Peripheral cytokine and chemokine alterations in depression: a meta‐analysis of 82 studies

Abstract

Objective To conduct a systematic review and meta‐analysis of studies that measured cytokine and chemokine levels in individuals with major depressive disorder (MDD) compared to healthy controls (HCs). Method The PubMed/MEDLINE, EMBASE, and PsycINFO databases were searched up until May 30, 2016. Effect sizes were estimated with random‐effects models. Result Eighty‐two studies comprising 3212 participants with MDD and 2798 HCs met inclusion criteria. Peripheral levels of interleukin‐6 (IL‐6), tumor necrosis factor (TNF)‐alpha, IL‐10, the soluble IL‐2 receptor, C‐C chemokine ligand 2, IL‐13, IL‐18, IL‐12, the IL‐1 receptor antagonist, and the soluble TNF receptor 2 were elevated in patients with MDD compared to HCs, whereas interferon‐gamma levels were lower in MDD (Hedge's g = −0.477, P = 0.043). Levels of IL‐1β, IL‐2, IL‐4, IL‐8, the soluble IL‐6 receptor (sIL‐6R), IL‐5, CCL‐3, IL‐17, and transforming growth factor‐beta 1 were not significantly altered in individuals with MDD compared to HCs. Heterogeneity was large (I2: 51.6–97.7%), and sources of heterogeneity were explored (e.g., age, smoking status, and body mass index). Conclusion Our results further characterize a cytokine/chemokine profile associated with MDD. Future studies are warranted to further elucidate sources of heterogeneity, as well as biosignature cytokines secreted by other immune cells.

Low tumor necrosis factor‐α levels predict symptom reduction during electroconvulsive therapy in major depressive disorder

“…Another meta‐analysis of inflammatory biomarkers in patients with MDD undergoing antidepressant treatment reported no decrease in the elevated baseline TNFα level. In that report, however, there was a decrease in the TNFα level in responders compared with nonresponders (Köhler et al., 2017). …”

A Comprehensive Database and Analysis Framework To Incorporate Multiscale Data Types and Enable Integrated Analysis of Bioactive Polyphenols

“…In regard to depression/anxiety, current evidence suggests that elevated expression of the pro-inflammatory cytokine inter-leukin-6 (IL-6) in the periphery and downregulation of Ras-related C3 botulinum toxin substrate-1 (Rac-1) expression in the nucleus accumbens (NAc) in the brain both play key roles in desensitizing the brain reward system, thereby increasing sensitivity to stress-mediated depression/anxiety phenotypes. 35–38 As highlighted by red arrows in Figure 3B, our integrative analysis revealed that IL-6 expression is significantly inhibited by select biologically available phenolic metabolites derived from BDPP treatment, particularly 3-(3′-hydroxyphenyl)propionic acid (3-HPP), dihydrocaffeic acid (DHCA), 3′- O -Me-epicatechin-5- O -glucuronide (Me-EC-Gln), and quercetin-3- O -glucuronide (Q-Gln). Moreover, Rac-1 expression is significantly induced by malvidin-glucoside, another BDPP metabolite.…”

Biomarkers for Antidepressant Efficacy of Electroconvulsive Therapy: An Exploratory Cerebrospinal Fluid Study

“…Based on the relative abundance on the relationship between the immune system and different aspects of depression [36][37][38], it is not surprising that the baseline CSF levels of sCD14 and to a lesser extent of IL-6, neopterin and sCD163 -all involved primarily in the innate immune response [14], were positively correlated with the antidepressant outcome of ECT, but this underlines the importance of understanding these interactions.…”