Serotonin Transporter mRNA Expression is Decreased by Lamivudine and Ribavirin and Increased by Interferon in Immune Cells

Tsao, Chiung–Wen; Lin, Yee‐Shin; Chang, Wen‐Wei; Chen, C. L.; Wu, S. R.; Fan, Chie Wei; Lo, Hanna

doi:10.1111/j.1365-3083.2005.01715.x

Cited by 14 publications

(12 citation statements)

References 60 publications

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“…These data are consistent with the hypothesis that IFN-induced psychiatric effects may be modulated by regulation of 5-HTT transcription. Treatment with IFN-α in humans increased 5-HTT expression, protein level and serotonin uptake, suggesting that increases in 5-HTT in circulating blood lymphocytes after IFN-α therapy may decrease levels of circulating serotonin, thereby causing depressive symptoms (44). …”

Section: Discussionmentioning

confidence: 99%

A Functional Serotonin Transporter Gene Polymorphism and Depressive Effects Associated With Interferon- Treatment

et al. 2010

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Interferon-alpha (IFN-α) treatment frequently induces depression, potentially leading to early dose reductions or a shorter duration of treatment, which can adversely affect outcomes, including the quality of life. Defining relevant risk factors for IFN-α induced depression is essential in order to identify prophylactic treatment strategies. We examined whether a functional polymorphism (5-HTTLPR) in the gene encoding the serotonin transporter moderates IFN-α-induced depressive symptoms in 1,015 patients with chronic hepatitis C (CHC) receiving pegylated IFN-α and ribavirin. Depressive symptoms were assessed at 0, 12, and 20 weeks of treatment. Depressive symptoms increased during antiviral treatment. 5-HTTLPR genotype moderated IFN-α-induced depressive symptoms in both Non-Hispanic Caucasians (NHCs; p = 0.009) and Hispanics (p = 0.036), though the opposite risk allele was associated with depression in the two populations. 5-HTTLPR may moderate risk for the development of depressive symptoms during IFN-α-therapy for CHC in a population-specific manner.

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Section: Discussionmentioning

confidence: 99%

A Functional Serotonin Transporter Gene Polymorphism and Depressive Effects Associated With Interferon- Treatment

et al. 2010

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“…Administration of the synthetic double-stranded RNA Poly I:C to rats increased expression of IFNα and SERT in the brain at the same time as it induced fatigue, as measured by decreased voluntary running wheel activity (Katafuchi et al 2006). Increased expression of SERT in response to IFNα was also observed in immune cells and in a T cell line (Tsao et al 2006). In the Jurkat T cell line, this effect was mediated by activation of mitogen-activated protein kinases (p38, ERK and JNK) (Tsao et al 2008).…”

Section: Cytokines and Depression - Animal Studiesmentioning

confidence: 91%

Inflammation-associated depression: From serotonin to kynurenine

Dantzer

O’Connor

Lawson

et al. 2011

Psychoneuroendocrinology

645

481

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In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasiexperimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptotphan degrading enzyme indoleamine 2,3 dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms.

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“…Serotonin is produced outside of the central nervous system, primarily in the gut, and is taken up by various cell types, including immune cells, which also contain serotonin receptors and transporters (Mossner and Lesch, 1998). Furthermore, there is increasing evidence for interaction between serotonin and cytokines in PBMCs (e.g., Tsao, et al, 2006). Together, these data present the intriguing possibility that pharmacologic manipulation of serotonin function may not only have an indirect effect on disease by reducing anxiety or facilitating more adaptive coping with stressors, but may also have a direct effect through modulation of immune function.…”

Section: Physiological Mechanisms Associated With Adverse Immune Outcmentioning

confidence: 99%

Personality and serotonin transporter genotype interact with social context to affect immunity and viral set-point in simian immunodeficiency virus disease

Capitanio

Abel

Mendoza

et al. 2008

Brain, Behavior, and Immunity

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From the beginning of the AIDS epidemic, stress has been a suspected contributor to the wide variation seen in disease progression, and some evidence supports this idea. Not all individuals respond to a stressor in the same way, however, and little is known about the biological mechanisms by which variations in individuals' responses to their environment affect disease-relevant immunologic processes. Using the simian immunodeficiency virus/rhesus macaque model of AIDS, we explored how personality (sociability) and genotype (serotonin transporter promoter) independently interact with social context (stable or unstable social conditions) to influence behavioral expression, plasma cortisol concentrations, SIV-specific IgG, and expression of genes associated with Type I interferon early in infection. SIV viral RNA set-point was strongly and negatively correlated with survival as expected. Set-point was also associated with expression of interferon-stimulated genes, with CXCR3 expression, and with SIV-specific IgG titers. Poorer immune responses, in turn, were associated with display of sustained aggression and submission. Personality and genotype acted independently as well as in interaction with social condition to affect behavioral responses. Together, the data support an "interactionist" perspective (Eysenck, 1991) on disease. Given that an important goal of HIV treatment is to maintain viral set-point as low as possible, our data suggest that supplementing anti-retroviral therapy with behavioral or pharmacologic modulation of other aspects of an organism's functioning might prolong survival, particularly among individuals living under conditions of threat or uncertainty.

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Serotonin Transporter mRNA Expression is Decreased by Lamivudine and Ribavirin and Increased by Interferon in Immune Cells

Cited by 14 publications

References 60 publications

A Functional Serotonin Transporter Gene Polymorphism and Depressive Effects Associated With Interferon- Treatment

A Functional Serotonin Transporter Gene Polymorphism and Depressive Effects Associated With Interferon- Treatment

Inflammation-associated depression: From serotonin to kynurenine

Personality and serotonin transporter genotype interact with social context to affect immunity and viral set-point in simian immunodeficiency virus disease

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