Although glucocorticoids and opioids may enhance some immune responses at very low concentrations, they are generally considered to be immunosuppressive. These contrasting responses may be controlled by the presence of multiple receptors for the same mediator that are coupled to stimulatory and inhibitory pathways. In fact, containment of the stress response may be the principal role of glucocorticoids. Glucocorticoids severely impair the phagocytic and cytotoxic activities of neutrophils and macrophages, their capacity to produce ROI and to induce iNOS, and secrete lysosomal enzymes in response to activation. Oxidative burst of professional phagocytes is also inhibited with epinephrine and -endorphin which activity is mediated via nonopioid receptors.
Histamine is a potent inhibitor of neutrophil microbicidal activity.
Adenosine provides an interesting example of how a single mediators may play dual roles. Adenosine, a vasodilator, is a potent anti-inflammatory agent released from damaged host cells. Neutrophil chemotaxis is activated by adenosine occupancy of receptors and inhibition of the respiratory burst triggered through receptors. Adenosine suppresses the respiratory burst only if it is added before the triggering agent, but it has no effect on the initiation or progress of degranulation. The interactions between platelets and neutrophils are essential for both cell types.