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FAAH-mediated modulation of TLR3-induced neuroinflammation in the rat hippocampus.

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Affiliations

  • 1. Physiology, School of Medicine, National University of Ireland, Galway, Ireland; NCBES Centre for Pain Research and Neuroscience Centre, National University of Ireland, Galway, Ireland.
      Authors
    • Henry RJ 1
    • Roche M 1
    (2 authors)
  • 2. Physiology, School of Medicine, National University of Ireland, Galway, Ireland; Pharmacology and Therapeutics, School of Medicine, National University of Ireland, Galway, Ireland; NCBES Centre for Pain Research and Neuroscience Centre, National University of Ireland, Galway, Ireland.
      Authors
    • Kerr DM 2
    (1 author)
  • 3. Pharmacology and Therapeutics, School of Medicine, National University of Ireland, Galway, Ireland; NCBES Centre for Pain Research and Neuroscience Centre, National University of Ireland, Galway, Ireland.
      Authors
    • Finn DP 3
    (1 author)

ORCIDs linked to this article

Journal of Neuroimmunology, 16 Sep 2014, 276(1-2):126-134
https://doi.org/10.1016/j.jneuroim.2014.09.002 PMID: 25245162 

Abstract 

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 IFNα, IFNγ and IL-6 expression following TLR3 activation and attenuated TLR3-induced IL-1β and TNFα expression. In comparison, central URB597 administration attenuated the TLR3-induced increase in TNFα and IFNγ 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.

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Read article at publisher's site: https://doi.org/10.1016/j.jneuroim.2014.09.002

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Science Foundation Ireland (1)