Inhibition of N-terminal ATPase on HSP90 attenuates colitis through enhanced Treg function

Mucosal Immunol. 2013 Sep;6(5):960-71. doi: 10.1038/mi.2012.134. Epub 2013 Jan 16.

Abstract

Inflammatory bowel disease (IBD) is a chronic inflammatory condition thought to reflect a failure of the enteral immune system to adequately regulate itself. Inflammatory stress drives upregulation of heat-shock proteins (HSPs), including the pro-inflammatory chaperone, HSP90. This protein sequesters the transcription factor, heat-shock factor 1 (HSF1) in the cytoplasm preventing transcription of a number of anti-inflammatory proteins. We hypothesized that inhibition of HSP90 would exert an anti-inflammatory effect and thereby attenuate intestinal inflammation in murine models of IBD. Inhibition of HSP90 with 17-allylaminogeldanamycin (17-AAG) reduced inflammation in acute dextran sodium sulfate and chronic CD45RB(High) colitis models coinciding with increased interleukin (IL)-10 production in the colon. Regulatory T cells (Tregs) from mice treated with 17-AAG demonstrated significantly greater suppressive capacity in vitro abolished in HSF1-/- or IL-10-/- cells. Finally, Tregs treated with 17-AAG exhibited increased nuclear localization of HSF1 with resultant upregulation of HSF1 response genes, including HSP70, HSP90 and IL-10.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphatases / metabolism*
  • Animals
  • Benzoquinones / pharmacology
  • Cell Nucleus / metabolism*
  • Cells, Cultured
  • Colitis / chemically induced
  • Colitis / drug therapy
  • Colitis / immunology*
  • Cytoplasm / metabolism*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Dextran Sulfate / administration & dosage
  • HSP90 Heat-Shock Proteins / metabolism*
  • Heat Shock Transcription Factors
  • Humans
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Lactams, Macrocyclic / pharmacology
  • Leukocyte Common Antigens / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Protein Transport / drug effects
  • Protein Transport / genetics
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / immunology*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Benzoquinones
  • DNA-Binding Proteins
  • HSF1 protein, human
  • HSP90 Heat-Shock Proteins
  • Heat Shock Transcription Factors
  • Lactams, Macrocyclic
  • Transcription Factors
  • Interleukin-10
  • tanespimycin
  • Dextran Sulfate
  • Leukocyte Common Antigens
  • Adenosine Triphosphatases