β-Adrenergic Stimulation Down-Regulates Neutrophil Priming for Superoxide Generation, but Not Elastase Release

Agonist- and Hydrogen Peroxide-Mediated Oxidation of the β2Adrenergic Receptor: Evidence of Receptor S-Sulfenation as Detected by a Modified Biotin-Switch Assay

“…These results have been corroborated by other groups using cardiomyocyte models of cardiomyopathy and heart failure, suggesting that the ROS-␤ 2 AR link is physiologically significant and, if unregulated, may be involved in pathophysiological states (Li et al, 2010;Xu et al, 2011). It is noteworthy that the agonism of ␤ 2 AR in human neutrophils facilitates a decrease in formyl-Met-Leu-Phe-mediated ROS generation (Opdahl et al, 1993;Anderson et al, 1996;Barnett et al, 1997), and others have shown that ␤ 2 AR agonism specifically decreases only extracellular ROS from these cells (Kopprasch et al, 1997). Together, these results suggest that ␤ 2 AR agonism may have cell type-specific differential effects on modulating ROS levels.…”

Suppressed neutrophil respiratory burst in patients with haemorrhagic stroke

“…The b2-adrenergic receptor is expressed on immune cells 10 and stimulation with b-adrenergic agonists, even at very low concentrations, down-regulates neutrophil priming for superoxide generation and inhibits chemotaxis to fMLP. [15][16][17] The present study also showed that there was a significant inverse correlation between the plasma noradrenalin concentration and the neutrophil CL response to fMLP. It is likely that increased intracranial pressure due to haemorrhage precipitated the suppression of neutrophil oxidative responsiveness through sympathetic nerve stimulation.…”

The impact of immunomodulator compound from the group of substituted thiadiazines on the course of stress reaction

“…Experiments with long-term infusion of α-receptor agonists showed not only a considerable reduction in TNF-α production but also increased production of IL-10 [20]. Moreover, activation of α2-AR reduces superoxide production by neutrophils; superoxide plays an important role in bactericidal activity by inhibiting chemotaxis [21], inhibiting chemotaxis [22][23][24], and inducing apoptosis [25].…”