Differential neuroendocrine and immune responses to acute psychosocial stress in women with type 1 bipolar disorder

Wieck, Andréa; Grassi‐Oliveira, Rodrigo; Prado, Carine Hartmann do; Rizzo, Lucas B.; Oliveira, Agatha Schommer de; Kommers-Molina, Júlia; Viola, Thiago Wendt; Teixeira, Antônio Lúcio; Bauer, Moisés Evandro

doi:10.1016/j.bbi.2013.07.005

Cited by 53 publications

(41 citation statements)

References 52 publications

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“…NF-κB is activated by acute stress (Bierhaus et al, 2003), as well as sleep loss (Irwin et al, 2008) and may have a role in mediating cellular responses to stressful life events, the latter of which have been strongly implicated in the relapse/remission course of MDD and BD (Slavich and Irwin, 2014; Johnson et al, 2008). The consequences of increased NF-κB inflammatory signaling may include increased expression of proinflammatory cytokines and attenuated neuroendocrine responses to stress (Wieck et al, 2013). NF-κB hyperactivation in BD may also be protective against cell loss, helping to compensate for the neurotoxic effects of repeated illness episodes (Barbosa et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…These studies have focused almost exclusively on circulating levels of proinflammatory cytokines (e.g., IL-6) in adults with established MDD or BD. Fewer studies have examined upstream inflammatory signaling mechanisms such as nuclear factor kappa B (NF-κB), despite evidence that activation of these transcription factors plays a key role in the regulation of the inflammatory cascade and in responses to psychological stress (Keri et al, 2014; Pace et al, 2006; Slavich and Irwin, 2014; Wieck et al, 2013). Compared to healthy volunteers, higher levels of NF-κB activity have been found in adults with BD during depressed (Spiliotaki et al, 2006) and euthymic states (e.g., Amoruso et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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Inflammatory cytokines and nuclear factor-kappa B activation in adolescents with bipolar and major depressive disorders

Miklowitz

Portnoff

Armstrong

et al. 2016

Psychiatry Research

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Adults with bipolar disorder (BD) and major depressive disorder (MDD) have higher circulating levels of proinflammatory cytokines than healthy controls. However, it is not known whether pediatric-onset patients with BD or MDD show increases in levels of inflammation or activation of nuclear factor kappa B (NF-κB), a key transcription factor in inflammatory signaling. Circulating levels of inflammatory cytokines, as well as spontaneous and stimulated levels of activated NF-κB in total peripheral blood mononuclear cells, monocytes and lymphocytes were measured in adolescents with BD (n=18), MDD (n=13), or no psychiatric history (n=20). Participants had a range of mood symptoms at time of testing. Adolescents with BD had significantly higher spontaneous levels of NF-κB in peripheral blood mononuclear cells, monocyte and lymphocyte populations, and higher plasma levels of IL-1β than healthy controls. Following stimulation with recombinant human TNF-α, participants with BD and MDD both had greater increases in NF-κB in monocytes than controls. Further, greater stimulated increases of NF-κB in monocytes were associated with the current severity of depressive symptoms. The results are limited by the small sample and cross-sectional design. Interventions that target early immunological dysregulation should be examined in relation to long-term outcomes in youth with bipolar and depressive disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inflammatory cytokines and nuclear factor-kappa B activation in adolescents with bipolar and major depressive disorders

Miklowitz

Portnoff

Armstrong

et al. 2016

Psychiatry Research

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“…Similar to aging, BD has been associated with an important immune imbalance toward low‐grade inflammation . While the underlying mechanisms involved with the low‐grade inflammatory status are largely unknown, expansion of peripheral‐activated T cells, low T reg cell numbers, and activation of intracellular signaling cascades (i.e., MAPKs, NF‐κB) have been reported in BD patients . The occurrence of low‐grade inflammation in BD might be considered a form of premature inflammaging, as it has been associated with comorbidities normally found in older adults, such as cardiovascular disease, functional impairment, and poor cognition …”

Section: Bd: a Possible Model Of Accelerated Agingmentioning

confidence: 99%

Neuroendocrine and viral correlates of premature immunosenescence

Bauer

Wieck

Petersen

et al. 2015

Annals of the New York Academy of Sciences

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Aging continuously remodels the immune system, a process known as immunosenescence. Here, we review evidence of premature immunosenescence in younger individuals under conditions of chronic psychological stress, chronic inflammation, or exposure to certain persistent viral infections. Chronic stress may accelerate various features of immunosenescence by activating key allostatic systems, notably the hypothalamic-pituitary-adrenal axis and increased cortisol levels. Chronic stress is associated with thymic involution, blunted T cell proliferation, increased serum proinflammatory markers, and shorter telomere lengths. Human cytomegalovirus (CMV) infection has been implicated in accelerating immunosenescence by shrinking the T cell receptor repertoire and causing clonal expansion of senescent CD8(+) CD28(-) T cells with a proinflammatory profile. These factors increase inflammation associated with aging, or "inflammaging," particularly as it relates to etiology of several age-related diseases and increased mortality. Patients with rheumatoid arthritis have been shown to have several signatures of premature immunosenescence, including expansion of senescent T cells associated with cognitive impairment. We end by speculating that bipolar disorder can be considered as a model of accelerated aging because it has been associated with shortened telomeres, higher CMV IgG titers, and expansion of senescent and regulatory T cells.

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Section: Stress: a Missing Link Between Illness And Inflammation In Bd?mentioning

confidence: 99%

“…For instance, euthymic BD patients exhibit blunted stress response as shown by reduced heart rate and salivary cortisol levels when exposed to acute stress [40]. In parallel to this altered neuroendocrine response, these patients present reduced lymphocyte sensitivity to glucocorticoids [40]. This HPA axis dysfunction in BD patients may indicate a defective neuroendocrine control over the immune system explaining, at least partially, why BD patients present increased circulating levels of pro-inflammatory cytokines.…”

Section: Stress: a Missing Link Between Illness And Inflammation In Bd?mentioning

confidence: 99%

The Immunology of Bipolar Disorder

Barbosa

Machado‐Vieira

Soares

et al. 2014

Neuroimmunomodulation

125

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Bipolar disorder (BD) is a psychiatric condition associated with elevated frequency of clinical comorbidities and cognitive impairment. The neurobiology of BD is not completely understood. Recent evidence has implicated immune dysfunction in its physiopathology. Here, we review several data supporting the presence of immunological dysfunction in BD: (i) increased frequency of autoimmune diseases; (ii) distinct immune cell profile; (iii) release of/altered cytokines by stimulated mononuclear cells; (iv) elevated levels of circulating immune markers, and (v) inflammatory changes in the central nervous system. We also discuss the interplay between immunological dysfunction and neuroprogression in BD.

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Differential neuroendocrine and immune responses to acute psychosocial stress in women with type 1 bipolar disorder

Cited by 53 publications

References 52 publications

Inflammatory cytokines and nuclear factor-kappa B activation in adolescents with bipolar and major depressive disorders

Inflammatory cytokines and nuclear factor-kappa B activation in adolescents with bipolar and major depressive disorders

Neuroendocrine and viral correlates of premature immunosenescence

The Immunology of Bipolar Disorder

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