Acute psychosocial stress induces differential short-term changes in catecholamine sensitivity of stimulated inflammatory cytokine production

The present findings extend our knowledge on changes in inflammatory target tissue sensitivity in response to acute psychosocial stress from glucocorticoid-dependent effects to catecholamine-dependent effects. Stress-induced decreases in catecholamine sensitivity thereby suggest intracellular processes aiding in maintaining a healthy endocrine-immune interplay. Longitudinal studies will have to investigate the processes leading from a supposedly beneficial short-term catecholamine resistance in response to acute stress to basal catecholamine resistance observed in relation to negative health outcomes.