Cytokines in bipolar disorder vs. healthy control subjects: A systematic review and meta-analysis

Munkholm, Klaus; Braüner, Julie Vestergaard; Kessing, Lars Vedel; Vinberg, Maj

doi:10.1016/j.jpsychires.2013.05.018

Cited by 365 publications

(251 citation statements)

References 144 publications

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“…Interestingly, we also found that levels of sEH in the parietal cortex from patients with major psychiatric disorders (depression, bipolar disorder, and schizophrenia) were higher than controls. Inflammation is also implicated in these psychiatric disorders (6)(7)(8)(9)(10)(47)(48)(49)(50). Recent studies showed that peripheral IL-6 is critical in regulating stress-related depression-like phenotypes in rodents (51)(52)(53).…”

Section: Discussionmentioning

confidence: 99%

Gene deficiency and pharmacological inhibition of soluble epoxide hydrolase confers resilience to repeated social defeat stress

Ren

Ishima

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

134

156

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Depression is a severe and chronic psychiatric disease, affecting 350 million subjects worldwide. Although multiple antidepressants have been used in the treatment of depressive symptoms, their beneficial effects are limited. The soluble epoxide hydrolase (sEH) plays a key role in the inflammation that is involved in depression. Thus, we examined here the role of sEH in depression. In both inflammation and social defeat stress models of depression, a potent sEH inhibitor, TPPU, displayed rapid antidepressant effects. Expression of sEH protein in the brain from chronically stressed (susceptible) mice was higher than of control mice. Furthermore, expression of sEH protein in postmortem brain samples of patients with psychiatric diseases, including depression, bipolar disorder, and schizophrenia, was higher than controls. This finding suggests that increased sEH levels might be involved in the pathogenesis of certain psychiatric diseases. In support of this hypothesis, pretreatment with TPPU prevented the onset of depression-like behaviors after inflammation or repeated social defeat stress. Moreover, sEH KO mice did not show depressionlike behavior after repeated social defeat stress, suggesting stress resilience. The sEH KO mice showed increased brain-derived neurotrophic factor (BDNF) and phosphorylation of its receptor TrkB in the prefrontal cortex, hippocampus, but not nucleus accumbens, suggesting that increased BDNF-TrkB signaling in the prefrontal cortex and hippocampus confer stress resilience. All of these findings suggest that sEH plays a key role in the pathophysiology of depression, and that epoxy fatty acids, their mimics, as well as sEH inhibitors could be potential therapeutic or prophylactic drugs for depression.brain-derived neurotrophic factor | depression | epoxyeicosatrienoic acid | soluble epoxide hydrolase | resilience

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Section: Discussionmentioning

confidence: 99%

Gene deficiency and pharmacological inhibition of soluble epoxide hydrolase confers resilience to repeated social defeat stress

Ren

Ishima

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

134

156

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“…In contrast to acute neuroinflammatory conditions in MDD, however, astroglia and microglia do not proliferate (Najjar et al, 2013), consistent with a continuous, low grade inflammation. As for BPD, peripheral IL-2, IL-4 and IL-6 are found to be increased in manic episodes (Brietzke et al, 2011) whereas another meta-analysis revealed significant elevation of soluble interleukin (IL)-2 receptor (sIL-2R), TNF-a, soluble tumor necrosis factor receptor type 1 (sTNFR1) and soluble interleukin (IL)-6 receptor (sIL-6R) (Munkholm et al, 2013). In the case of schizophrenia, TNF-a, IFN-g, IL-12 and IL-2 are consistently elevated in chronic schizophrenic patients, while IL-1b, IL-6 and TGF-b correlate positively with disease activity (Miller et al, 2011).…”

Section: Purinergic Regulation Of Neuroinflammation In Cns Disordersmentioning

confidence: 99%

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

et al. 2016

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a b s t r a c tThe principle functions of neuroinflammation are to limit tissue damage and promote tissue repair in response to pathogens or injury. While neuroinflammation has utility, pathophysiological inflammatory responses, to some extent, underlie almost all neuropathology. Understanding the mechanisms that control the three stages of inflammation (initiation, propagation and resolution) is therefore of critical importance for developing treatments for diseases of the central nervous system. The purinergic signaling system, involving adenosine, ATP and other purines, plus a host of P1 and P2 receptor subtypes, controls inflammatory responses in complex ways. Activation of the inflammasome, leading to release of pro-inflammatory cytokines, activation and migration of microglia and altered astroglial function are key regulators of the neuroinflammatory response. Here, we review the role of P1 and P2 receptors in mediating these processes and examine their contribution to disorders of the nervous system. Firstly, we give an overview of the concept of neuroinflammation. We then discuss the contribution of P2X, P2Y and P1 receptors to the underlying processes, including a discussion of cross-talk between these different pathways. Finally, we give an overview of the current understanding of purinergic contributions to neuroinflammation in the context of specific disorders of the central nervous system, with special emphasis on neuropsychiatric disorders, characterized by chronic low grade inflammation or maternal inflammation. An understanding of the important purinergic contribution to neuroinflammation underlying neuropathology is likely to be a necessary step towards the development of effective interventions.

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“…In a study by Cunha et al [12], it was reported that serum high-sensitive C-reactive protein (hsCRP) was increased in manic patients compared to euthymic and healthy controls. A meta-analysis showed that elevated levels of serum TNF-α receptor 1, TNF-α, and serum soluble IL-2 receptor were associated with manic episodes; TNF-α levels were also elevated among depressed patients, suggesting that TNF-α may be a potential marker of the disease [8]. In addition, Pandey et al [39] suggested that the mRNA levels of membrane-bound receptors for proinflammatory cytokines could be a potential biomarker of BD.…”

Section: Discussionmentioning

confidence: 99%

“…The biological mechanisms of BD still remain unclear, but it can be effectively conceptualized as a multi-systemic inflammatory disease [3]. To date, changes in peripheral inflammatory markers have been reported in BD such as cytokine profiles [4][5][6][7][8][9][10][11], acute phase proteins [12][13][14], and lymphocyte cell activation [5,[15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil/lymphocyte and platelet/lymphocyte ratios in all mood states of bipolar disorder

Ayhan¹,

Çiçek²,

İnanlı³

et al. 2017

Psychiatry and Clinical Psychopharmacology

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Objectives: This study aims at researching the inflammatory cells and their ratios as inflammation markers in different phases of patients with bipolar disorder (BD). Methods: In this retrospective study, 79 manic, 61 depressed, 59 euthymic drug-naive patients with BD, and 86 control subjects have been evaluated for their complete blood count. Results: Neutrophil/lymphocyte ratio (NLR) was found to be significantly higher in manic, euthymic, and depressed patients with BD compared to control group. However, no difference was found between all patient and control groups regarding platelet/lymphocyte ratio (PLR). There was no difference among different phases of patient groups in terms of NLR and PLR. Conclusions: Our findings suggest that inflammatory process may have a role in all mood episodes of BD and NLR may be a useful trait inflammation marker for BD independent of mood episodes. However, further studies need to be conducted on the effect of inflammatory mechanisms on mood states of BD. ARTICLE HISTORY

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Cytokines in bipolar disorder vs. healthy control subjects: A systematic review and meta-analysis

Cited by 365 publications

References 144 publications

Gene deficiency and pharmacological inhibition of soluble epoxide hydrolase confers resilience to repeated social defeat stress

Gene deficiency and pharmacological inhibition of soluble epoxide hydrolase confers resilience to repeated social defeat stress

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

Neutrophil/lymphocyte and platelet/lymphocyte ratios in all mood states of bipolar disorder

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