Modulation of neuroinflammation: Role and therapeutic potential of TRPV1 in the neuro-immune axis.
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.
Department of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, Hubei, China.
Wei-Lin
WL
Kong
Department of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, Hubei, China.
Yuan-Yuan
YY
Peng
Department of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, Hubei, China. Electronic address: pengbiwen@whu.edu.cn.
Bi-Wen
BW
Peng
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D004660:Encephalitis / Q000188:drug therapy* / Q000276:immunology* / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D051379:Mice; D009457:Neuroglia / Q000276:immunology / Q000378:metabolism; D009474:Neurons / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction; D050916:TRPV Cation Channels / Q000276:immunology / Q000378:metabolism*
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human; C493921:TRPV1 protein, mouse
Bimodal effect; Glia; Inflammatory mediators; Neuroinflammation; Neurological disorders; TRPV1