Plasma Levels of IL-23 and IL-17 before and after Antidepressant Treatment in Patients with Major Depressive Disorder

Kim, Jae Won; Kim, Yong Ku; Hwang, Jaehoon; Yoon, Ho Kyoung; Ko, Young Hoon; Han, Changsu; Lee, Heon Jeong; Ham, Byung Joo; Lee, Hong Seock

doi:10.4306/pi.2013.10.3.294

Cited by 63 publications

(50 citation statements)

References 36 publications

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“…Few studies, however, have investigated the connection between depression and high levels of IL-17. In the study of Han et al [41], levels of IL-17 and IL-23 were measured in the plasma of patients with severe depression, but no correlation was found. In contrast, Liu et al [57] found a link between high IL-17 levels and depression, but they investigated patients with rheumatoid arthritis (RA).…”

Section: Does Il-17 Have a Role In Depression?mentioning

confidence: 96%

The role of IL-17 in CNS diseases

2015

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Cytokines of the IL-17 family are uniquely placed on the border between immune cells and tissue. Although IL-17 was originally found to induce the activation and mobilization of neutrophils to sites of inflammation, its tissue-specific function is not yet fully understood. The best-studied IL-17 family members, IL-17A and IL-17F, are both typically produced by immune cells such as Th17, γδ T cells and innate lymphoid cells group 3. However, the cells that respond to these cytokines are mostly found in inflamed tissue. As seen in psoriatic skin lesions or in joints of rheumatoid arthritis patients, high levels of IL-17 have been detected in the central nervous system (CNS) during inflammatory responses. Here, we provide a general review of the molecular function of IL-17 and its role in the CNS in particular. Of the different inflammatory conditions of the CNS, we found multiple sclerosis (MS) to be the one most associated with the presence of Th17 cells and IL-17. In particular, many studies using the murine model for MS, experimental autoimmune encephalomyelitis, found a clear association of Th17 and IL-17 with disease severity and progression. We summarize the recent advances made in correlating the presence of IL-17 with impaired blood-brain barrier integrity as well as the activation of astrocytes and microglia and the consequences for disease progression. There is also evidence that IL-17 plays a pathogenic role in the post-ischemic phase of stroke as well as its experimental model. We review the limited but promising data on the sources of post-stroke IL-17 production and its effects on CNS-resident target cells. In addition to MS and stroke, there is also evidence linking high levels of IL-17 to depression, as a frequent comorbidity of several inflammatory diseases, as well as to different types of infections of the CNS. The evidence we supply here suggests that inhibiting the function of the IL-17 cytokine family could have a beneficial effect on pathogenic conditions in the CNS.

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Section: Does Il-17 Have a Role In Depression?mentioning

confidence: 96%

The role of IL-17 in CNS diseases

2015

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“…In order to explore whether fluoxetine effects on inflammation depend on the quality of the living environment, we analyzed hippocampal expression levels of seven immune mediators reportedly involved in antidepressant drug action (Carvalho et al, 2013;Chen et al, 2010;Eller et al, 2008;Hannestad et al, 2011;Kim et al, 2013;Lanquillon et al, 2000;Song et al, 2009;Tuglu et al, 2003) and affected by environmental stimuli (Chabry et al, 2015;Goshen et al, 2008;Singhal et al, 2014;Wohleb et al, 2011). In particular, we focused on IL-6, TNFα and IL-1β, which are pro-inflammatory cytokines among the most studied in relation to antidepressant effects (Carvalho et al, 2013;Eller et al, 2008;Hannestad et al, 2011).…”

Section: Fluoxetine Affects Hippocampal Inflammatory Mediatorsmentioning

confidence: 99%

“…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.…”

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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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“…Therefore, based on the presented data, it may be concluded that one of the main mechanisms of these drugs is to downregulate IL-17A expression and to diminish the number of Th17 lymphocytes. In contrast, there are studies revealing that some antidepressant drugs lack these effects; for instance, Kim et al reported that serum levels of IL-17A and its related cytokine, IL-23, were not altered after antidepressant treatment (32). Furthermore, it has been established that ladasten is unable to change the expression of IL-17A in mice with experimental depression-like syndrome (33).…”

Section: Il-17a and Depressionmentioning

confidence: 99%

The Role of Interleukin-17A (IL-17A) in Depression

Fathalizadeh

Mirzabeigi

et al. 2016

Iran Red Crescent Med J

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Context: The aim of this review was to address the recent data regarding the role of IL-17A in the pathogenesis of depression and its complications, such as cancer. Evidence Acquisition: This review article summarizes the recent data on the role of IL-17A in depression, using the PubMed and Google Scholar databases. Results: It has been documented that depression may alter the immune response via unknown mechanism/s. It is possible that immune responses and depression are linked via several molecules, including cytokines. IL-17A, a pro-inflammatory cytokine, participates in the pathogenesis of several inflammatory-based diseases, such as autoimmunity. Conclusions: Due to the comorbidity of depression and chronic inflammatory processes, and depression's effect on the immune system, it may be hypothesized that the IL-17A cytokine plays a key role in the pathogenesis of depression.

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Plasma Levels of IL-23 and IL-17 before and after Antidepressant Treatment in Patients with Major Depressive Disorder

Cited by 63 publications

References 36 publications

The role of IL-17 in CNS diseases

The role of IL-17 in CNS diseases

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

The Role of Interleukin-17A (IL-17A) in Depression

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