Inhibition of TRPV1 Channel Activity in Human CD4(+) T Cells by Nanodiamond and Nanoplatinum Liquid, DPV576

Background: 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. Here, we sought to examine the effect of DPV576 in modulating the functions of human CD4(+) T lymphocytes and whether the modulation is mediated via TRPV channels. Materials and methods: Human primary CD4(+) T cells were activated with anti CD3/CD28 with and without DPV576 at 1:10 and 1:100 dilutions for 24 h in vitro. TRPV receptor expression (TRPV1 and TRPV4) on CD4(+) T cells were 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-alpha, IFN-gamma, and IL-10 using specific ELISA kits. Results: DPV576 treatment of CD4(+) T cells that were activated with anti CD3/CD28 resulted in decreased expression of the TRPV1 channel, but had no effect on TRPV4. This was accompanied by decreased secretion of IFN-gamma and reduced expression of TRPV1 in capsaicin activated CD4(+) T cells. In addition, DPV576 inhibited the capsaicin, induced the production of IFN-gamma, and enhanced the secretion of IL-10. Conclusion: 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.