Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 52, Issue -, Pages 152-160Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2012.11.006
Keywords
TRPV1; TRPV4; IL-17A; IL-17RA; ERK; NF kappa B
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Funding
- Deutsche Forschungsgemeinschaft [SCHA 404/13-2]
- Bundesministerium fur Forschung und Technologie (BMBF, program Immunopain)
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In addition to the proinflammatory cytokines tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta, the cytokine interleukin-17 (IL-17) is considered an important mediator of autoimmune diseases such as rheumatoid arthritis. Because tumor necrosis factor-alpha and interleukin-1 beta have the potential to influence the expression of transduction molecules such as transient receptor potential vanilloid 1 (TRPV1) in dorsal root ganglion (DRG) neurons and thus to contribute to pain we explored in the present study whether IL-17A activates DRG neurons and influences the expression of TRPV1. The IL-17A receptor was visualized in most neurons in dorsal root ganglion (DRG) sections as well as in cultured DRG neurons. Upon long-term exposure to IL-17A, isolated and cultured rat DRG neurons showed a significant upregulation of extracellular-regulated kinase (ERK) and nuclear factor kappa B (NF kappa B). Long-term exposure of neurons to IL-17A did not upregulate the expression of TRPV1. However, we found a pronounced upregulation of transient receptor potential vanilloid 4 (TRPV4) which is considered a candidate transduction molecule for mechanical hyperalgesia. Upon the injection of zymosan into the paw, IL-17A-deficient mice showed less mechanical hyperalgesia than wild type mice but thermal hyperalgesia was not attenuated in IL-17A-deficient mice. These data show, therefore, a particular role of IL-17 in mechanical hyperalgesia, and they suggest that this effect is linked to an activation and upregulation of TRPV4. (c) 2012 Elsevier Inc. All rights reserved.
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