Comparison of inflammatory cytokine levels among type I/type II and manic/hypomanic/euthymic/depressive states of bipolar disorder

Bai, Ya Mei; Su, Tung Ping; Tsai, Shih‐Jen; Chiou, Wen-Fei; Li, Cheng Ta; Tu, Pei-Chi; Chen, Mu‐Hong

doi:10.1016/j.jad.2014.05.009

Cited by 98 publications

(78 citation statements)

References 48 publications

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“…Also depressed patients had signifi cantly lower levels of sTNF-R1 than the patients in manic/hypomanic episode and euthymic patients. These results in combination with the clinical data mentioned previously might suggest a role for sTNF-R1 in the staging of BD (Bai et al 2014 ).…”

Section: Neurochemical Datasupporting

confidence: 81%

Staging of Bipolar Disorder

Fountoulakis

2014

Bipolar Disorder

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Section: Neurochemical Datasupporting

confidence: 81%

Staging of Bipolar Disorder

Fountoulakis

2014

Bipolar Disorder

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“…The current findings provide strong evidence that the correlation between psychopathology and inflammatory dysregulation (e.g., (Bai, Su et al 2014;Stepanichev, Dygalo et al 2014) is important in behavioral outcomes. Moreover, Melcer and colleagues found that susceptibility to PTSD was related to Traumatic Brain Injury (TBI) severity in combat veterans (Melcer, Walker et al 2014), further suggesting that central inflammation is related to the development of PTSD.…”

Section: Discussionmentioning

confidence: 52%

The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning

Jones

Lebonville

Barrus

et al. 2014

Neuropsychopharmacol

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Posttraumatic stress disorder (PTSD) has been shown to be associated with pro-inflammatory markers, including elevated plasma levels of interleukin-1β (IL-1β). However, the precise role of neuroinflammation and central immune signaling on the development of this debilitating psychological disorder is not known. Here, we used stress-enhanced fear learning (SEFL), an animal model of the disorder, to examine the role of central IL-1β in PTSD. The results show that the severe stressor in SEFL induces a time-dependent increase in IL-1β immunoreactivity and mRNA expression within the dentate gyrus of the dorsal hippocampus (DH). There was no increase in IL-1β in the basolateral amygdala or the perirhinal cortex. Moreover, blocking the action of IL-1β following the severe stressor with IL-1 receptor antagonist (10 μg, intracerebroventricular (i.c.v.), 24 and 48 h after the stressor) prevented the development of SEFL. To provide further support for the role of IL-1β in the development of SEFL, we show that systemic morphine, a treatment which is known to reduce both PTSD and SEFL, also reduces IL-1β expression in the DH induced by the severe stressor. These studies provide the first evidence that IL-1 is involved SEFL and suggest that IL-1 signaling in the brain may have a critical role in the development of PTSD.

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“…Neuropsychological data (Lin et al, 2015) also showed that patients with SBP performed significantly better than did patients with BP-I in set shifting and visual-spatial memory and that patients with SBP performed similarly to those with BP-II in all of the cognitive domains. Bai et al (2014) compared inflammatory cytokine levels in BP-I and-II and reported that patients with BP-II had significantly lower levels of soluble (s)TNF-R1 than did patients with BP-I, but there were no data on SBP patients. Our study provided comparable evidence supporting their claim that along the BD spectrum, BP-I is strongly associated with inflammatory cytokines dysregulation and that SBP and BP-II have no significant differences in levels of inflammatory changes, which was consistent with other studies (Angst et al, 2003, 2010; Benazzi and Akiskal, 2006; Lin et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, there are few investigations of the differences in biomarker along the BP continuum of BP-I, BP-II, and SBP (Bai et al, 2014). We believe studies of the possible biological differences along the BP spectrum will provide support in addition to epidemiological data for the classification of BP-II and SBP.…”

Section: Introductionmentioning

confidence: 99%

“…Although patients with MDD also have higher-than-normal range levels of peripheral inflammatory cytokines (Miller et al, 2009) and lower-than-normal range BDNF levels (Polyakova et al, 2015), studies have hypothesized that the disturbance of inflammation (Bai et al, 2015) and BDNF expression (Li et al, 2014) were more severe in BP than in MDD and indicated the potential differential roles of these biomarkers (Li et al, 2014). …”

Section: Introductionmentioning

confidence: 99%

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The Differential Levels of Inflammatory Cytokines and BDNF among Bipolar Spectrum Disorders

Wang

Lee

Chung

et al. 2016

IJNPPY

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Objective:Emerging evidence suggests that inflammation and neurodegeneration underlies bipolar disorder. To investigate biological markers of cytokines and brain-derived neurotrophic factor between bipolar I, bipolar II, and other specified bipolar disorder with short duration hypomania may support the association with inflammatory dysregulation and bipolar disorder and, more specifically, provide evidence for other specified bipolar disorder with short duration hypomania patients were similar to bipolar II disorder patients from a biological marker perspective.Methods:We enrolled patients with bipolar I disorder (n=234), bipolar II disorder (n=260), other specified bipolar disorder with short duration hypomania (n=243), and healthy controls (n=140). Their clinical symptoms were rated using the Hamilton Depression Rating Scale and Young Mania Rating Scale. Inflammatory cytokine (tumor necrosis factor-α, C-reactive protein, transforming growth factor-β1, and interleukin-8) and brain-derived neurotrophic factor levels were measured in each group. Multivariate analysis of covariance and linear regression controlled for possible confounders were used to compare cytokine and brain-derived neurotrophic factor levels among the groups.Results:Multivariate analysis of covariance adjusted for age and sex and a main effect of diagnosis was significant (P<.001). Three of the 5 measured biomarkers (tumor necrosis factor-α, transforming growth factor-β1, and interleukin-8) were significantly (P=.006, .01, and <.001) higher in all bipolar disorder patients than in controls. Moreover, covarying for multiple associated confounders showed that bipolar I disorder patients had significantly higher IL-8 levels than did bipolar II disorder and other specified bipolar disorder with short duration hypomania patients in multivariate analysis of covariance (P=.03) and linear regression (P=.02) analyses. Biomarkers differences between bipolar II disorder and other specified bipolar disorder with short duration hypomania patients were nonsignificant.Conclusion:The immunological disturbance along the bipolar spectrum was most severe in bipolar I disorder patients. Other specified bipolar disorder with short duration hypomania patients and bipolar II disorder patients did not differ in these biological markers.

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Comparison of inflammatory cytokine levels among type I/type II and manic/hypomanic/euthymic/depressive states of bipolar disorder

Cited by 98 publications

References 48 publications

Staging of Bipolar Disorder

Staging of Bipolar Disorder

The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning

The Differential Levels of Inflammatory Cytokines and BDNF among Bipolar Spectrum Disorders

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