title: Immunological differences between patients with major depression and somatization syndrome.
abstract: There is some evidence that major depression is accompanied by activation of the inflammatory response system (IRS). There is also evidence that proinflammatory cytokines and induction of IRS activation are associated with sickness behavior in experimental animals. However, no research has examined the IRS in somatization disorder. The aim of this study was to examine possible immunological differences between major depression, somatization and healthy controls. We measured the following IRS variables in patients with major depression (n=36), somatization syndrome (SSI-8; n=37), major depression and somatization (n=40) and healthy controls (n=37): interleukin-6 (IL-6); interleukin-1-receptor-antagonist (IL-1RA); plasma soluble interleukin-6 receptor (IL-6R); soluble suppressor/cytotoxic antigen (CD8); leukemia inhibitory factor (LIF-R); and Clara cell protein (CC16), an endogenous anticytokine. Serum CD8 concentrations were significantly increased in patients with major depression compared with concentrations in patients with somatization syndrome, whereas concentrations in normal controls were intermediate between those of the two groups of patients. Serum CC16 was significantly lower in major depression than in healthy controls. The highest CC16 scores were found in patients with somatization syndrome. Somatizing patients have significantly lower serum IL-6 values than normal controls and depressed patients. The present results indicate (1) an activation of the IRS in depression with signs of T-cell activation (increased CD8), monocytic activation (IL-1RA) and a lowered anti-inflammatory capacity of the serum (lower CC16) and (2) an immune alteration in somatizing syndrome, such as monocytic activation (increased IL-1RA) and indicators of lowered T-lymphocytic activity (lowered CD8 and IL-6). These results suggest different immune alterations in somatization syndrome and depression.
authors.affiliation: Klinik Roseneck, Center for Behavioral Medicine, Prien am Chiemsee, Germany. rief@mailer.uni-marburg.de
authors.forename: W
authors.initials: W
authors.lastname: Rief
authors.forename: F
authors.initials: F
authors.lastname: Pilger
authors.forename: D
authors.initials: D
authors.lastname: Ihle
authors.forename: E
authors.initials: E
authors.lastname: Bosmans
authors.forename: B
authors.initials: B
authors.lastname: Egyed
authors.forename: M
authors.initials: M
authors.lastname: Maes
mesh_terms: D000328:Adult; D016827:CD8 Antigens / Q000097:blood / Q000276:immunology*; D015897:Comorbidity; D003865:Major Depressive Disorder / Q000453:epidemiology / Q000276:immunology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood* / Q000276:immunology*; D053577:Interleukin-1 Receptor Accessory Protein; D008297:Male; D015995:Prevalence; D011569:Psychiatric Status Rating Scales; D017472:Receptors, Interleukin-1 / Q000097:blood / Q000276:immunology*; D019947:Receptors, Interleukin-6 / Q000097:blood / Q000276:immunology*; D013001:Somatoform Disorders / Q000453:epidemiology / Q000276:immunology*
chemical_list: D016827:CD8 Antigens; C407643:IL1RAPL1 protein, human; D018836:Inflammation Mediators; D053577:Interleukin-1 Receptor Accessory Protein; D017472:Receptors, Interleukin-1; D019947:Receptors, Interleukin-6