In a recent study published in the journal Cytokine, Michela Manni, Richard Granstein and Georges Maestroni, from the Center for Experimental Pathology, Locarno, Switzerland, provide new evidence suggesting that catecholamines, through activation of beta2-adrenoreceptors (ARs) on immune cells, may drive, in certain conditions, Th17 immune responses.
The authors report that the beta2-AR agonist salbutamol is able to modulate cytokine production in dendritic cells (DCs) stimulated with MDP or simultaneously by both TLR-2 and NOD2 ligands, resulting in a cytokine pattern that directs Th17 priming.
Contrary to the concept that beta2-AR agonists are immunosuppressive agents, this report indicates that in combination with TLR-2 and/or NOD2 activation, stimulation of beta2-ARs on dendritic cells may enhance an IL-17-type immune response.
Catecholamines and β2-ARs might be involved in the defense against extracellular bacteria and in the pathogenesis of inflammatory diseases by modulating Th17 polarization.
These findings may have implications for conditions such as asthma/allergy, autoimmunity or psoriasis, where sympathetic-immune dysfunction or stress-induced exacerbations have been described.
For example, as IL-17 is increased in skin inflammatory disorders such as psoriasis, this study suggest that stress-induced release of catecholamines by the sympathetic nervous system with consequent stimulation of Th17-type immunity may contribute to stress induced exacerbation of psoriasis.