Published online Oct 26, 2016. doi: 10.4330/wjc.v8.i10.584
Peer-review started: March 15, 2016
First decision: April 20, 2016
Revised: July 27, 2016
Accepted: August 17, 2016
Article in press: August 18, 2016
Published online: October 26, 2016
Processing time: 230 Days and 9.1 Hours
Core tip: In evaluating the relationship between sympathetic activation and inflammatory cytokine production in heart failure, we demonstrated that norepinephrine (NE) has reduced ability to suppress the production of the proinflammatory cytokine tumor necrosis factor-alpha, and increase anti-inflammatory interleukin-10, in human isolated monocytes from heart failure compared to healthy subjects. It appears to be mediated through beta-adrenergic, and not alpha-adrenergic, receptors based on monocytic THP-1 cells dose-response experiments. This suggests that the diminished immunomodulatory activity of NE in heart failure is primarily due to altered beta-adrenergic receptor function, and may represent an immunologic mechanism for the positive effects of beta-adrenergic blocking agents.