Raised levels of plasma interleukin‐1β in major and postviral depression

Owen, Bruce M; Eccleston, D.; Ferrier, I. N.; Young, Andrew

doi:10.1034/j.1600-0447.2001.00162.x

Cited by 160 publications

(91 citation statements)

References 12 publications

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“…73,74 In addition, disorders which affect the immunological system such as autoimmune disorders or chronic viral infections such as HIV are often associated with depressive disorders. Several investigators [75][76][77][78] have found increased levels in IL-1b in patients with dysthymia or major depressive disorder. Similarly, TNF-a has been found to be increased in the plasma of patients with depressive mood 79 or with major depressive disorder 80 and even IL-6 has sometimes been found to be over expressed in elderly patients with major depressive disorder.…”

Section: Resultsmentioning

confidence: 99%

“…Administration of proinflammatory cytokines in animals induce a depression-like status 73,74 Depression has been reported to accompany diseases affecting the immune system (HIV, autoimmune illnesses) where cytokines are strongly dysregulated 71 Patients with depression have increased level of proinflammatory cytokines [75][76][77][78][79][80][81][82][83][84] Cytokine therapy may cause depression as side effect 72,[88][89][90][91][92] Antidepressive drugs may prevent depression induced by cytokine therapy in human 91,92 Antidepressive drugs may have a cytokine-linked anti-inflammatory effect 91,106,107 Inhibitors of proinflammatory cytokines may relieve depressive symptoms in humans 108 Anti-inflammatory drugs able to inhibit proinflammatory cytokine production may have antidepressive effect 109 mainly based on cytokine plasma level determinations and such circulating molecule concentrations do not necessarily reflect the activity of cytokines within the CNS. The activation of brain cytokines might involve different mechanisms and currently it is not possible to measure cytokines in specific areas of living human brain.…”

Section: Findings Referencesmentioning

confidence: 99%

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The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

et al. 2006

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Although poststroke depression is unlikely to represent a single disorder and numerous etiologies for different kinds of poststroke depression will likely emerge as the result of future research, we believe that a number of poststroke depressive disorders are likely to be the result of specific changes in brain pathology and neurophysiology. Nevertheless, there are relatively few hypotheses about the pathophysiology of poststroke depression. This paper, therefore, proposes a new hypothesis for poststroke depression involving increased production of proinflammatory cytokines resulting from brain ischemia in cerebral areas linked to the pathogenesis of mood disorders. This paper reviews the evidence supporting the hypothesis that proinflammatory cytokines are involved in the occurrence of stroke as well as mood disorders linked to the brain damage. The increased production of proinflammatory cytokines such as IL-1b, TNF-a or IL-18 resulting from stroke may lead to an amplification of the inflammatory process, particularly in limbic areas, and widespread activation of indoleamine 2,3-dioxygenase (IDO) and subsequently to depletion of serotonin in paralimbic regions such as the ventral lateral frontal cortex, polar temporal cortex and basal ganglia. The resultant physiological dysfunction may lead to poststroke depression. Future investigations may explore this hypothesis through more extensive studies on the role of proinflammatory cytokines, such as IL-1b, TNF-a or even IL-18, in patients with poststroke depression. Molecular Psychiatry (2006) 11, 984-991.

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Section: Resultsmentioning

confidence: 99%

Section: Findings Referencesmentioning

confidence: 99%

The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

et al. 2006

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“…88 According to the sickness behavior hypothesis, the cytokines TNF-a, IL-1 and IL-6 have frequently been investigated in MD. A considerable number of studies showed elevated serum levels of TNF-a 70,86,[89][90][91][92][93] and IL-1b [94][95][96] in depressed patients, whereas only few investigators reported unchanged levels of these cytokines. 97 A study on elevated mRNA levels of TNF-a in peripheral mononuclear cells of depressed patients confirms the majority of findings on elevated serum levels.…”

