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Inflammation in depression: the role of cytokines

Year 2012, Volume: 2 Issue: 3, 103 - 107, 30.01.2014

Abstract

Recent studies support the concept that inflammatory mechanisms play a crucial role in the pathomechanisms of major depression. Major depression shares similarities with ‘sickness behavior’, a normal response to inflammatory cytokines. Elevations in proinflammatory cytokines and other inflammation-related proteins in major depression were found in plasma and cerebrospinal fluid (CSF). Clinical progress of the disease may also be predicted by the changes in proinflammatory cytokine levels. Antidepressant treatment can lead to a normalization of elevated cytokine levels in major depression. The new hypothesis of depression provided some new opportunities in treatment of depression.


Key words: Cytokine, inflammation, depression, antidepressant

References

  • Maes M. Evidence for an immune response in major depression: a review and hypothesis. Prog Neuropsychopharmacol Biol Psychiatry. 1995;19(1):11–38.
  • Maes M. The immune pathophysiology of major depression. Depression: Neurobiological, Psychopathological and Therapeutic Advances. 1st ed. London: John Wiley; 1997. p. 197-215.
  • Raison CL, Capuron L, Miller AH. Cytokines sing the blues: Inflammation and the pathogenesis of major depression. Trend Immunol. 2006;27:24-31.
  • Maes M, Galecki P, Chang YS, Berk M. A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):676- 692.
  • Maes M, Leonard BE, Myint AM, Kubera M, Verkerk R. The new ‘5-HT’ hypothesis of depression: cell-mediated immune activation induces indoleamine 2,3-dioxygenase, which leads to lower plasma tryptophan and an increased synthesis of detrimental tryptophan catabolites (TRYCATs), both of which contribute to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):702-721.
  • Song C, Wang H. Cytokines mediated inflammation and decreased neurogenesis in animal models of depression. 2011;35(3):760-768.
  • Kubera M, Obuchowicz E, Goehler L, Brzeszcz J, Maes M. In animal models, psychosocial stress-induced (neuro)inflammation, apoptosis and reduced neurogenesis are associated to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):744-759.
  • Maes M, Leonard B, Fernandez A, Kubera M, Nowak G, Veerhuis R, Gardner A, Ruckoanich P, Geffard M, Altamura C, Galecki P, Berk M. Editorial: (Neuro)inflammation and neuroprogression as new pathways and drug targets in depression: From antioxidants to kinase inhibitors. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):659-663.
  • Miller AH, Maletic V, Raison CL. Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression. Biol Psychiatry. 2009;65:732-741.
  • Khairova RA, Machado-Vieira R, Du J, Manji HK. A potential role for pro-inflammatory cytokines in regulating synaptic plasticity in major depressive disorder. Int J Neuropsychopharmacol. 2009;12(4):561- 578.
  • Sommer N, Löschmann PA, Northoff GH, Weller M, Steinbrecher JP, Lichtenfels R, Meyermann R, Riethmüller A, Fontana A. The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis. Nature Medicine. 1995;1:244-248.
  • Navikas V, Matusecicus D, Söderström M, Pirskanen R, Fredrikson S, Link H. The phosphodiesterase i.v. inhibitor rolipram in vitro reduces the numbers of MBP-reactive IFN-gamma and TNF-alpha mRNA expressing blood mononuclear cells in patients with multiple sclerosis. Clin Neuropharmacol. 1998;21(4):236-244.
  • Suzuki E, Shintani F, Kanba S, Asai M, Nakaki T. Induction of interleukin1β and interleukin1 receptor antagonist mRNA by chronic treatment with various psychotropics in widespread area of rat brain. Neurosci Lett. 1996;215:201-204.
  • Shirayama Y, Mitsushio H, Takashima M, Ichikawa H, Takahashi K. Reduction of substance P after chronic antidepressants treatment in the striatum, substantia nigra and amygdala of the rat. Brain Res. 1996;739:70-78.
  • Müller N, Schwarz MJ, Dehning S, Douhe A, Cerovecki A, Goldstein- Müller B, Spellmann I, Hetzel G, Maino K, Kleindienst N, Möller HJ, Arolt V, Riedel M. The cyclooxygenase-2 inhibitor celecoxib has therapeutic effects in major depression: results of a double-blind, randomized, placebo controlled, add-on pilot study to reboxetine. Mol Psychiatry. 2006;11(7):680-684.
  • Stafford L, Berk M. The use of statins after a cardiac intervention is associated with reduced risk of subsequent depression: proof of concept for the inflammatory and oxidative hypotheses of depression? J Clin Psychiatry. 2011;72(9):1229-1235.
  • Wang Y, Yang F, Liu YF, Gao F, Jiang W. Acetylsalicylic acid as an augmentation agent in fluoxetine treatment resistant depressive rats. Neurosci Lett. 2011;499(2):74-79.
  • Pae CU, Marks DM, Han C, Patkar AA. Does minocycline have antidepressant effect? Biomed Pharmacother. 2008;62(5):308-311.
  • Lin PY, Su KP. A meta-analytic review of double-blind, placebo- controlled trials of antidepressant efŞcacy of omega-3 fatty acids. J Clin Psychiatry. 2007;68(7):1056-1061.
  • Song C, Wang H. Cytokines mediated inflammation and decreased neurogenesis in animal models of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):760-768.
  • Jiang Y, Deacon R, Anthony DC, Campbell SJ. Inhibition of peripheral TNF can block the malaise associated with CNS inflammatory diseases. Neurobiol Dis. 2008;32(1):125-132.
  • Kulkarni S, Dhir A, Akula KK. Potentials of curcumin as an antidepressant. Sci World J. 2009;9:1233-1241.
  • Loix S, De Kock M, Henin P. The anti-inflammatory effects of ketamine: state of the art. Acta Anaesthesiol Belg. 2011;62(1):47-58.
  • Rook GAW, Raison CL, Lowry CA. Can we vaccinate against depression? Drug Discovery Today. 2012;17(9/10):451-458.

