Beta-adrenergic receptor activation primes microglia cytokine production

J Neuroimmunol. 2013 Jan 15;254(1-2):161-4. doi: 10.1016/j.jneuroim.2012.08.007. Epub 2012 Sep 1.

Abstract

Exaggerated pro-inflammatory cytokine production by primed microglia is thought to mediate pathology during stress, aging, and neurodegeneration. Recently, it was demonstrated that beta-adrenergic receptor (β-AR) antagonism prevents priming of microglia in mice exposed to chronic stress. To determine if β-AR stimulation is sufficient to prime microglia, rats were intra-cerebroventricularly administered isoproterenol (β-AR agonist) or vehicle and 24 h later hippocampal microglia were placed in culture with media or LPS. Prior isoproterenol treatment significantly enhanced IL-1β and IL-6, but not TNF-α production following LPS stimulation. These data suggest that central β-AR stimulation is sufficient to prime microglia cytokine responses.

MeSH terms

  • Adrenergic beta-Agonists / pharmacology
  • Analysis of Variance
  • Animals
  • CD11b Antigen / metabolism
  • Cytokines / metabolism*
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Hippocampus / cytology*
  • Hippocampus / drug effects
  • Isoproterenol / pharmacology
  • Lipopolysaccharides / pharmacology
  • Male
  • Microglia / drug effects
  • Microglia / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adrenergic, beta / physiology*

Substances

  • Adrenergic beta-Agonists
  • CD11b Antigen
  • Cytokines
  • Lipopolysaccharides
  • Receptors, Adrenergic, beta
  • Isoproterenol