injections of ghrelin (5 mug/kg/day) from day 1 to 35 significantly reduced the clinical severity of EAE. The suppression of EAE was accompanied by reduced mRNA levels of proinflammatory cytokines such as TNF-alpha, IL-1beta, and IL-6 in the spinal cord cellular infiltrates and microglia from ghrelin-treated mice at the peak of disease, suggesting the role of ghrelin as an antiinflammatory hormone. Consistently, ghrelin significantly suppressed the production of proinflammatory cytokines in LPS-stimulated microglia in vitro. These results shed light on the new role of ghrelin in the regulation of inflammation with possible implications for management of human diseases.

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CRRD ID: 12905041
Created: 2017-06-01
Species: All species
Last Modified: 2017-06-01
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.