Depresyonda inflamasyon: sitokinlerin rolü

Year 2012, Volume: 2 Issue: 3, 103 - 107, 30.01.2014

Abstract

Son yıllarda yapılan çalışmalar majör depresyonun patolojisinde inflamatuvar mekanizmaların önemli rol oynadığını göstermektedir. Majör depresyonda, inflamatuvar sitokinlere verilen yanıt olan “hastalık davranışı”na benzer belirtiler görülmektedir. Depresif hastaların plazma ve beyin omurilik sıvılarında proinflamatuvar sitokinler ve inflamasyonla bağlantılı proteinlerin miktarında artış gözlenir. Hastalığın prognozu da sitokin değerlerindeki değişmelerle paralellik göstermektedir. Antidepresan tedavi ile sitokin seviyeleri normale çevrilebilmektedir. Depresyonun bu yeni hipotezi, tedavide de yenilikleri gündeme getirmiştir.


Anahtar Kelimeler : Sitokin, inflamasyon, depresyon, antidepresan

References

  • Maes M. Evidence for an immune response in major depression: a review and hypothesis. Prog Neuropsychopharmacol Biol Psychiatry. 1995;19(1):11–38.
  • Maes M. The immune pathophysiology of major depression. Depression: Neurobiological, Psychopathological and Therapeutic Advances. 1st ed. London: John Wiley; 1997. p. 197-215.
  • Raison CL, Capuron L, Miller AH. Cytokines sing the blues: Inflammation and the pathogenesis of major depression. Trend Immunol. 2006;27:24-31.
  • Maes M, Galecki P, Chang YS, Berk M. A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):676- 692.
  • Maes M, Leonard BE, Myint AM, Kubera M, Verkerk R. The new ‘5-HT’ hypothesis of depression: cell-mediated immune activation induces indoleamine 2,3-dioxygenase, which leads to lower plasma tryptophan and an increased synthesis of detrimental tryptophan catabolites (TRYCATs), both of which contribute to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):702-721.
  • Song C, Wang H. Cytokines mediated inflammation and decreased neurogenesis in animal models of depression. 2011;35(3):760-768.
  • Kubera M, Obuchowicz E, Goehler L, Brzeszcz J, Maes M. In animal models, psychosocial stress-induced (neuro)inflammation, apoptosis and reduced neurogenesis are associated to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):744-759.
  • Maes M, Leonard B, Fernandez A, Kubera M, Nowak G, Veerhuis R, Gardner A, Ruckoanich P, Geffard M, Altamura C, Galecki P, Berk M. Editorial: (Neuro)inflammation and neuroprogression as new pathways and drug targets in depression: From antioxidants to kinase inhibitors. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):659-663.
  • Miller AH, Maletic V, Raison CL. Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression. Biol Psychiatry. 2009;65:732-741.
  • Khairova RA, Machado-Vieira R, Du J, Manji HK. A potential role for pro-inflammatory cytokines in regulating synaptic plasticity in major depressive disorder. Int J Neuropsychopharmacol. 2009;12(4):561- 578.
  • Sommer N, Löschmann PA, Northoff GH, Weller M, Steinbrecher JP, Lichtenfels R, Meyermann R, Riethmüller A, Fontana A. The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis. Nature Medicine. 1995;1:244-248.
  • Navikas V, Matusecicus D, Söderström M, Pirskanen R, Fredrikson S, Link H. The phosphodiesterase i.v. inhibitor rolipram in vitro reduces the numbers of MBP-reactive IFN-gamma and TNF-alpha mRNA expressing blood mononuclear cells in patients with multiple sclerosis. Clin Neuropharmacol. 1998;21(4):236-244.
  • Suzuki E, Shintani F, Kanba S, Asai M, Nakaki T. Induction of interleukin1β and interleukin1 receptor antagonist mRNA by chronic treatment with various psychotropics in widespread area of rat brain. Neurosci Lett. 1996;215:201-204.
