Pro-inflammatory cytokines and treatment response to escitaloprsam in major depressive disorder

被引:245
作者
Eller, Triin [1 ]
Vasar, Veiko [1 ]
Shlik, Jakov [2 ]
Maron, Eduard [1 ,3 ]
机构
[1] Univ Tartu, Dept Psychiat, EE-50090 Tartu, Estonia
[2] Univ Ottawa, Dept Psychiat, Ottawa, ON K1N 6N5, Canada
[3] N Estonia Reg Hosp, Psychiat Clin, Tallinn, Estonia
关键词
Cytokines; escitalopram; interleukin-8; major depression; soluble interleukin-2 receptor; tumor necrosis factor alpha;
D O I
10.1016/j.pnpbp.2007.09.015
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Alterations in the immune system may have importance for the pathophysiology of depression. Several studies have linked increased production of pro-inflammatory cytokines to depression and depressive symptoms. There is growing evidence that antidepressive treatment may influence the production of pro-and anti-inflammatory cytokines. In the present study we aimed to find associations between the levels of soluble interleukin-2 receptor (sIL-2R), interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) and the response to antidepressant treatment in patients with major depression. Our study group consisted of 100 patients (35 males and 65 females) who were treated with escitalopram 10-20 mg/day for 12 weeks. Responders and non-responders were identified according to Montgomery-Asberg's Depression Rating Scale (MADRS) scores. The levels of cytokines were measured at baseline and at 4th and 12th week of the treatment and compared to cytokine concentrations in healthy volunteers (n =45; 19 males and 26 females). Our data indicated that a higher level of TNF-alpha might predict a non-response to treatment with escitalopram and that changes in concentrations of sIL-2R during the treatment were different in responders and non-responders. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:445 / 450
页数:6
相关论文
共 38 条
[1]   Further evidence for the depressive effects of cytokines: Anhedonia and neurochemical changes [J].
Anisman, H ;
Kokkinidis, L ;
Merali, Z .
BRAIN BEHAVIOR AND IMMUNITY, 2002, 16 (05) :544-556
[2]   IL-6 levels decrease with SSRI treatment in patients with major depression [J].
Basterzi, AD ;
Aydemir, Ç ;
Kisa, C ;
Aksaray, S ;
Tuzer, V ;
Yazici, K ;
Göka, E .
HUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL, 2005, 20 (07) :473-476
[3]   Immunotherapy with interferon-alpha in patients affected by chronic hepatitis C induces an intercorrelated stimulation of the cytokine network and an increase in depressive and anxiety symptoms [J].
Bonaccorso, S ;
Puzella, A ;
Marino, V ;
Pasquini, M ;
Biondi, M ;
Artini, M ;
Almerighi, C ;
Levrero, M ;
Egyed, B ;
Bosmans, E ;
Meltzer, HY ;
Maes, M .
PSYCHIATRY RESEARCH, 2001, 105 (1-2) :45-55
[4]   Interleukin-1β and tumor necrosis factor-α in children with major depressive disorder or dysthymia [J].
Brambilla, F ;
Monteleone, P ;
Maj, M .
JOURNAL OF AFFECTIVE DISORDERS, 2004, 78 (03) :273-277
[5]   A new chapter opens in anti-inflammatory treatments: The antidepressant bupropion lowers production of tumor necrosis factor-alpha and interferon-gamma in mice [J].
Brustolim, D. ;
Ribeiro-dos-Santos, R. ;
Kast, R. E. ;
Altschuler, E. L. ;
Soares, M. B. P. .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2006, 6 (06) :903-907
[6]   Cytokines and psychopathology:: Lessons from interferon-α [J].
Capuron, L ;
Miller, AH .
BIOLOGICAL PSYCHIATRY, 2004, 56 (11) :819-824
[7]   Interferon-alpha-induced changes in tryptophan metabolism: Relationship to depression and paroxetine treatment [J].
Capuron, L ;
Neurauter, G ;
Musselman, DL ;
Lawson, DH ;
Nemeroff, CB ;
Fuchs, D ;
Miller, AH .
BIOLOGICAL PSYCHIATRY, 2003, 54 (09) :906-914
[8]   Depressive symptoms and production of proinflammatory cytokines by peripheral blood mononuclear cells stimulated in vitro [J].
Cyranowski, Jill M. ;
Marsland, Anna L. ;
Bromberger, Joyce T. ;
Whiteside, Theresa L. ;
Chang, Yuefang ;
Matthews, Karen A. .
BRAIN BEHAVIOR AND IMMUNITY, 2007, 21 (02) :229-237
[9]  
DAIMOND M, 2006, EUROPEAN NEUROPSYCHO, V16, P481
[10]   Successful antidepressant therapy restores the disturbed interplay between TNF-α system and HPA axis [J].
Himmerich, Hubertus ;
Binder, Elisabeth B. ;
Kuenzel, Heike E. ;
Schuld, Andreas ;
Lucae, Susanne ;
Uhr, Manfred ;
Pollmaecher, Thomas ;
Holsboer, Florian ;
Ising, Marcus .
BIOLOGICAL PSYCHIATRY, 2006, 60 (08) :882-888