title: Monocyte proinflammatory cytokine release is higher and glucocorticoid sensitivity is lower in middle aged men than in women independent of cardiovascular risk factors.
abstract: OBJECTIVE
  To investigate whether stimulated monocyte cytokine release and its inhibition by glucocorticoids differs between men and women.
  
  
  METHODS
  In vitro monocyte interleukin 6 (IL-6) and tumour necrosis factor alpha (TNFalpha) release after lipopolysaccharide stimulation were assessed with and without co-incubation with increasing doses of dexamethasone and hydrocortisone separately. Glucocorticoid sensitivity was defined as the amount of a particular glucocorticoid required to inhibit lipopolysaccharide stimulated monocyte cytokine release by 50%. The established cardiovascular risk factors of age, body mass index, number of cigarettes smoked daily, low density cholesterol to high density cholesterol ratio, systolic and diastolic blood pressure, and haemoglobin A1c were used as covariates.
  
  
  METHODS
  Aircraft manufacturing plant in southern Germany.
  
  
  METHODS
  269 middle aged male and 36 middle aged female employees.
  
  
  RESULTS
  Release of monocyte IL-6 and TNFalpha (each p = 0.001) was higher in samples from men than in those from women. Inhibition of lipopolysaccharide stimulated IL-6 and TNFalpha release by either glucocorticoid was less pronounced in samples from men than in those from women (IL-6: dexamethasone p = 0.033, hydrocortisone p = 0.029; TNFalpha: dexamethasone p < 0.001, hydrocortisone p = 0.089).
  
  
  CONCLUSIONS
  The finding suggests that proinflammatory activity of circulating monocytes is higher in men than in women independent of cardiovascular risk factors, thereby providing one explanation for the relatively greater coronary risk in men.
authors.affiliation: Institute of Clinical Psychology II, University of Zurich, Zurich, Switzerland.
authors.forename: P H
authors.initials: PH
authors.lastname: Wirtz
authors.forename: R
authors.initials: R
authors.lastname: von Känel
authors.forename: N
authors.initials: N
authors.lastname: Rohleder
authors.forename: J E
authors.initials: JE
authors.lastname: Fischer
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002318:Cardiovascular Diseases / Q000209:etiology*; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000378:metabolism*; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D012307:Risk Factors; D012737:Sex Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism; D000093242:Interleukin-6 Inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D003907:Dexamethasone; D006854:Hydrocortisone; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors