Anti-inflammatory effects of nicotinic acid in human monocytes are mediated by GPR109A dependent mechanisms.

ABSTRACT:

Objective

Nicotinic acid (NA) treatment has been associated with benefits in atherosclerosis that are usually attributed to effects on plasma lipoproteins. The NA receptor GPR109A is expressed in monocytes and macrophages, suggesting a possible additional role for NA in modulating function of these immune cells. We hypothesize that NA has the potential to act directly on monocytes to alter mediators of inflammation that may contribute to its antiatherogenic effects in vivo.

Methods and results

In human monocytes activated by Toll-like receptor (TLR)-4 agonist lipopolysaccharide, NA reduced secretion of proinflammatory mediators: TNF-α (by 49.2±4.5%); interleukin-6 (by 56.2±2.8%), and monocyte chemoattractant protein-1 (by 43.2±3.1%) (P<0.01). In TLR2 agonist, heat-killed Lis

SUBMITTER: Digby JE 

PROVIDER: S-EPMC3392598 | biostudies-literature | 2012 Mar

REPOSITORIES: biostudies-literature