Abstract

Background: Both depressive disorders (DD) and post-traumatic stress disorders (PTSD) are caused by immune system dysfunction. Affected individuals show increased proinflammatory cytokine concentration levels. Also, it has been hypothesized that DD and PTSD might be associated with a generalized proinflammatory cytokine signature. The study assessed the concentration of IL-1β, IL-4, IL-8 and IL-10 in depression alone and with PTSD. Methods: The study involved 460 participants. Out of them, 420 subjects comprised a study group and 40 subjects comprised a control group. Each study group consisted of 60 patients with mild depression (MD), moderate depression (MOD), severe depression (SeD), MD and PTSD (MD + PTSD), MOD and PTSD (MOD + PTSD), SeD and PTSD (SeD + PTSD), and with PTSD alone. All patients had serum concentration of IL-1β, IL-4, IL-8 and IL-10 measured with ELISA. Results: DD and PTSD are reflected in IL-1β, IL-4, IL-8 and IL-10 concentration levels. It was reported that mean levels of IL-1β, IL-4, IL-8 increase as depression became more severe. A regular decrease in IL-10 concentration levels was noted with the onset and exacerbation of depressive symptoms. Conclusion: The findings might be useful when considering chronic inflammation as a potential target or biomarker in depression and PTSD treatment.

Highlights

  • Depression has been reported to be a global disease affecting people in all communities worldwide [1]

  • The aim of this study was to assess changes in the concentration of interleukin 1β (IL-1β), IL-4, IL-8 and IL-10 among patients with mild depression (MD), moderate depression (MOD), severe depression (SeD), MD and post-traumatic stress disorders (PTSD) (MD + PTSD), MOD and PTSD (MOD + PTSD), SeD and PTSD (SeD + PTSD), and with PTSD alone, in order to find potential markers of altered stress reactivity associated with both depression and PTSD

  • The analysis was performed for the control group [comprising 40 subjects] and for the study groups described in the Material and Methods section [each group comprised 60 subjects]

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Summary

Introduction

Depression has been reported to be a global disease affecting people in all communities worldwide [1]. The proper functioning of the immune system and the occurrence of the clinical symptoms of PTSD and/or depressive disorder (DD) are interdependent Both inflammatory diseases and DD share a common risk factor, namely the activation of the immune system. The role of the pro-inflammatory phenotype, which creates a potential genetic basis for the elevated risk of DD and/or PTSD, seems to be decisive in terms of the order of developing either disease The pathophysiology of both DD and PTSD involves abnormalities in the HPA-axis. Indoleamine 2,3-dioxygenase (IDO), (Han et al, 2015) is claimed to be a factor that links “cytokine theory” with “monoamine theory” in DD [2,3] Both depressive disorders (DD) and post-traumatic stress disorders (PTSD) are caused by immune system dysfunction. Conclusion: The findings might be useful when considering chronic inflammation as a potential target or biomarker in depression and PTSD treatment

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