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Modulation of TRPV1 Function in Human CD4+ T Cells by Nanodiamond and Nanoplatinum Liquid, DPV576

Modulation of TRPV1 Function in Human CD4+ T Cells by Nanodiamond and Nanoplatinum Liquid, DPV576

Authors :
James K. Gimzewski
Anshu Agrawal
Hideki Katano
Aya D Ghoneum
Mamdooh Ghoneum
Publication Year :
2018
Publisher :
MDPI AG, 2018.

Abstract

Transient receptor potential vanilloid (TRPV) channels act as sensors of pain, temperature, and other external stimuli. We have recently shown that DPV576, an aqueous mixture of nanodiamond (ND) and nanoplatinum (NP), can modulate the activity of TRPV on human primary keratinocytes, suggesting their potential as a possible pain modulator [1]. CD4+ T lymphocytes also express TRPV channels, and we sought with special interest to examine the effect of DPV576 in modulating the functions of TRPV channel expression and secretion of cytokines on human CD4+ T lymphocytes. Human primary CD4+ T cells were activated with anti CD3/CD28 with and without DPV576 at 1:25 and 1:100 dilutions for 24 hours in vitro. TRPV Receptor expression (TRPV1 and TRPV4) on CD4+ T cells was examined by flow cytometry. The capacity of DPV576 to modulate the activity of TRPV1 agonist capsaicin in CD4+ T cells was also determined. Activation of CD4+ T cells was determined by production of cytokines TNF-α, IFN-γ, and IL-10 using specific ELISA kits. DPV576 treatment of CD4+ T cells that were activated with anti CD3/CD28, resulted in increased expression of TRPV1 channel but had no effect on TRPV4. This was accompanied by increased secretion of IFN-g and reduced expression of TRPV1 in capsaicin activated CD4+ T cells. In addition, DPV576 inhibited the capsaicin, induced the production of both IFN-g and TNF-α, and enhanced the secretion of IL-10. We conclude that short term exposure to DPV576 inhibits the activity of TRPV1 channels in CD4+ T lymphocytes, which may suggest its possible beneficial use for pain management.&nbsp

Details

Database :
OpenAIRE
Accession number :
edsair.doi.dedup.....0ce82804490cc9e06c0d232f5f60f1a1
Full Text :
https://doi.org/10.20944/preprints201804.0354.v1