Catecholamine effects depend on the distance from catecholamine source. α- and β-adrenoceptors (ARs) show different binding affinities for catecholamines. Norepinephrine, the main neurotransmitter in the sympathetic nervous system (SNS), binds with higher affinity to α-ARs than β-ARs. Simultaneous expression of these receptors on immune cells (for example, macrophages (MΦ)) provides these cells with a passive means to determine the distance to the next catecholamine source. In close proximity to the catecholamine source (for example, sympathetic nerve terminal or catecholamine-producing tyrosine hydroxylase (TH)-positive cell) the concentration is high enough to activate β-ARs, whereas at a greater distance only α-ARs are activated. In the case of innate immune cells, like macrophages, this directly translates into anti-inflammatory (for example, increases in interleukin (IL)-10 via β-AR) or proinflammatory activity (for example, increases in tumor necrosis factor (TNF) via α-AR). Therefore, the simultaneous expression of α-ARs and β-ARs on immune cells provides a mean to regulate inflammatory processes dependent on the distance to the catecholamine source. We hypothesize that the body uses this system to promote local inflammation by repulsion of sympathetic nerve fibers from inflamed areas (zone of inflammation) and, at the same time, locally confines the inflammatory process by suppression of bystander activation in the zone of anti-inflammation.