Section: The Inflammatory Hypothesis Of Depressionmentioning

confidence: 99%

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

2007

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Beside the well-known deficiency in serotonergic neurotransmission as pathophysiological correlate of major depression (MD), recent evidence points to a pivotal role of increased glutamate receptor activation as well. However, cause and interaction of these neurotransmitter alterations are not understood. In this review, we present a hypothesis integrating current concepts of neurotransmission and hypothalamus-pituitary-adrenal (HPA) axis dysregulation with findings on immunological alterations and alterations in brain morphology in MD. An immune activation including increased production of proinflammatory cytokines has repeatedly been described in MD. Proinflammatory cytokines such as interleukin-2, interferon-c, or tumor necrosis factor-a activate the tryptophan-and serotonin-degrading enzyme indoleamine 2,3-dioxygenase (IDO). Depressive states during inflammatory somatic disorders are also associated with increased proinflammatory cytokines and increased consumption of tryptophan via activation of IDO. An enhanced consumption of serotonin and its precursor tryptophan through IDO activation could well explain the reduced availability of serotonergic neurotransmission in MD. An increased activation of IDO and its subsequent enzyme kynurenine monooxygenase by proinflammatory cytokines, moreover, leads to an enhanced production of quinolinic acid, a strong agonist of the glutamatergic N-methyl-D-aspartate receptor. In inflammatory states of the central nervous system, IDO is mainly activated in microglial cells, which preferentially metabolize tryptophan to the NMDA receptor agonist quinolinic acid, whereas astrocytes -counteracting this metabolism due to the lack of an enzyme of this metabolism -have been observed to be reduced in MD. Therefore the type 1/type 2 immune response imbalance, associated with an astrocyte/microglia imbalance, leads to serotonergic deficiency and glutamatergic overproduction. Astrocytes are further strongly involved in re-uptake and metabolic conversion of glutamate. The reduced number of astrocytes could contribute to both, a diminished counterregulation of IDO activity in microglia and an altered glutamatergic neurotransmission. Further search for antidepressant agents should take into account anti-inflammatory drugs, for example, cyclooxygenase-2 inhibitors, might exert antidepressant effects by acting on serotonergic deficiency, glutamatergic hyperfunction and antagonizing neurotoxic effects of quinolinic acid. Molecular Psychiatry (2007) 12, 988-1000; doi:10.1038/sj.mp.4002006; published online 24 April 2007 Keywords: major depression; psychoneuroimmunology; IDO; glutamate; immune system; serotonin Glutamate in depressionGlutamatergic neurotransmission is involved in depression and interacts with the serotonergic and noradrenergic systems The common therapeutic mechanism of antidepressant drugs is the enhancement of serotonergic and/or noradrenergic neurotransmission. On the basis of this pharmacological profile of antidepressant drugs, neurochemical research on major depression ...

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“…Some of the results showed an increase in the blood or cerebrospinal levels of this cytokine in depressed patients (Levine et al, 1999;Anisman et al, 1999;Owen et al, 2001). Furthermore, cerebrospinal IL-1beta levels were correlated with the severity of depression (Levine et al, 1999), age of onset (Anisman et al, 1999), and duration of illness (Anisman et al, 1999).…”

Section: Introductionmentioning

confidence: 97%

Association Study of the Interleukin-1beta (C-511T) Genetic Polymorphism with Major Depressive Disorder, Associated Symptomatology, and Antidepressant Response

Yu¹,

Chen

Hong

et al. 2003

Neuropsychopharmacol

135

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Proinflammatory cytokines, including interleukin (IL)-1beta, are suggested to have a role in the pathogenesis of major depressive disorder (MDD) and be related to the therapeutic effects of antidepressants. To elucidate a genetic predisposition of MDD, we studied biallelic polymorphism in the promoter region (position -511) of the IL-1beta gene in 157 patients with MDD and in 112 controls. We also examined the association of this polymorphism and fluoxetine therapeutic response in 119 MDD patients who received a 4-week fluoxetine treatment. No significant difference was found in the genetic polymorphism between MDD patients and controls. However, MDD patients who were homozygous for the -511T allele of the IL-1beta gene had a trend of less severity of depressive symptoms and more favorable fluoxetine therapeutic response than -511C carriers. Further study with a larger sample is needed to clarify the role of the IL-1beta genetic polymorphisms in the symptoms and treatment effects in MDD.

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Raised levels of plasma interleukin‐1β in major and postviral depression

Cited by 160 publications

References 12 publications

The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

Association Study of the Interleukin-1beta (C-511T) Genetic Polymorphism with Major Depressive Disorder, Associated Symptomatology, and Antidepressant Response

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