Diazepam Impairs Innate and Adaptive Immune Responses and Ameliorates Experimental Autoimmune Encephalomyelitis

FALCON C; FERNANDEZ HURST N; VIVINETTO AL; LOPEZ PHH; ZURITA A; GATTI G; . CERVI L.; MONFERRAN C; ROTH G

Frontiers in Immunology

American Chemical Society

Año: 2021

1664-3224

urrently there is increasing attention on the modulatory effects of benzodiazepines on theimmune system. Here, we evaluate how Diazepam (DZ) affects both innate and adaptiveimmunity. We observed that treatment with DZ and Lipopolysaccharide (LPS) onmacrophages or dendritic cells (DCs) induced a defective secretion of IL-12, TNF-a, IL-6and a lesser expression of classical activation markers as NO production and CD40 incomparison with LPS condition. More importantly, mice pre-treated with DZ and thenchallenged to LPS induced-septic shock showed reduced death. The DZ treatment shiftedthe LPS-induced pro-inflammatory cytokine production of peritoneal cells (PCs) to an antiinflammatory profile commanded by IL-10. In agreement with this, DZ treatment preventedLPS-induced DC ability to initiate allogeneic Th1 and Th17 responses in vitro whencompared with LPS-matured DC. Since these inflammatory responses are the key in thedevelopment of the experimental autoimmune encephalomyelitis (EAE), we