Open Access Maced J Med Sci. 2019 Sep 12;7(18):3064-3069. doi: 10.3889/oamjms.2019.779. eCollection 2019 Sep 30.
The Impact of Immunological Factors on Depression Treatment - Relation Between Antidepressants and Immunomodulation Agents.
Open access Macedonian journal of medical sciences
Jovana Vojvodic, Goran Mihajlovic, Petar Vojvodic, Dusan Radomirovic, Aleksandra Vojvodic, Tatjana Vlaskovic-Jovicevic, Zorica Peric-Hajzler, Dusica Matovic, Sanja Dimitrijevic, Goran Sijan, Maria Grazia Roccia, Massimo Fioranelli, Torello Lotti
Affiliations
Affiliations
- Clinic for Psychiatric Disorders "Dr. Laza Lazarevic", Belgrade, Serbia.
- Faculty of Medical Sciences, Department of Psychiatry, University of Kragujevac, Kragujevac, Serbia.
- Faculty of Medicine, University of Nis, Serbia.
- Department of Dermatology and Venereology, Military Medical Academy, Belgrade, Serbia.
- Military Medical Academy, Belgrade, Serbia.
- Department of Gynecology, Military Medical Academy, Belgrade, Serbia.
- Clinic for Plastic Surgery and Burns, Military Medical Academy, Belgrade, Serbia.
- Department of Nuclear Physics, Sub-nuclear and Radiation, G. Marconi University, Rome, Italy.
- Department of Dermatology, University of G. Marconi, Rome, Italy.
PMID: 31850124
PMCID: PMC6910782 DOI: 10.3889/oamjms.2019.779
Abstract
It is determined that 30% of patients with depression are resistant to antidepressant medication. The increased concentration of inflammation factors, such as C-reactive protein, and pro-inflammatory cytokines, have been detected in serum in these patients. It is necessary to establish new therapeutic possibilities and protocols that are created to overcome the difficulties caused by increased concentration of inflammatory biomarkers in depressive patients. The Selective Serotonin Reuptake Inhibitors (SSRIs) are considered to be the most powerful antidepressants, increasing the level of serotonin in endogenous depression, as well as in that caused by immunological mechanisms. It is believed that agents that influence cytokines, immunological signal pathways and cytokine syntheses, like the inhibitors of cyclooxygenase enzyme and other non-steroidal anti-inflammatory drugs (NSAIDs), are very important in the potential treatment of residual symptoms of depression. Treatment with cytokine antagonists is one of the potential adjuvant therapies, along with antidepressants. Signal pathways blockers, such as the inhibitors of cyclooxygenase and other NSAIDs, are in the phase of research, in terms of their antidepressant effects. Also, it has been shown that the inhibition of indolamin-2,3 deoxygenase (IDO) and kynurenine (KYN) signal pathways in the synthesis of neurotransmitters, by application of IDO antagonists, are leading to suppression of pro-inflammatory cytokine effects. Antidepressants may have anti-inflammatory effects, depending on dose and type, and they achieve this effect through the decrease of pro-inflammatory cytokine production and increase of anti-inflammatory cytokines. Also, antidepressants modulate the humoral and cellular immune system. This work aims to summarise certain neurobiological and neuroimmunological specificities that have been observed in patients with depression, antidepressants and immunomodulation agents. The understanding of complex and heterogenic pathophysiology of depression through the prism of the altered immune system, is of major importance, in terms of better optimisation of pharmacotherapy, and options for a personalised approach in depressive disorder treatment.
Copyright: © 2019 Jovana Vojvodic, Goran Mihajlovic, Petar Vojvodic, Dusan Radomirovic, Aleksandra Vojvodic, Tatjana Vlaskovic-Jovicevic, Zorica Peric-Hajzler, Dusica Matovic, Sanja Dimitrijevic, Goran Sijan, Maria Grazia Roccia, Massimo Fioranelli, Torello Lotti.
Keywords: Antidepressants; Cytokines; Depression; Inflammation
References
- JAMA Psychiatry. 2013 Jan;70(1):31-41 - PubMed
- Neuroscience. 2013 Aug 29;246:199-229 - PubMed
- Int J Mol Sci. 2016 May 14;17(5): - PubMed
- J Neuroimmune Pharmacol. 2013 Sep;8(4):900-20 - PubMed
- J Clin Psychiatry. 2014 Sep;75(9):975-7 - PubMed
- Pharmacopsychiatry. 2016 May;49(3):85-96 - PubMed
- PLoS One. 2013 Sep 27;8(9):e77227 - PubMed
- Pharmacopsychiatry. 2013 Jan;46(1):29-34 - PubMed
- Transl Psychiatry. 2012 Feb 21;2:e79 - PubMed
- Dialogues Clin Neurosci. 2017 Mar;19(1):55-63 - PubMed
- PLoS One. 2016 Nov 9;11(11):e0164337 - PubMed
- Biol Psychiatry. 2016 Jul 1;80(1):33-9 - PubMed
- Neuropsychiatr Dis Treat. 2017 May 10;13:1245-1262 - PubMed
- Int J Neuropsychopharmacol. 2014 Oct 31;18(3):null - PubMed
- Trends Immunol. 2006 Jan;27(1):24-31 - PubMed
- Psychiatr Danub. 2013 Sep;25(3):292-8 - PubMed
- BMC Med. 2016 Oct 28;14(1):173 - PubMed
- World J Psychiatry. 2016 Sep 22;6(3):283-93 - PubMed
- Expert Rev Neurother. 2012 Sep;12(9):1143-61 - PubMed
- Brain Behav Immun. 2017 Jan;59:265-272 - PubMed
- Mediators Inflamm. 2017;2017:6280925 - PubMed
- Transl Psychiatry. 2012 Aug 14;2:e151 - PubMed
- Pharmacol Ther. 2011 May;130(2):226-38 - PubMed
- Psychopharmacology (Berl). 2016 May;233(9):1707-14 - PubMed
- Adv Ther. 2017 Jan;34(1):78-90 - PubMed
- Curr Neuropharmacol. 2016;14(7):674-87 - PubMed
- Basic Clin Pharmacol Toxicol. 2016 Jul;119(1):10-8 - PubMed
- Brain Behav. 2015 Aug;5(8):e00338 - PubMed
- Int J Neuropsychopharmacol. 2016 Jan 16;:null - PubMed
Publication Types