title: Evidence for a positive correlation between serum cortisol levels and IL-1beta production by peripheral mononuclear cells in anorexia nervosa.
abstract: A hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis has been reported in anorexia nervosa (AN), together with some immunological abnormalities, involving citokine - and particularly Tumor Necrosis-Factor-alpha (TNF-alpha) - production by polymorphonuclear cells. The ability of pro-inflammatory cytokines to activate the HPA axis is well known; however, there are no data demonstrating an interdependence between immunological and endocrine response in AN. To investigate the presence of a correlation between immune response and pituitary-adrenal function, plasma ACTH and serum cortisol concentrations were measured in 13 AN patients and in the same number of controls. TNF-alpha and interleukin (IL)-1beta production by ex-vivo unstimulated and LPS-stimulated peripheral mononuclear cells was also assessed. Circulating cortisol concentrations were higher (p<0.01) in AN (156.7 +/- 45.1 microg/l, mean +/- SD) than in controls (105.9 +/- 25.7 microg/l). Unstimulated IL-1beta release in supernatants of mononuclear cell cultures was slightly but not significantly higher in AN than in controls, while TNF-alpha release was similar in the two groups. A positive correlation was found between IL-1beta concentrations in unstimulated culture supranatants and serum cortisol levels in AN (r=0.782, p=0.002), while in normal subjects there was a trend toward a negative correlation; a slight positive correlation, while not significant, between IL-1beta and plasma ACTH, as well as between TNF-alpha and serum cortisol was also found in AN. These data suggest that the normal relationship between pro-inflammatory cytokines release, particularly IL-1beta, and cortisol secretion is deranged in AN.
authors.affiliation: Department of Internal Medicine, University of Turin, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Limone
authors.forename: A
authors.initials: A
authors.lastname: Biglino
authors.forename: F
authors.initials: F
authors.lastname: Bottino
authors.forename: B
authors.initials: B
authors.lastname: Forno
authors.forename: P
authors.initials: P
authors.lastname: Calvelli
authors.forename: S
authors.initials: S
authors.lastname: Fassino
authors.forename: C
authors.initials: C
authors.lastname: Berardi
authors.forename: P
authors.initials: P
authors.lastname: Ajmone-Catt
authors.forename: A
authors.initials: A
authors.lastname: Bertagna
authors.forename: R P
authors.initials: RP
authors.lastname: Tarocco
authors.forename: G G
authors.initials: GG
authors.lastname: Rovera
authors.forename: G M
authors.initials: GM
authors.lastname: Molinatti
mesh_terms: D000293:Adolescent; D000311:Adrenal Glands / Q000503:physiopathology; D000328:Adult; D000856:Anorexia Nervosa / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007031:Hypothalamus / Q000503:physiopathology; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D010902:Pituitary Gland / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D006854:Hydrocortisone