IL-10 inhibits miR-155 induction by toll-like receptors

J Biol Chem. 2010 Jul 2;285(27):20492-8. doi: 10.1074/jbc.M110.102111. Epub 2010 Apr 30.

Abstract

IL-10 is a potent anti-inflammatory cytokine that is crucial for down-regulating pro-inflammatory genes, which are induced by Toll-like receptor (TLR) signaling. In this study, we have examined whether modulation of microRNAs plays a role in the inhibitory effect of IL-10 on TLR4 signaling. Analyzing microRNAs known to be induced by TLR4, we found that IL-10 could inhibit the expression of miR-155 in response to lipopolysaccharide but had no effect on miR-21 or miR-146a. IL-10 inhibited miR-155 transcription from the BIC gene in a STAT3-dependent manner. This inhibitory effect of IL-10 on miR-155 led to an increase in the expression of the miR-155 target, SHIP1. This is the first example of IL-10 playing a role in microRNA function and suggests that through its inhibitory effect on miR-155, IL-10 has the ability to promote anti-inflammatory gene expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DNA, Complementary / genetics
  • Enzyme-Linked Immunosorbent Assay / methods
  • Genes, Reporter
  • Humans
  • Interleukin-10 / pharmacology*
  • Kinetics
  • Luciferases / genetics
  • Mice
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / genetics*
  • RNA, Messenger / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • STAT3 Transcription Factor / physiology
  • Toll-Like Receptor 4 / physiology*
  • Transcription, Genetic / drug effects

Substances

  • DNA, Complementary
  • MIRN155 microRNA, human
  • MicroRNAs
  • Mirn155 microRNA, mouse
  • RNA, Messenger
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Stat3 protein, mouse
  • TLR4 protein, human
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Interleukin-10
  • Luciferases