Literature DB >> 28342781

Modulation of neuroinflammation: Role and therapeutic potential of TRPV1 in the neuro-immune axis.

Wei-Lin Kong1, Yuan-Yuan Peng1, Bi-Wen Peng2.   

Abstract

Transient receptor potential vanilloid type 1 channel (TRPV1), as a ligand-gated non-selective cation channel, has recently been demonstrated to have wide expression in the neuro-immune axis, where its multiple functions occur through regulation of both neuronal and non-neuronal activities. Growing evidence has suggested that TRPV1 is functionally expressed in glial cells, especially in the microglia and astrocytes. Glial cells perform immunological functions in response to pathophysiological challenges through pro-inflammatory or anti-inflammatory cytokines and chemokines in which TRPV1 is involved. Sustaining inflammation might mediate a positive feedback loop of neuroinflammation and exacerbate neurological disorders. Accumulating evidence has suggested that TRPV1 is closely related to immune responses and might be recognized as a molecular switch in the neuroinflammation of a majority of seizures and neurodegenerative diseases. In this review, we evidenced that inflammation modulates the expression and activity of TRPV1 in the central nervous system (CNS) and TRPV1 exerts reciprocal actions over neuroinflammatory processes. Together, the literature supports the hypothesis that TRPV1 may represent potential therapeutic targets in the neuro-immune axis.
Copyright © 2017 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Bimodal effect; Glia; Inflammatory mediators; Neuroinflammation; Neurological disorders; TRPV1

Mesh:

Substances:

Year:  2017        PMID: 28342781     DOI: 10.1016/j.bbi.2017.03.007

Source DB:  PubMed          Journal:  Brain Behav Immun        ISSN: 0889-1591            Impact factor:   7.217


  33 in total

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Journal:  Front Cell Neurosci       Date:  2017-07-24       Impact factor: 5.505

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10.  N-Acylethanolamine-Hydrolyzing Acid Amidase Inhibition, but Not Fatty Acid Amide Hydrolase Inhibition, Prevents the Development of Experimental Autoimmune Encephalomyelitis in Mice.

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