TPL-2-mediated activation of MAPK downstream of TLR4 signaling is coupled to arginine availability

Sci Signal. 2010 Aug 17;3(135):ra61. doi: 10.1126/scisignal.2000934.

Abstract

The innate immune response is influenced by the nutrient status of the host. Mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase 1 (ERK1) and ERK2, are activated after the stimulation of macrophages with bacterial lipopolysaccharide (LPS) and are necessary for the optimal production of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha). We uncovered a role for the extracellular nutrient arginine in the activation of ERK1/2 in LPS-stimulated macrophages. Arginine facilitated the activation of MAPKs by preventing the dephosphorylation and inactivation of the MAPK kinase kinase tumor-promoting locus 2 (TPL-2). Starvation of mice decreased the concentration of arginine in the plasma and impaired the activation of ERK1/2 by LPS. Supplementation of starved mice with arginine promoted the subsequent activation of ERK1/2 and the production of TNF-alpha in response to LPS. Thus, arginine is critical for two aspects of the innate immune response in macrophages: It is the precursor used in the generation of the antimicrobial mediator nitric oxide, and it facilitates MAPK activation and consequently cytokine production.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acids / blood
  • Animals
  • Arginine / metabolism*
  • Arginine / pharmacology
  • Blotting, Western
  • Chromatography, Ion Exchange
  • Enzyme Activation / drug effects
  • Enzyme Activation / immunology*
  • Immunity, Innate / physiology*
  • Immunohistochemistry
  • Lipopolysaccharides
  • MAP Kinase Kinase Kinases / genetics
  • MAP Kinase Kinase Kinases / metabolism*
  • Macrophages / immunology*
  • Mice
  • Mice, Knockout
  • Mitogen-Activated Protein Kinases / metabolism*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Signal Transduction / immunology*
  • Toll-Like Receptor 4 / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Amino Acids
  • Lipopolysaccharides
  • Proto-Oncogene Proteins
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Arginine
  • Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase Kinases
  • Map3k8 protein, mouse