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. Author manuscript; available in PMC: 2019 Jun 7.
Published in final edited form as: Brain Behav Immun. 2016 Dec 21;61:60–68. doi: 10.1016/j.bbi.2016.12.017

Figure 4.

Figure 4

β2-AR but not β1-AR antagonists reverse the inhibitory effect of Isoproterenol (Iso) on LPS-induced TNF production by monocytes. Washed whole blood cells from 5 healthy donors were pre-incubated with (A) CGP 12177A (highly selective β1-blocker, 0–10−5M), (B) ICI 118551 (highly selective β2-blocker, 0–10−5M) or (C) betaxolol (β-blocker with low β1/β2 selectivity, 0–10−5M) for 20 min prior to incubation with LPS (200 pg/mL) and isoproterenol (10−8M). Results are expressed as mean ± SEM of % TNF+ monocytes. Black bars (left) indicate cells treated with LPS plus isoproterenol, and clear bars (right) indicate cells treated with LPS only as references (without blockers). ICI 118551 and high concentrations of betaxolol, but not CGP20712A (black circles) reversed the inhibitory effect of Iso (*p < .05; **p < .01; ***p < .001). Blockers did not affect LPS-stimulated TNF expression by themselves (clear circles).