Attenuation of contact hypersensitivity by cell-permeable heat shock protein 70 in BALB/c mouse model

Exp Dermatol. 2012 Dec;21(12):969-71. doi: 10.1111/exd.12044.

Abstract

In contact hypersensitivity (CHS), multiple cells, inflammatory mediators and cytokines are known to be involved in the regulation of the immune response. Previously, we revealed the reactive oxygen species generation by 2, 4, 6-trinitrobenzene sulphonic acid (TNBS) in vivo, followed by heat shock protein 70 (Hsp70) carbonylation and the exogenous antioxidant role of cell-permeable Hsp70. Here, we demonstrate the role of Hsp70 using cell-permeable Hsp70 in the mouse CHS model. Pretreatment of cell-permeable Hsp70: (i) suppressed ear swelling; (ii) down-regulated phosphorylated p38, but up-regulated phosphorylated extracellular signal-regulated kinase; (iii) increased population of CD4(+) CD25(+) Foxp3(+) T cells; (iv) decreased secretion of tumor necrosis factor-α (TNF-α), IL-12, interferon-γ and IL-2 and (v) but up-regulated IL-4 and transforming growth factor beta (TGF-β) in the lymph nodes. In conclusion, cell-permeable Hsp70 attenuates CHS through modulation of MAPK pathway and regulation of Th1, Th2 and regulatory T cells.

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Topical
  • Animals
  • Dermatitis, Contact / metabolism*
  • Dermatitis, Contact / therapy*
  • Disease Models, Animal
  • Female
  • Genetic Therapy / methods
  • HSP70 Heat-Shock Proteins / genetics*
  • HSP70 Heat-Shock Proteins / metabolism*
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Signal Transduction / physiology*
  • Transduction, Genetic / methods

Substances

  • HSP70 Heat-Shock Proteins
  • Hspa14 protein, human