PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
In Major Depression, Increased Serum Dynorphin and Kappa Opioid Receptor Levels are Positively Associated with Mu Opioid Receptor Levels and Immune Activation and Are Attenuated by Nicotine Dependence
Version 1
: Received: 14 April 2019 / Approved: 16 April 2019 / Online: 16 April 2019 (09:49:14 CEST)
How to cite:
Al-Hakeim, H.; Al-Fadhel, S.; Al-Dujaili, A. H.; Maes, M. In Major Depression, Increased Serum Dynorphin and Kappa Opioid Receptor Levels are Positively Associated with Mu Opioid Receptor Levels and Immune Activation and Are Attenuated by Nicotine Dependence. Preprints2019, 2019040176. https://doi.org/10.20944/preprints201904.0176.v1
Al-Hakeim, H.; Al-Fadhel, S.; Al-Dujaili, A. H.; Maes, M. In Major Depression, Increased Serum Dynorphin and Kappa Opioid Receptor Levels are Positively Associated with Mu Opioid Receptor Levels and Immune Activation and Are Attenuated by Nicotine Dependence. Preprints 2019, 2019040176. https://doi.org/10.20944/preprints201904.0176.v1
Al-Hakeim, H.; Al-Fadhel, S.; Al-Dujaili, A. H.; Maes, M. In Major Depression, Increased Serum Dynorphin and Kappa Opioid Receptor Levels are Positively Associated with Mu Opioid Receptor Levels and Immune Activation and Are Attenuated by Nicotine Dependence. Preprints2019, 2019040176. https://doi.org/10.20944/preprints201904.0176.v1
APA Style
Al-Hakeim, H., Al-Fadhel, S., Al-Dujaili, A. H., & Maes, M. (2019). In Major Depression, Increased Serum Dynorphin and Kappa Opioid Receptor Levels are Positively Associated with Mu Opioid Receptor Levels and Immune Activation and Are Attenuated by Nicotine Dependence. Preprints. https://doi.org/10.20944/preprints201904.0176.v1
Chicago/Turabian Style
Al-Hakeim, H., Arafat Hussein Al-Dujaili and Michael Maes. 2019 "In Major Depression, Increased Serum Dynorphin and Kappa Opioid Receptor Levels are Positively Associated with Mu Opioid Receptor Levels and Immune Activation and Are Attenuated by Nicotine Dependence" Preprints. https://doi.org/10.20944/preprints201904.0176.v1
Abstract
Background: There is now evidence that immune and opioid systems show functional reciprocal relationships and that both systems may participate in the pathophysiology of major depression (MDD). Objective: The present study was carried out to delineate differences between MDD patients and healthy controls in dynorphin and kappa opioid receptor (KORs) in association with levels of β-endorphins and mu opioid receptors (MORs), interleukin-6 (IL-6) and IL-10. Method: The present study recruited 60 drug-free male participants with MDD aged 24-70 year and 30 age-matched healthy males as control group and measured serum levels of dynorphin, KOR, β-endorphin, MOR, IL-6 and IL-10. Results: Serum dynorphin, KOR, β-endorphin and MOR are significantly increased in MDD as compared with controls. The increases in the dynorphin/KOR system and β-endorhin/MOR system are significantly intercorrelated and are both strongly associated with increased IL-6 and IL-10 levels. Dynorphin, β-endorphin, KOR and both cytokines showed a good diagnostic performance for MDD versus controls, whereby both opioid peptides and cytokines show a bootstrapped (n=2000) area under the receiver operating curve of 0.972. KOR and the dynorphin/KOR system are both significantly decreased in depressed subjects with comorbid nicotine dependence. Conclusion: Our findings suggest that in MDD, immune activation is associated with a simultaneous activation of dynorphin/KOR and β-endorhin/MOR signaling and that these opioid systems may participate in the pathophysiology of depression by a) exerting immune regulatory activities attenuating the primary immune response; and b) modulating reward responses and mood as well as emotional and behavioral responses to stress.
Medicine and Pharmacology, Psychiatry and Mental Health
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.