4.5 Article

Dendritic cells do not transduce inflammatory stimuli via the capsaicin receptor TRPV1

Journal

FEBS LETTERS
Volume 579, Issue 23, Pages 5135-5139

Publisher

WILEY
DOI: 10.1016/j.febslet.2005.08.023

Keywords

dendritic cells; transient receptor potential channel vanilloid type 1; vanilloid receptor 1; capsaicin; inflammation; substance

Funding

  1. NIAID NIH HHS [AI054450] Funding Source: Medline

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Inflammatory stimuli provide critical activation signals for dendritic cells (DC). Signaling through the capsaicin receptor TRPV1 is reported to initiate DC maturation and migration. We attempted to characterize TRPV1 channels in DC. Capsaicin or extracellular protons failed to elicit a change in intracellular [Ca2+] or membrane current in DC. In contrast, capsaicin evoked a sustained increase in [Ca2+] and large inwards currents in sensory neurons and TRPV1-expressing HEK293 cells. TRPV1 expression was confirmed by RT-PCR in sensory neurons, but was undetectable in DC. Interestingly, and in contrast to capsaicin, the inflammatory neuropeptide substance P evoked Ca2+ transients in DC. Thus, our data do not support the hypothesis that DC express TRPV1 channels. Rather, signaling through TRPV1 in sensory nerves may modulate DC via neurogenic actions. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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