Stress hormones modulate neutrophil and lymphocyte activity in vitro

There is increasing evidence that stress hormones and neurotransmitters may represent an information channel between the immune, endocrine, and central nervous systems. The goal of this investigation was to determine the in vitro effect of selected stress hormones on neutrophil and lymphocyte function using leukocytes from healthy volunteers. The following hormones were tested using a complete dose response curve including dosages within the physiological range; cortisol, epinephrine, norepinephrine, and glucagon. Cortisol did not affect neutrophil function, but did suppress lymphocyte blastogenesis. The catecholamines, epinephrine, and norepinephrine inhibited only neutrophil chemotaxis, while glucagon impaired both neutrophil chemotactic and bactericidal activity. When the individual hormones were combined into hormone cocktails, the inhibitory effect of both epinephrine and glucagon on neutrophil function was lost, while the inhibitory effect of cortisol on lymphocyte blastogenesis was greatly reduced. In fact, incubation of neutrophils in the stress hormone cocktail resulted in the neutrophils becoming hypermetabolic. Although the in vitro effects of these hormones on neutrophil and lymphocyte function do not fully correlate with the in vivo effect of trauma on immune function, these studies do support the general concept that the stress hormones may represent a link between the immune and endocrine systems.