Peer-Reviewed Journal Details
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Henry, RJ,Kerr, DM,Finn, DP,Roche, M
2014
November
Journal Of Neuroimmunology
FAAH-mediated modulation of TLR3-induced neuroinflammation in the rat hippocampus
Published
WOS: 15 ()
Optional Fields
Fatty acid amide hydrolase Cannabinoid Anandamide Cytokine Interferon Virus TOLL-LIKE RECEPTORS MURINE ENCEPHALOMYELITIS VIRUS FOCAL CEREBRAL-ISCHEMIA CENTRAL-NERVOUS-SYSTEM IMMUNOLOGICALLY INDUCED FATIGUE BRAIN INTERFERON-ALPHA ENDOCANNABINOID SYSTEM MULTIPLE-SCLEROSIS MICROGLIAL CELLS CHRONIC NEURODEGENERATION
276
126
134
The present study examined the effect of enhancing fatty acid amide hydrolase (FAAH) substrate levels in vivo on Toll-like receptor (TLR)3-induced neuroinflammation. Systemic and central (i.c.v.) administration of the FAAH inhibitor URB597 increased hippocampal levels of the N-acylethanolamines palmitoylethanolamide and oleoylethanolamide, but not anandamide. Systemic URB597 increased IFN alpha, IFN gamma and IL-6 expression following TLR3 activation and attenuated TLR3-induced IL-1 beta and TNF alpha. expression. In comparison, central URB597 administration attenuated the TLR3-induced increase in TNF alpha and IFN-gamma expression (and associated downstream genes IP-10 and SOCS1), while concurrently increasing IL-10 expression. These data support an important role for FAAH-mediated regulation of TLR3-induced neuroinflammatory responses. (C) 2014 Elsevier B.V. All rights reserved.
10.1016/j.jneuroim.2014.09.002
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