Heat shock protein 90 is involved in IL-17-mediated skin inflammation following thermal stimulation

  • Authors:
    • Bo-Kyung Kim
    • Minhwa Park
    • Ji-Yon Kim
    • Kyung-Ho Lee
    • So-Youn Woo
  • View Affiliations

  • Published online on: June 7, 2016     https://doi.org/10.3892/ijmm.2016.2627
  • Pages: 650-658
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The pathogenesis of inflammatory skin diseases involves interactions between immune cells and keratinocytes, including the T helper 17 (Th17)-mediated immune response. Several chemokines [chemokine (C-X-C motif) ligand (CXCL)1, CXCL5 and CXCL8] and antimicrobial peptides [β-defensin 1 (BD1), LL-37, S100A8 and S100A9] were transcriptionally upregulated in the keratinocyte cell line HaCaT upon stimulation with interleukin (IL)-17. Balneotherapy, the treatment of disease by bathing, is an alternative therapy that has frequently been used for the treatment of inflammatory skin diseases. Immersion in pools of thermal mineral water is often considered to have chemical, thermal, mechanical and immunomodulatory benefits. We examined the effect of thermal treatment on IL-17-mediated inflammation in a model of skin disease. As Act1 is required for IL-17 signaling and is a client protein of heat shock protein 90 (HSP90), we evaluated the effect of HSP90 inhibition on IL-17-mediated cytokine and antimicrobial peptide expression in keratinocytes following heat treatment. We found that after thermal stimulation, Act1 binding to HSP90α was significantly increased in the presence of IL-17 (100 ng/ml) and 17-N-allylamino-17-demethoxygeldanamycin (17-AAG, 1 µM). Antimicrobial peptide and chemokine expression generally increased after heat treatment; Act1 knockdown and 17‑AAG reversed this effect. These observations demonstrate the possible immunomodulatory effect of heat on keratinocytes during the progression of IL-17-mediated inflammatory skin diseases.
View Figures
View References

Related Articles

Journal Cover

August-2016
Volume 38 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Kim B, Park M, Kim J, Lee K and Woo S: Heat shock protein 90 is involved in IL-17-mediated skin inflammation following thermal stimulation. Int J Mol Med 38: 650-658, 2016.
APA
Kim, B., Park, M., Kim, J., Lee, K., & Woo, S. (2016). Heat shock protein 90 is involved in IL-17-mediated skin inflammation following thermal stimulation. International Journal of Molecular Medicine, 38, 650-658. https://doi.org/10.3892/ijmm.2016.2627
MLA
Kim, B., Park, M., Kim, J., Lee, K., Woo, S."Heat shock protein 90 is involved in IL-17-mediated skin inflammation following thermal stimulation". International Journal of Molecular Medicine 38.2 (2016): 650-658.
Chicago
Kim, B., Park, M., Kim, J., Lee, K., Woo, S."Heat shock protein 90 is involved in IL-17-mediated skin inflammation following thermal stimulation". International Journal of Molecular Medicine 38, no. 2 (2016): 650-658. https://doi.org/10.3892/ijmm.2016.2627