Effects of eicosapentaenoic acid and fluoxetine on plasma cortisol, serum interleukin-1beta and interleukin-6 concentrations in patients with major depressive disorder

Jazayeri, Shima; Keshavarz, Seyed Ali; Tehrani‐Doost, Mehdi; Djalali, Mahmood; Hosseini, Mostafa; Amini, Homayoun; Chamari, Maryam; Djazayery, Abolghassem

doi:10.1016/j.psychres.2009.04.013

Cited by 102 publications

(82 citation statements)

References 25 publications

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“…Indeed, the literature describing the effects of standard antidepressants on systemic inflammation is highly mixed. Although some studies have demonstrated that antidepressants decrease inflammatory cytokines (38,39), others report either no effect (31,40,41) or even increased levels (42,43). This discrepancy is likely due to a number of factors, including the class of antidepressant used for treatment or the heterogeneity of the patient population (44).…”

Section: Significancementioning

confidence: 99%

Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress

Hodes

Pfau

Leboeuf

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

586

506

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Significance Depression and anxiety have been linked to increased inflammation. However, we do not know if inflammatory status predates onset of disease or whether it contributes to depression symptomatology. We report preexisting individual differences in the peripheral immune system that predict and promote stress susceptibility. Replacing a stress-naive animal’s peripheral immune system with that of a stressed animal increases susceptibility to social stress including repeated social defeat stress (RSDS) and witness defeat (a purely emotional form of social stress). Depleting the cytokine IL-6 from the whole body or just from leukocytes promotes resilience, as does sequestering IL-6 outside of the brain. These studies demonstrate that the emotional response to stress can be generated or blocked in the periphery, and offer a potential new form of treatment for stress disorders.

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Section: Significancementioning

confidence: 99%

Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress

Hodes

Pfau

Leboeuf

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

586

506

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“…However, due to the heterogeneity of depression, not all clinical studies have reported consistent results. For example, Jazayeri [21] showed that serum IL-6 and IL-1β do not change significantly after antidepressant treatments. Can inflammatory biomarkers be used to predict or diagnose depression?…”

Section: Infl Ammatory Biomarkers Of Depressionmentioning

confidence: 99%

Inflammation: a mechanism of depression?

Han

2014

Neurosci. Bull.

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In recent decades, major depression has become more prevalent and research has shown that immune activation and cytokine production may be involved. This review is mainly focused on the contribution of infl ammation to depression. We fi rst briefl y introduce the infl ammatory biomarkers of depression, then discuss the sources of cytokines in the brain, and fi nally describe the neuroimmunological mechanisms underlying the association between infl ammation and depression.Keywords: depression; infl ammation; cytokines; hypothalamic-pituitary-adrenal axis; 5-HT; neuroplasticity ·Review· IntroductionThe prevalence of major depression has increased dramatically over the past few decades [1] , and women are nearly twice as likely as men to develop depressive disorder [2] . Depression is classified as a brain disorder, but its symptomatology includes some behaviors that also occur during chronic infl ammatory stress [3] . Research has shown that immune activation and the production of cytokines may be involved in depression [4] , so this relationship has received much attention. In fact, three causal pathways have been proposed: depression to inflammation, inflammation to depression, and a bidirectional relationship [5] . In this review, we focus on the impact of inflammation on depression and the underlying mechanisms. Cytokines are small cell-signaling proteins that mediate and regulate immune responses and inflammation, and can be divided into two categories:the pro-inflammatory cytokines interleukin (IL)-1 β, IL-6, IL-8, and tumor necrosis factor (TNF)-α, and the anti-inflammatory cytokines IL-1Rα, IL-4, IL-10, and transforming growth factor (TGF)-β1. Generally, t he proinfl ammatory cytokines promote systemic infl ammation and are essential for the initiation of an infl ammatory response to disease [6] , while the anti-inflammatory cytokines antagonize these actions to reduce inflammation and promote healing [6,7] . Moreover, some cytokines play dual roles [8] . In the central nervous system (CNS), the cellular source, function, and mechanisms of action of cytokines differ from those in the periphery. In the following, we briefl y introduce the current research on infl ammatory biomarkers of depression. Infl ammatory Biomarkers of DepressionSo far, there are neither universally accepted or defi nitive biomarkers of depression [9] , nor effective methods to assess the severity, endophenotypes, or response to treatment [10] .However, sufficient evidence has suggested changes in the circulating levels of cytokines in depressed patients, which can be reversed by antidepressant treatments [11,12] .So, many studies have aimed to clarify the neurobiological changes in depression and to establish inflammatory biomarkers. The peripheral levels of IL-6, TNF-α, and IL-1β are increased in patients with depression [13][14][15][16][17] , and antidepressant treatments reverse this effect [18][19][20] . These consistent results demonstrate that IL-6, TNF-α, and IL-1β are putative biomarkers for depression. However, due to the he...

