title: Neuroendocrine measures and lymphocyte subsets in depressive illness: influence of a clinical interview concerning life experiences.
abstract: The effects of a clinical interview concerning either positive or negative day-to-day events on lymphocyte subpopulations, and on plasma cortisol, ACTH and norepinephrine, were determined in depressive patients (major depressive and dysthymic) and in normal controls. Irrespective of its content, the interview provoked an elevation of circulating natural killer (NK) cells, suggesting that this effect was related to either a change in mood state (regardless of its valence) or to the stress associated with the interview procedure. Since the interview did not influence plasma cortisol, ACTH or norepinephrine, it is likely that the NK cell variations were independent of these endocrines. Although basal NK cells were elevated in the depressive group relative to controls, the extent of the NK cell increase provoked by the interview was comparable in depressive and control subjects. The failure to detect differences between these populations could not be attributed to ceiling effects precluding more pronounced alterations in the depressed subjects. Indeed, variations of circulating cell subtypes were found to be exquisitely sensitive to differences in stressor intensity. In a subset of control subjects, a more potent stressor (anticipation of an academic examination) increased the plasma endocrine levels, increased circulating NK cell number beyond that associated with the interview stress, and provoked an increase of several T cell subsets (CD3, CD4 and CD8). Evidently, while a clinical interview may be sufficiently stressful to influence circulating NK cells, the stress of such a procedure seems no greater in depressed than in control subjects. It is suggested that although depressed patients may exhibit higher basal NK levels, this effect is likely not related to increased reactivity to stressors.
authors.affiliation: Department of Psychiatry, University of Ottawa, Ontario, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Griffiths
authors.forename: A V
authors.initials: AV
authors.lastname: Ravindran
authors.forename: Z
authors.initials: Z
authors.lastname: Merali
authors.forename: H
authors.initials: H
authors.lastname: Anisman
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000328:Adult; D000339:Affect / Q000502:physiology; D001143:Arousal / Q000502:physiology*; D003866:Depressive Disorder / Q000276:immunology* / Q000523:psychology; D019263:Dysthymic Disorder / Q000276:immunology* / Q000523:psychology; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007406:Interview, Psychological; D008016:Life Change Events; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood*; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D012016:Reference Values; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D009638:Norepinephrine