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TRPV1 Mediates Capsaicin-Stimulated Metabolic Activity but not Cell Death or Inhibition of Interleukin-1β Release in Human THP-1 Monocytes


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Abstract
Human monocytes and dendritic cells express transient receptor potential vanilloid 1 (TRPV1) which may play a role in mediating the inflammatory, immune and cancer surveillance responses of these cells. The aim of the present study was to investigate TRPV1 expression and function in THP-1 monocytic cells. RT-PCR and Western blot were used to detect TRPV1. The metabolic activity and viability of THP-1 cells following exposure to vanilloids was assessed using resorufin production from rezazurin. Cytokine release was measured using ELISA. TRPV1 was expressed in cultured THP-1 monocytic cells and naïve monocytes. Lower concentrations (250 M, all agonists decreased metabolic activity. Capsaicin-stimulated THP-1 metabolic activity was blocked by the TRPV1 antagonist, 5-iodo-resiniferatoxin (5’-IRTX), whereas the decline in resorufin production by THP-1 cells at higher capsaicin concentrations (due to cell death), was not affected by 5’-IRTX. Finally, capsaicin (125 M) significantly increased lipopolysaccharide-stimulated IL-6 and TNF- release from THP-1 cells, whereas phytohaemagglutinin-stimulated IL-1, TNF-, MCP-1 and IL-6 release were concentration-dependently inhibited by capsaicin. Modulation of IL-1release was not TRPV1 mediated. Overall, these results show that functional TRPV1 channels are present in naïve monocytes and THP-1 cells, and when activated, increase cell metabolic activity. In addition, capsaicin modifies cytokine release from THP-1 cells and induces cell death, most likely by a mechanism that is independent of TRPV1 activation.
Item Type: | Article |
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Authors/Creators: | Kunde, DA and Yingchoncharoen, J and Jurkovic, S and Geraghty, DP |
Keywords: | TRPV1; capsaicin; cytokines; immunomodulation; monocytes |
Journal or Publication Title: | Toxicology and Applied Pharmacology |
Publisher: | Academic Press Inc Elsevier Science |
ISSN: | 0041-008X |
DOI / ID Number: | 10.1016/j.taap.2018.09.025 |
Copyright Information: | © 2018 Elsevier Inc. |
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