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“…However, other clinical studies obtained opposite results, demonstrating no or even pro-inflammatory effects of antidepressant treatment (Chen et al, 2010;Haastrup et al, 2012;Hannestad et al, 2011;Jazayeri et al, 2010;Kim et al, 2013;Song et al, 2009). Experimental studies reflect the incongruence of clinical findings.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, though many studies showed that antidepressants have anti-inflammatory effects (Basterzi et al, 2005;Kagaya et al, 2001;Lanquillon et al, 2000;Leo et al, 2006;Tuglu et al, 2003;Yoshimura et al, 2009), an increasing number of studies are reporting a proinflammatory action (Chen et al, 2010;Haastrup et al, 2012;Hannestad et al, 2011;Jazayeri et al, 2010;Kim et al, 2013;Song et al, 2009). In addition, the bi-directional crosstalk between SSRI administration and inflammation has been described also by studies investigating the effects of antiinflammatory drugs on antidepressant efficacy.…”

mentioning

confidence: 99%

“…For instance, some studies report a decrease of IL-1β expression following fluoxetine administration in mice exposed to stress (Cheng et al, 2016;Lu et al, 2014), while others do not (Wilson et al, 2014). The variable SSRI effects on cytokine levels have also been described in the peripheral inflammatory markers of depressed patients (Jazayeri et al, 2010;Song et al, 2009). …”

mentioning

confidence: 99%

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Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment

Alboni

Poggini

Garofalo

et al. 2016

Brain, Behavior, and Immunity

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It has been hypothesized that selective serotonin reuptake inhibitors (SSRIs), the most common treatment for major depression, affect mood through changes in immune function. However, the effects of SSRIs on inflammatory response are contradictory since these act either as anti-or pro-inflammatory drugs. Previous experimental and clinical studies showed that the quality of the living environment moderates the outcome of antidepressant treatment. Therefore, we hypothesized that the interplay between SSRIs and the environment may, at least partially, explain the apparent incongruence regarding the effects of SSRI treatment on the inflammatory response. In order to investigate such interplay, we exposed C57BL/6 mice to chronic stress to induce a depression-like phenotype and, subsequently, to fluoxetine treatment or vehicle (21days) while being exposed to either an enriched or a stressful condition. At the end of treatment, we measured the expression levels of several anti-and pro-inflammatory cytokines and inflammatory mediators in the whole hippocampus and in isolated microglia. We also determined microglial density, distribution, and morphology to investigate their surveillance state. Results show that the effects of fluoxetine treatment on inflammation and microglial function, as compared to vehicle, were dependent on the quality of the living environment. In particular, fluoxetine administered in the enriched condition increased the expression of pro-inflammatory markers compared to vehicle, while treatment in a stressful condition produced anti-inflammatory effects. These findings provide new insights regarding the effects of SSRIs on inflammation, which may be crucial to devise pharmacological strategies aimed at enhancing antidepressant efficacy by means of controlling environmental conditions. AbstractIt has been hypothesized that selective serotonin reuptake inhibitors (SSRIs), the most common treatment for major depression, affect mood through changes in immune function. However, the effects of SSRIs on inflammatory response are contradictory since these drugs act either as anti-or proinflammatory. Previous experimental and clinical studies showed that the quality of the living environment moderates the outcome of antidepressant treatment. Therefore, we hypothesized that the interplay between SSRIs and environment may, at least partially, explain the apparent incongruence regarding the effects of SSRI treatment on the inflammatory response. In order to investigate such interplay, we exposed C57BL/6 mice to chronic stress to induce a depression-like phenotype and, subsequently, to fluoxetine treatment or vehicle (21 days) while being exposed to either an enriched or a stressful condition. At the end of treatment, we measured the expression levels of several anti-and pro-inflammatory cytokines and inflammatory mediators in the whole hippocampus and in isolated microglia. We also determined microglial density, distribution, and morphology to investigate their surveillance state. Results show that...

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Effects of eicosapentaenoic acid and fluoxetine on plasma cortisol, serum interleukin-1beta and interleukin-6 concentrations in patients with major depressive disorder

Cited by 102 publications

References 25 publications

Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress

Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress

Inflammation: a mechanism of depression?

Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment

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