Toll-like receptor 2 (TLR2) mediates activation of stress-activated MAP kinase p38

J Leukoc Biol. 2002 Mar;71(3):503-10.

Abstract

Early events in the response of cells to lipopolysaccharide (LPS) include activation of NF-kappaB and stress-activated MAP kinase p38. Recent studies have shown that the human Toll-like receptor 2 (TLR2) mediates activation of NF-kappaB in response to commercial preparations of LPS (comLPS), membrane lipoproteins, and Gram-positive bacterial products. Here, we show that expression of TLR2 in human embryonic kidney 293 cells enabled p38 phosphorylation in response to comLPS, a synthetic bacterial lipoprotein, and B. subtilis. Activation of p38 was confirmed by an in vitro kinase assay using ATF2 as substrate and by an assay measuring activation of the downstream effector of p38, MAP kinase-activated protein kinase in cells. Thus, TLR2 initiated the signaling pathway for p38 in response to bacterial products.

MeSH terms

  • Cell Line
  • Drosophila Proteins*
  • Embryo, Mammalian
  • Enzyme Activation / drug effects
  • Humans
  • Lipopolysaccharides / pharmacology
  • Membrane Glycoproteins / physiology*
  • Mitogen-Activated Protein Kinases / physiology*
  • Phosphorylation
  • Receptors, Cell Surface / physiology*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Toll-Like Receptor 2
  • Toll-Like Receptors
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Drosophila Proteins
  • Lipopolysaccharides
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • TLR2 protein, human
  • Toll-Like Receptor 2
  • Toll-Like Receptors
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases