Evidence for a systemic immune activation during depression: results of leukocyte enumeration by flow cytometry in conjunction with monoclonal antibody staining

Maes, Michaël; Lambrechts, Jos; Bosmans, Eugène; Jacobs, Joannes F M; Suy, E.; Vandervorst, C.; Jonckheere, C. De; Minner, B.; Raus, Jef

doi:10.1017/s0033291700032712

Cited by 258 publications

(127 citation statements)

References 54 publications

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“…Further to the findings on sickness behavior (Hart, 1988), initial evidence for the role of inflammation in depression came from the observation that experimental administration of pro-inflammatory cytokines produced a clinical response resembling major depression (the 'macrophage theory' of depression; Smith, 1991) and that depressed patients showed systemic immune activation (Maes et al, 1992). Metaanalyses of clinical and population studies showed that depressed individuals have a small elevation in levels of several inflammation biomarkers (Howren et al, 2009).…”

Section: Observational Studies In Humansmentioning

confidence: 99%

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Danese

Lewis

2016

Neuropsychopharmacol

293

191

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The brain and the immune system are not fully formed at birth, but rather continue to mature in response to the postnatal environment. The two-way interaction between the brain and the immune system makes it possible for childhood psychosocial stressors to affect immune system development, which in turn can affect brain development and its long-term functioning. Drawing from experimental animal models and observational human studies, we propose that the psychoneuroimmunology of early-life stress can offer an innovative framework to understand and treat psychopathology linked to childhood trauma. Earlylife stress predicts later inflammation, and there are striking analogies between the neurobiological correlates of early-life stress and of inflammation. Furthermore, there are overlapping trans-diagnostic patterns of association of childhood trauma and inflammation with clinical outcomes. These findings suggest new strategies to remediate the effect of childhood trauma before the onset of clinical symptoms, such as anti-inflammatory interventions and potentiation of adaptive immunity. Similar strategies might be used to ameliorate the unfavorable treatment response described in psychiatric patients with a history of childhood trauma.

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Section: Observational Studies In Humansmentioning

confidence: 99%

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Danese

Lewis

2016

Neuropsychopharmacol

293

191

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“…Some cases of idiopathic depression with no co-morbid conditions showed an increase in the circulating pro-inflammatory biomarkers [8] [29] [30] [31]. Many studies done on idiopathic major depression showed that circulating biomarkers such as TNF-α, IL-6, their soluble receptors, and CRP have risen in this group of patients [29] [30] [31].…”

Section: Inflammatory State and Depressionmentioning

confidence: 99%

“…Many studies done on idiopathic major depression showed that circulating biomarkers such as TNF-α, IL-6, their soluble receptors, and CRP have risen in this group of patients [29] [30] [31]. Furthermore, CSF examination in depressed patients showed an increase in the level of some cytokines [32] [33] [34].…”

Section: Inflammatory State and Depressionmentioning

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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“…Furthermore, it appears that depression may be associated with variations of either circulating cytokine levels (ie, cell signalling factors released from activated macrophages), or cytokine production from mitogenstimulated lymphocytes, including interleukin-2 (IL-2), soluble IL-2 receptors (sIL-2R), IL-1␤, IL-1 receptor antagonist (IL-1Ra), IL-6, soluble IL-6 receptor (sIL-6R), and ␥-interferon (IFN). [209][210][211][212][213][214][215][216] While there have been reports that the elevated levels of IL-1␤, IL-6 and ␣1-acid glycoprotein normalized with antidepressant medication, 217 the unregulated production of sIL-2R, IL-6 and sIL-6R was not attenuated with antidepressant agents, leading to the suggestion that the latter factors may be trait markers of the illness. 208 Although severity of depressive illness is likely fundamental in determining cytokine levels, 208 the possibility cannot be ignored that chronic depression (or chronic stress) may induce cytokine changes to a greater extent than those observed following acute episodes (as in the case of major depression).…”

Section: Cytokines and Depressive Illnessmentioning

confidence: 99%

Dysthymia: a review of pharmacological and behavioral factors

et al. 2000

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Although dysthymia, a chronic, low-grade form of depression, has a morbidity rate as high as that of major depression, and increases the risk for major depressive disorder, limited information is available concerning the etiology of this illness. In the present report we review literature concerning the biological and characterological features of dysthymia, the effectiveness of antidepressant treatments, the influence of stressors in the precipitation and maintenance of the disorder, and both quality of life and psychosocial correlates of the illness. We also provisionally suggest that dysthymia may stem from disturbances of neuroendocrine and neurotransmitter functioning (eg, corticotropin releasing hormone and arginine vasopressin within the hypothalamus, or alternatively monoamine variations within several extrahypothalamic sites), and may also involve cytokine activation. The central disturbances may reflect phenotypic variations of neuroendocrine processes or sensitization of such mechanisms. It is suggested that chronic stressor experiences or stressors encountered early in life lead to the phenotypic neurochemical alterations, which then favor the development of the dysthymic state. Owing to the persistence of the neurochemical disturbances, vulnerability to double depression is increased, and in this instance treatment with antidepressants may attenuate the symptoms of major depression but not those of the basal dysthymic state. Moreover, the residual features of depression following treatment may be indicative of underlying neurochemical disturbances, and may also serve to increase the probability of illness recurrence or relapse. Molecular Psychiatry (2000) 5, 242-261.

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Evidence for a systemic immune activation during depression: results of leukocyte enumeration by flow cytometry in conjunction with monoclonal antibody staining

Cited by 258 publications

References 54 publications

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

The Role of Immune System in Depression Disorder

Dysthymia: a review of pharmacological and behavioral factors

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