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Dendritic cells do not transduce inflammatory stimuli via the capsaicin receptor TRPV1
Author(s) -
O’Connell Peta J.,
Pingle Sandeep C.,
Ahern Gerard P.
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.08.023
Subject(s) - trpv1 , capsaicin , extracellular , chemistry , microbiology and biotechnology , intracellular , sensory system , receptor , neuroscience , transient receptor potential channel , signal transduction , biology , biochemistry
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 [Ca 2+ ] or membrane current in DC. In contrast, capsaicin evoked a sustained increase in [Ca 2+ ] 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 Ca 2+ 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.