BACKGROUND: Previous studies have suggested that regulation of the proinflammatory cytokine interleukin (IL)-6 is abnormal in patients with major depression. This study was undertaken to determine whether IL-6 concentrations in cerebrospinal fluid (CSF) differ between depressed patients and healthy control subjects. METHODS: Lumbar puncture with a standardized procedure was performed on 18 drug-free patients meeting DSM-IV criteria for unipolar major depression and 26 age- and sex-matched healthy volunteers. CSF was assayed for IL-6 using a quantitative 'sandwich' enzyme immunoassay technique. RESULTS: Mean+/-S.D. CSF IL-6 levels did not differ between depressed (2.2+/-1.0 pg/ml) and healthy control (2.4+/-1.9 pg/ml) subjects. LIMITATIONS: This study had adequate power (0.8) to detect a large (d=0.88) effect size at alpha = 0.05. Although sample sizes were comparable to or larger than those of previous CSF studies, it is possible that a less robust difference between depressed and healthy subjects was not detected. CONCLUSIONS: These findings fail to support speculation that immune activation may be causally involved in the pathogenesis of depression.
BACKGROUND: Previous studies have suggested that regulation of the proinflammatory cytokine interleukin (IL)-6 is abnormal in patients with major depression. This study was undertaken to determine whether IL-6 concentrations in cerebrospinal fluid (CSF) differ between depressedpatients and healthy control subjects. METHODS: Lumbar puncture with a standardized procedure was performed on 18 drug-free patients meeting DSM-IV criteria for unipolar major depression and 26 age- and sex-matched healthy volunteers. CSF was assayed for IL-6 using a quantitative 'sandwich' enzyme immunoassay technique. RESULTS: Mean+/-S.D. CSF IL-6 levels did not differ between depressed (2.2+/-1.0 pg/ml) and healthy control (2.4+/-1.9 pg/ml) subjects. LIMITATIONS: This study had adequate power (0.8) to detect a large (d=0.88) effect size at alpha = 0.05. Although sample sizes were comparable to or larger than those of previous CSF studies, it is possible that a less robust difference between depressed and healthy subjects was not detected. CONCLUSIONS: These findings fail to support speculation that immune activation may be causally involved in the pathogenesis of depression.
Authors: Claudia Ditzen; Ning Tang; Archana M Jastorff; Larysa Teplytska; Alexander Yassouridis; Giuseppina Maccarrone; Manfred Uhr; Thomas Bronisch; Christine A Miller; Florian Holsboer; Christoph W Turck Journal: Neuropsychopharmacology Date: 2011-12-14 Impact factor: 7.853
Authors: Gabriela D Colpo; Marion Leboyer; Robert Dantzer; Mahdukar H Trivedi; Antonio L Teixeira Journal: Expert Rev Neurother Date: 2017-11-27 Impact factor: 4.618
Authors: Emily S Miller; Allie Sakowicz; Archana Roy; Amy Yang; John T Sullivan; William A Grobman; Katherine L Wisner Journal: Am J Obstet Gynecol Date: 2018-12-14 Impact factor: 8.661