title: Acute psychosocial stress induces differential short-term changes in catecholamine sensitivity of stimulated inflammatory cytokine production.
abstract: BACKGROUND
  We have previously shown that psychosocial stress induces acute changes in glucocorticoid (GC) sensitivity of pro-inflammatory cytokine production. However, hormones of the sympathetic adrenal medullary system complement endocrine regulation of inflammatory responses. The current study therefore aimed at investigating the effects of repeated acute stress exposure on catecholamine sensitivity of inflammatory cytokine production.
  
  
  METHODS
  Twenty healthy male participants were subjected to the Trier Social Stress Test on two consecutive days. Blood samples were taken before and repeatedly after stress. Whole blood was stimulated with lipopolysaccharide and incubated with increasing concentrations of epinephrine (E) and norepinephrine (NE) for 18h. Tumor-necrosis-factor (TNF) alpha and interleukin (IL)-6 were measured in culture supernatants.
  
  
  RESULTS
  Overall, incubation with E and NE induced dose-dependent suppression of TNF-alpha (NE: F=77.66, p<.001; E: F=63.38, p<.001), and IL-6 production (NE: F=28.79, p<.001; E: F=24.66, p<.001). Acute stress exposure resulted in reduced sensitivity of TNF-alpha (NE: F=6.36, p<.001; E: F=4.86, p=.005), but not IL-6 (NE: F=1.07, p=.38; E: F=0.88, p=.50) to the inhibitory signals of E and NE. No evidence of habituation of these effects was found (all p⩾.22).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Psychology, University of Marburg, Marburg, Germany.
authors.forename: Jana
authors.initials: J
authors.lastname: Strahler
authors.affiliation: Department of Psychology & Volen National Center for Complex Systems, Brandeis University, Waltham, MA, USA.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Rohleder
authors.affiliation: Department of Psychology & Volen National Center for Complex Systems, Brandeis University, Waltham, MA, USA. Electronic address: jmw@brandeis.edu.
authors.forename: Jutta M
authors.initials: JM
authors.lastname: Wolf
mesh_terms: D000328:Adult; D001773:Blood Cells / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007249:Inflammation / Q000097:blood* / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D012463:Saliva / Q000737:chemistry; D013315:Stress, Psychological / Q000097:blood* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*; D055815:Young Adult
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine
keywords: Acute psychosocial stress; Catecholamine sensitivity; Catecholamines; Cortisol; Cytokines; Inflammation; Sympathetic nervous system