Possible Interaction: Epinephrine and Interleukin-10

“Further, in LPS-stimulated blood, the increase on IL-10 levels caused by epinephrine only marginally contributed to concurrent inhibition of TNF production.”

“In separate in vitro experiments in whole blood, epinephrine increased LPS-induced IL-10 release by a combined effect on alpha and beta adrenergic receptors.”

“Acetylcholine and epinephrine contribute with IL-10 and other mediators to the anti-inflammatory compensatory response initiated to dampen the inflammatory process.”

“Gene expression of TNF-alpha, IL-6, and IL-10 was markedly enhanced by epinephrine in EMCV-inoculated mice.”

“The 16-hour treatment of M2a macrophages with 1 μmol/L epinephrine led to a significant upregulation of the cytokines IL-10 (P = .0131), TNF (P = .0012) and IL-6 (P = .0001), while no M1 marker IL-12 was detected (Figure 1A-D).”

“Notably, a positive association was found between Epi and IL-1β, IL-10 , Eotaxin, IL-8, and MCP-1.”

“Endogenous catecholamine, epinephrine and norepinephrine, and isoproterenol concentration-dependently induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inhibited that of IL-10 in human peripheral blood mononuclear cells (PBMC).”

“In blood of … volunteers, epinephrine reduced the LPS-stimulated synthesis of TNFalpha by 62.5% (P< 0.0001), of IL-6 by 39% (P< 0.0001), and of IL-1beta by 40% (P= 0.015), and increased the LPS-stimulated IL-10 production by 77.8% (P < 0.0001).”

“Finally, the combination of adrenaline and exogenous IL-10 led to a more pronounced suppression of TNF synthesis after LPS stimulation compared to suppression by IL-10 or adrenaline alone.”

“In this in vitro model adrenaline enhanced the LPS-induced synthesis of IL-10 with parallel suppression of TNF synthesis.”

“ Epinephrine significantly increased IL-10 production, but attenuated TNF-alpha release exclusively through beta2 adrenergic receptors, and is independent of IL-10 production.”

“For example, adrenalin in a concentration-dependent manner inhibits the endotoxin-induced increase in the content of TNFα in blood and monocytes [6, 9] and increases the level of “protective” IL-10 [1, 8, 9].”