Adrenergic β2 Receptor Activation Stimulates Anti-Inflammatory Properties of Dendritic Cells In Vitro

• DOI: 10.1371/journal.pone.0085086
• Publication Date: 2014-01-22T22:28:04Z
• Authors: Laurens E. Nijhuis; Brenda J. Olivier; Shobit Dhawan; Francisca W. Hilbers; Louis Boon; Monika C. Wolkers; Janneke N. Samsom; Wouter J. de Jonge
• Keywords: 0301 basic medicine; Epinephrine; Science; Bone Marrow Cells; Interleukin-23; Mice; 03 medical and health sciences; Animals; Albuterol; Cells, Cultured; Interleukin-6; Q; R; Dextrans; Forkhead Transcription Factors; Dendritic Cells; Adrenergic beta-Agonists; Flow Cytometry; Interleukin-12; Endocytosis; Interleukin-10; EMC MM-04-54-07; Medicine; Cytokines; Female; Inflammation Mediators; Fluorescein-5-isothiocyanate; Research Article

Vagal nerve efferent activation has been shown to ameliorate the course of many inflammatory disease states. This neuro-modulatory effect suggested rest on acetylcholine receptor (AChR) tissue macrophages or dendritic cells (DCs). In more recent studies, vagal anti-inflammatory activity was involve adrenergic, splenic, pathways. Here we provide evidence that rather than cholinergic, bone marrow derived DCs results in enhanced endocytosis uptake, IL-10 production but a decreased IL-6, IL-12p70 and IL-23 production. antigen specific T cell stimulation assays, adrenergic β2 led an potential induce Foxp3 positive suppressive Treg cells. These effects were independent IL10-R activation, TGFβ release, retinoic acid (RA) secretion. Hence, modulates DC function resulting skewing towards phenotypes.