Interferon-α-induced serotonin uptake in Jurkat T cells via mitogen-activated protein kinase and transcriptional regulation of the serotonin transporter

Tsao, Chiung–Wen; Lin, Yee‐Shin; Cheng, Juei‐Tang; Lin, Chiou–Feng; Wu, Hung–Tsung; Wu, S. R.; Tsai, Wan–Hua

doi:10.1177/0269881107082951

Cited by 41 publications

(40 citation statements)

References 60 publications

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“…Previous studies have found a significant association between other inflammatory markers (that we did not explore), including IFN α, γ and 5-HTT in animal models (Katafuchi et al, 2006;Morikawa et al, 1998;Tsao et al, 2008).…”

Section: I]mentioning

confidence: 57%

“…This potential link is supported by findings from preclinical studies in rodent models that directly link proinflammatory cytokines with brain 5-HTT availability through activation of MAPK pathways (Baganz and Blakely, 2013;Couch et al, 2013;Katafuchi et al, 2006;Malynn et al, 2013;Morikawa et al, 1998;Ramamoorthy et al, 1995;Samuvel, 2005;Tsao et al, 2008).…”

Section: Introductionmentioning

confidence: 84%

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Circulating tumour necrosis factor is highly correlated with brainstem serotonin transporter availability in humans

Krishnadas

Nicol

Sassarini

et al. 2016

Brain, Behavior, and Immunity

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Circulating Tumour Necrosis Factor is highly correlated with brainstem serotonin transporter availability in humans, Brain, Behavior, and Immunity (2015), doi: http://dx.doi.org/ 10. 1016/j.bbi.2015.08.005 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: I]mentioning

confidence: 57%

Section: Introductionmentioning

confidence: 84%

Circulating tumour necrosis factor is highly correlated with brainstem serotonin transporter availability in humans

Krishnadas

Nicol

Sassarini

et al. 2016

Brain, Behavior, and Immunity

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“…Third, BDNF and inflammatory cytokines both influence serotonin transporter transcription and function (Mossner et al, 2000;Mossner et al, 1998;Zhu et al, 2006;Zhu et al, 2010). IFN-a increases serotonin transporter transcription via the MAP kinase intracellular signaling pathway (Tsao et al, 2008), and both BDNF and inflammatory cytokines share overlapping intracellular signal transduction pathways including MAP kinases (Duman et al, 2007;Zhu et al, 2010) and NF-kappaB (Kairisalo et al, 2009). Fourth, the BDNF Met allele has been associated with an elevated cortical response to a dexamethasone/corticosterone releasing hormone challenge (Schule et al, 2006), which is notable given that there is a greater cortical response to the initial injection of IFN-a in those at increased risk for subsequent depression (Raison et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

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Depression has been associated with inflammation, and inflammation may both influence and interact with growth factors such as brainderived neurotrophic factor (BDNF). Both the functional Val66Met BDNF polymorphism (rs6265) and BDNF levels have been associated with depression. It is thus plausible that decreased BDNF could mediate and/or moderate cytokine-induced depression. We therefore prospectively employed the Beck Depression Inventory-II (BDI-II), the Hospital Anxiety and Depression Scale (HADS), and the Montgomery-Asberg Depression Rating Scale (MADRS) in 124 initially euthymic patients during treatment with interferon-alpha (IFN-a), assessing serum BDNF and rs6265. Using mixed-effect repeated measures, lower pretreatment BDNF was associated with higher depression symptoms during IFN-a treatment (F 144,17.2 ¼ 6.8; Po0.0001). However, although the Met allele was associated with lower BDNF levels (F 1,83.0 ¼ 5.0; P ¼ 0.03), it was only associated with increased MADRS scores (F 4,8.9 ¼ 20.3; Po0.001), and not the BDI-II or HADS. An exploratory comparison of individual BDI-II items indicated that the Met allele was associated with suicidal ideation, sadness, and worthlessness, but not neurovegetative symptoms. Conversely, the serotonin transporter promoter polymorphism (5-HTTLPR) short allele was associated with neurovegetative symptoms such as insomnia, poor appetite and fatigue, but not sadness, worthlessness, or suicidal ideation. IFN-a therapy further lowered BDNF serum levels (F 4,37.7 ¼ 5.0; P ¼ 0.003), but this decrease occurred regardless of depression development. The findings thus do not support the hypothesis that decreasing BDNF is the primary pathway by which IFN-a worsens depression. Nonetheless, the results support the hypothesis that BDNF levels influence resiliency against developing inflammatory cytokine-associated depression, and specifically to a subset of symptoms distinct from those influenced by 5-HTTLPR. Neuropsychopharmacology (2013) 38, 985-995;

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“…Besides, there is a positive association between the functional effects of 5-HT and the increase in the level of IL-6. Furthermore, evidence shows that expression and function of 5-HTT is elevated as a response to IL-6 cytokine [91] [92] [93] [94].…”

Section: Serotonin (5-ht)mentioning

confidence: 99%

The Role of Immune System in Depression Disorder

Hoseinzadeh¹,

Abadi²,

Agheltar³

et al. 2016

Health

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In order to diagnose a major depressive disorder, patients must have at least 5 depressive symptoms out of 9 criteria, present for at least two weeks. Depressive symptoms include absence of concentration, fatigue and suicidal ideation. The intensity of depression symptoms affects the severity of depression and the degree of the impact on the quality of life. Major depressive disorders (MDD) are defined as a significant health problem, and are estimated to rise in prevalence in the future years. Immune cytokine, associated with major depression for instance, is the interleukin IL-6 and tumor necrosis factor (TNF-α) which is defined as pro-inflammatory cytokines, can activate an inflammatory response. The effects of other inflammatory cytokines on the central nervous system are of controversy. There is an increasing interest about the effect of cytokines derived from innate immune system on the brain and behavior. Cytokines are defined as large sized proteins, mainly produced by immune cells. Two subtypes of cytokines exist: pro-inflammatory cytokines, facilitating inflammatory responses and neural activities; and anti-inflammatory cytokines, inhibiting inflammatory processes. Besides microglia and astrocytes, immune cells such as monocytes, macrophages, and lymphocytes also produce cytokines. At the times of immunological alterations, infections or inflammation, cytokines will be in an activated form. The main goal of the current review study is to investigate the role of the immune system in the depression disorder.

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Interferon-α-induced serotonin uptake in Jurkat T cells via mitogen-activated protein kinase and transcriptional regulation of the serotonin transporter

Cited by 41 publications

References 60 publications

Circulating tumour necrosis factor is highly correlated with brainstem serotonin transporter availability in humans

Circulating tumour necrosis factor is highly correlated with brainstem serotonin transporter availability in humans

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

The Role of Immune System in Depression Disorder

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