A relative resistance of T cells to dexamethasone in bipolar disorder

Knijff, Esther M.; Breunis, M. Nadine; Geest, Marielle C. van; Kupka, Ralph; Ruwhof, Cindy; Wit, Harm J. de; Nolen, Willem A.; Drexhage, Hemmo A.

doi:10.1111/j.1399-5618.2006.00359.x

Cited by 46 publications

(23 citation statements)

References 86 publications

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“…31 Combined immunological and endocrinological investigations have also revealed the presence of Tcell steroid resistance as a potential trait marker in BD. 32 Similar findings in major depressive disorder, 33 and schizophrenia, 34,35 suggest that such HPA axis dysfunction may represent a trait marker across the broader affective and psychotic disorder spectrum.…”

Section: Hypothalamic-pituitary-adrenal Axissupporting

confidence: 53%

Neurobiological trait abnormalities in bipolar disorder

Langan

McDonald

2009

Mol Psychiatry

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Dissecting trait neurobiological abnormalities in bipolar disorder (BD) from those characterizing episodes of mood disturbance will help elucidate the aetiopathogenesis of the illness. This selective review highlights the immunological, neuroendocrinological, molecular biological and neuroimaging abnormalities characteristic of BD, with a focus on those likely to reflect trait abnormalities by virtue of their presence in euthymic patients or in unaffected relatives of patients at high genetic liability for illness. Trait neurobiological abnormalities of BD include heightened pro-inflammatory function and hypothalamic-pituitary-adrenal axis dysfunction. Dysfunction in the intracellular signal transduction pathway is indicated by elevated protein kinase A activity and altered intracellular calcium signalling. Consistent neuroimaging abnormalities include the presence of ventricular enlargement and white matter abnormalities in patients with BD, which may represent intermediate phenotypes of illness. In addition, spectroscopy studies indicate reduced prefrontal cerebral N-acetylaspartate and phosphomonoester concentrations. Functional neuroimaging studies of euthymic patients implicate inherently impaired neural networks subserving emotional regulation, including anterior limbic, ventral and dorsal prefrontal regions. Despite heterogeneous samples and conflicting findings pervading the literature, there is accumulating evidence for the existence of neurobiological trait abnormalities in BD at various scales of investigation. The aetiopathogenesis of BD will be better elucidated by future clinical research studies, which investigate larger and more homogenous samples and employ a longitudinal design to dissect neurobiological abnormalities that are underlying traits of the illness from those related to episodes of mood exacerbation or pharmacological treatment.

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Section: Hypothalamic-pituitary-adrenal Axissupporting

confidence: 53%

Neurobiological trait abnormalities in bipolar disorder

Langan

McDonald

2009

Mol Psychiatry

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“…Blood was collected in clotting tubes for serum preparation (stored at −80°C) and in sodium-heparin tubes for peripheral blood mononuclear cell (PBMC) preparation as described in detail elsewhere 20. CD14 positive monocytes were isolated from frozen PBMCs by magnetic cell sorting system (Miltenyi Biotec, Bergisch Gladbach, Germany) according to the manufacturer's recommendations.…”

Section: Methodsmentioning

confidence: 99%

The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis

Brkić

Bon

Cossu

et al. 2016

Annals of the Rheumatic Diseases

140

113

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“…Cytokines play a key role in the activation of the HPA-axis and peripheral glucocorticoid signaling. Recent reports provide support for T-cell-associated resistance to glucocorticoids and altered glucocorticoid-signaling cascades in BD (Knijff et al 2006;Spiliotaki et al 2006). Glucocorticoid release from the adrenal glands induces a pro-inflammatory response in microglia.…”

Section: Hypothalamic-pituitary Adrenal Axismentioning

confidence: 96%

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

et al. 2010

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The aim of this review is to evaluate the evidentiary base supporting the hypothesis that the increased hazard for obesity in mood disorder populations (and vice versa) is a consequence of shared pathophysiological pathways. We conducted a PubMed search of all English-language articles with the following search terms: obesity, inflammation, hypothalamic-pituitary-adrenal axis, insulin, cognition, CNS, and neurotransmitters, cross-referenced with major depressive disorder and bipolar disorder. The frequent co-occurrence of mood disorders and obesity may be characterized by interconnected pathophysiology. Both conditions are marked by structural and functional abnormalities in multiple cortical and subcortical brain regions that subserve cognitive and/or affective processing. Abnormalities in several interacting biological networks (e.g. immuno-inflammatory, insulin signaling, and counterregulatory hormones) contribute to the co-occurence of mood disorders and obesity. Unequivocal evidence now indicates that obesity and mood disorders are chronic low-grade pro-inflammatory states that result in a gradual accumulation of allostatic load. Abnormalities in key effector proteins of the pro-inflammatory cascade include, but are not limited to, cytokines/adipokines such as adiponectin, leptin, and resistin as well as tumor necrosis factor alpha and interleukin-6. Taken together, the bidirectional relationship between obesity and mood disorders may represent an exophenotypic manifestation of aberrant neural and inflammatory networks. The clinical implications of these observations are that, practitioners should screen individuals with obesity for the presence of clinically significant depressive symptoms (and vice versa). This clinical recommendation is amplified in individuals presenting with biochemical indicators of insulin resistance and other concurrent conditions associated with abnormal inflammatory signaling (e.g. cardiovascular disease).

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A relative resistance of T cells to dexamethasone in bipolar disorder

Abstract: A relative T-cell resistance to steroids, as has been observed in MD previously, may be a trait phenomenon of BD, independent of mood state.

Cited by 46 publications

References 86 publications

Neurobiological trait abnormalities in bipolar disorder

Neurobiological trait abnormalities in bipolar disorder

The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

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