Changes in cytokine and chemokine expression distinguish dysthymic disorder from major depression and healthy controls

Ho, Pei‐Shen; Yen, Che-Hung; Chen, Chun‐Yen; Huang, San-Yuan; Liang, Chih‐Sung

doi:10.1016/j.psychres.2016.12.014

Cited by 34 publications

(23 citation statements)

References 35 publications

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“…A multiplex bead array assay was used to examine plasma levels of cytokines. The detailed procedures for detection of soluble cytokines by multiplex bead array assays have been previously reported [26,27]. Three cytokines (IL-1β, IL-1 receptor antagonist (RA), and IL-33) were determined by using a customized human cytokine magnetic bead panel (Bio-Rad; Yu-Shing Biotech., Ltd., Taipei, Taiwan) according to the manufacturer's instructions (Bio-Rad; Genmall Biotechnology Co., Ltd., Taipei, Taiwan).…”

Section: Plasma Levels Of Cytokinesmentioning

confidence: 99%

The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

Liang

Tsai

et al. 2020

Alz Res Therapy

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Background: The neuroprotective role of interleukin (IL)-33 is supported by numerous preclinical studies, but it remains uninvestigated in clinical studies of Alzheimer's disease (AD). We aimed to examine the association between human blood levels of IL-33 and cognitive preservation in amnestic mild cognitive impairment (aMCI) and AD. Methods: A total of 100 participants (26 controls, 35 aMCI patients, and 39 AD patients) completed two Mini-Mental State Examinations (MMSEs) over a 1-year interval. In all 100 participants at the second MMSE, we examined the plasma levels of IL-33, IL-β, IL-1 receptor agonist (IL-1RA), beta amyloid (Aβ), and tau and apolipoprotein E (ApoE) genotyping; we also performed Hopkins Verbal Learning Test, Trail Making Test, forward and backward digit span, and Clinical Dementia Rating. Results: IL-33 expression showed a positive trend among controls (1/26 = 3.8%), aMCI (9/35 = 25.7%), and AD (17/39 = 43.6%) (trend analysis: P < 0.001). Patients expressing IL-33 preserved their cognitive function compared with IL-33 nonexpressing patients (1-year ΔMMSE, 0.16 ± 1.6 vs − 1.5 ± 2.6; P = 0.006). The cognitive preservation was not associated with the lower levels of Aβ, tau, and ApoE ε4, while higher levels of ApoE ε4 and phosphorylated tau were indeed associated with cognitive decline. The aMCI patients with AD conversion during study period had higher proportion of IL-33(−) than non-AD converters (90.9% vs 53.3%, P = 0.04). Conclusions: IL-33 or its associated signaling pathways may represent a new treatment paradigm for aMCI and AD.

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Section: Plasma Levels Of Cytokinesmentioning

confidence: 99%

The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

Liang

Tsai

et al. 2020

Alz Res Therapy

Self Cite

View full text Add to dashboard Cite

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“…A multiplex bead array assay was used to examine plasma levels of cytokines. The detailed procedures for detection of soluble cytokines by multiplex bead array assays have been previously reported [23,24]. Three cytokines (IL-1β, IL-1 receptor antagonist (RA), and IL-33) were determined by using a customized human cytokine magnetic bead panel (Bio-Rad; Yu-Shing Biotech., Ltd, Taipei, Taiwan) according to the manufacturer's instructions (Bio-Rad; Genmall Biotechnology Co., LTD., Taipei, Taiwan).…”

Section: Plasma Levels Of Cytokinesmentioning

confidence: 99%

The Role of Interleukin-33 in Patients with Mild Cognitive Impairment and Alzheimer's Disease