  • Shirayama Y, Mitsushio H, Takashima M, Ichikawa H, Takahashi K. Reduction of substance P after chronic antidepressants treatment in the striatum, substantia nigra and amygdala of the rat. Brain Res. 1996;739:70-78.
  • Müller N, Schwarz MJ, Dehning S, Douhe A, Cerovecki A, Goldstein- Müller B, Spellmann I, Hetzel G, Maino K, Kleindienst N, Möller HJ, Arolt V, Riedel M. The cyclooxygenase-2 inhibitor celecoxib has therapeutic effects in major depression: results of a double-blind, randomized, placebo controlled, add-on pilot study to reboxetine. Mol Psychiatry. 2006;11(7):680-684.
  • Stafford L, Berk M. The use of statins after a cardiac intervention is associated with reduced risk of subsequent depression: proof of concept for the inflammatory and oxidative hypotheses of depression? J Clin Psychiatry. 2011;72(9):1229-1235.
  • Wang Y, Yang F, Liu YF, Gao F, Jiang W. Acetylsalicylic acid as an augmentation agent in fluoxetine treatment resistant depressive rats. Neurosci Lett. 2011;499(2):74-79.
  • Pae CU, Marks DM, Han C, Patkar AA. Does minocycline have antidepressant effect? Biomed Pharmacother. 2008;62(5):308-311.
  • Lin PY, Su KP. A meta-analytic review of double-blind, placebo- controlled trials of antidepressant efŞcacy of omega-3 fatty acids. J Clin Psychiatry. 2007;68(7):1056-1061.
  • Song C, Wang H. Cytokines mediated inflammation and decreased neurogenesis in animal models of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):760-768.
  • Jiang Y, Deacon R, Anthony DC, Campbell SJ. Inhibition of peripheral TNF can block the malaise associated with CNS inflammatory diseases. Neurobiol Dis. 2008;32(1):125-132.
  • Kulkarni S, Dhir A, Akula KK. Potentials of curcumin as an antidepressant. Sci World J. 2009;9:1233-1241.
  • Loix S, De Kock M, Henin P. The anti-inflammatory effects of ketamine: state of the art. Acta Anaesthesiol Belg. 2011;62(1):47-58.
  • Rook GAW, Raison CL, Lowry CA. Can we vaccinate against depression? Drug Discovery Today. 2012;17(9/10):451-458.
There are 24 citations in total.

Details

Primary Language Turkish
Journal Section Articles
Authors

Salih Gümrü This is me

Feyza Arıcıoğlu

Publication Date January 30, 2014
Submission Date January 30, 2014
Published in Issue Year 2012 Volume: 2 Issue: 3

Cite

APA Gümrü, S., & Arıcıoğlu, F. (2014). Depresyonda inflamasyon: sitokinlerin rolü. Clinical and Experimental Health Sciences, 2(3), 103-107.
AMA Gümrü S, Arıcıoğlu F. Depresyonda inflamasyon: sitokinlerin rolü. Clinical and Experimental Health Sciences. February 2014;2(3):103-107.
Chicago Gümrü, Salih, and Feyza Arıcıoğlu. “Depresyonda Inflamasyon: Sitokinlerin Rolü”. Clinical and Experimental Health Sciences 2, no. 3 (February 2014): 103-7.
EndNote Gümrü S, Arıcıoğlu F (February 1, 2014) Depresyonda inflamasyon: sitokinlerin rolü. Clinical and Experimental Health Sciences 2 3 103–107.
IEEE S. Gümrü and F. Arıcıoğlu, “Depresyonda inflamasyon: sitokinlerin rolü”, Clinical and Experimental Health Sciences, vol. 2, no. 3, pp. 103–107, 2014.
ISNAD Gümrü, Salih - Arıcıoğlu, Feyza. “Depresyonda Inflamasyon: Sitokinlerin Rolü”. Clinical and Experimental Health Sciences 2/3 (February 2014), 103-107.
JAMA Gümrü S, Arıcıoğlu F. Depresyonda inflamasyon: sitokinlerin rolü. Clinical and Experimental Health Sciences. 2014;2:103–107.
MLA Gümrü, Salih and Feyza Arıcıoğlu. “Depresyonda Inflamasyon: Sitokinlerin Rolü”. Clinical and Experimental Health Sciences, vol. 2, no. 3, 2014, pp. 103-7.
Vancouver Gümrü S, Arıcıoğlu F. Depresyonda inflamasyon: sitokinlerin rolü. Clinical and Experimental Health Sciences. 2014;2(3):103-7.

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