Liang

Tsai

et al. 2020

SSRN Journal

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Background: The neuroprotective role of Interleukin (IL)-33 is supported in numerous pre-clinical studies but remains mostly uninvestigated in clinical studies of Alzheimer's disease (AD). We aimed to examine the association between human blood levels of IL-33 and cognitive preservation in amnestic mild cognitive impairment (aMCI) and AD. Methods: A total of 100 participants (26 controls, 35 aMCI patients, and 39 AD patients) were completed twice Mini Mental State Examination (MMSE) over a 1-year interval. At the second MMSE, the 100 participants examined the plasma levels of IL-33, IL-β, IL-1 receptor agonist (IL-1RA), beta amyloid (Aβ), and tau and apolipoprotein E (ApoE) genotyping, and Hopkins Verbal Learning Test, Trail Making Test, forward and backward digit span, and Clinical Dementia Rating were performed as well. Results: IL-33 expression showed a positive trend among controls (1/26 = 3.8%), aMCI (9/35 = 25.7%), and AD (17/39 = 43.6%) (trend analysis: P < 0.001). The patients expressing IL-33 preserved their cognitive function compared with IL-33 non-expressing patients (1-year ΔMMSE: 0.16 ± 1.6 vs-1.5 ± 2.6; P = 0.006). The cognitive preservation was not associated with the lower levels of Aβ, tau, and AopE ε4, while higher levels of AopE ε4 and phosphorylated tau were indeed associated with cognitive decline. The aMCI patients with AD conversion during study period had higher proportion of IL-33(-) than non-AD converters (0.9% vs 53.3%, P = 0.04). Conclusions: IL-33 or its associated signaling pathways may represent a new treatment paradigm for aMCI and AD.

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“…4C). Furthermore, activated glial cells including microglia and astrocytes are the key sources of neuroin ammation and central cytokines [9,10,54]. To examine the involvement of microglia and astrocytes in LPS induced neuroin ammation, glial cell activation markers of glial brillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (Iba-1) expression was determined by immuno uorescence.…”

Section: Ibrutinib Alleviated Lps Induced Neuroin Ammationmentioning

confidence: 99%

“…Moreover, increased cytokine levels have also been detected in the brain sample of MDD patients committing suicide. Additionally, psychoneuroimmunologic perspectives also suggest that neuroin ammation can lead to depression [7,[10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Ibrutinib alleviated LPS-induced neuroinflammation and synaptic defects in a mouse model of depression

Ali

et al. 2020

Preprint

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Background Previous studies indicate a close association between the altered immune system and major depressive disorders. and inhibition of neuroinflammation may represent an alternative mechanism to treat depression. Recently, the anti-inflammatory activity of ibrutinib has been reported, however, the effect of ibrutinib on neuroinflammation allied depression and its underlying mechanism has not been comprehensively studied. Therefore, we aimed to elucidate the potential anti-depressive role and mechanism of ibrutinib against neuroinflammation induced depression as well as synaptic defects. Methods Adult C57BL/6J male mice weighing 25–30 g (age 7–8 weeks) were treated with LPS (2 mg/kg BW i.p) and 50 mg/kg BW ibrutinib, orally. Depressive-like behaviors were assessed by FST and SPT, cytokine levels were determined by ELISA, ROS, TBARs, and Nitric oxides were measured via biochemical assays, Iba-1 and GFAP expression were determined by immunofluorescence. Further, spine density was measured by Golgi staining, while NF-kB, Nrf2, SOD2, HO-1, NLRP3, P38, Caspase-1, BDNF, PSD95, and synaptophysin were measured by immunoblotting. Results Our results showed that ibrutinib treatment significantly reduced LPS induced depressive-like behaviors and neuroinflammation via inhibiting NF-kB activation, decreasing pro-inflammatory cytokines level, normalizing redox signaling and it’s a downstream component including Nrf2, HO-1, and SOD2 as well as glial cells activation markers such as Iba-1 and GFAP expression. Further, ibrutinib treatment inhibited LPS activated inflammasome activation by targeting NLRP3/P38/Caspase-1 signaling. Interestingly, LPS reduced dendritic spines numbers, expression of BDNF and synaptic related markers including PSD95, snap25, and synaptophysin were improved by ibrutinib treatment in the hippocampal area of the mice brain. Conclusion In conclusion, our finding suggested that ibrutinib could alleviate neuroinflammation and synaptic defects, rendering its antidepressant potential against LPS induced neuroinflammation and depression.

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Changes in cytokine and chemokine expression distinguish dysthymic disorder from major depression and healthy controls

Cited by 34 publications

References 35 publications

The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

The Role of Interleukin-33 in Patients with Mild Cognitive Impairment and Alzheimer's Disease

Ibrutinib alleviated LPS-induced neuroinflammation and synaptic defects in a mouse model of depression

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