Interleukin-10 level is associated with post-stroke depression in acute ischaemic stroke patients

Chi, Chu-huai; Huang, Yuanyuan; Ye, Suzhen; Shao, Mengmeng; Ming-xia, Jiang; Yang, Mengyao; Wu, Qian; Shao, Baiqi; Li, Xian‐Mei

doi:10.1016/j.jad.2021.06.037

Cited by 25 publications

(23 citation statements)

References 44 publications

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“…We observed that compared with the non-PSD group, PSD group showed a higher proportion of female (40.80% vs. 20.37%, p = 0.024), lower years of education (9 [6-12] vs. 12 [9][10][11][12][13][14][15][16]; p = 0.044), higher stroke severity (NIHSS score: 5 [1.5-8.5] vs. 2 [1-4.5]; p = 0.046), worse cognitive function (MMSE score: 24 [22][23][24][25][26][27] vs. 27 [23-29]; p = 0.027) and lower monocyte count (0.50 [0.35-0.60] vs. 0.50 [0.48-0.70]; p = 0.007). BMI, pulmonary infection, medicines (antibiotic, statin and antiplatelet agents), vascular risk factors (hypertension, diabetes mellitus, heart disease, hyperlipidemia, smoking, drinking and previous stroke), stroke type including TOAST classification, stroke hemisphere, stroke location, the times from stroke onset to chest CT scan and to the blood sample collection, complete blood count parameters (leukocyte, neutrophil, lymphocyte and platelet counts, platelet-tolymphocyte ratio, neutrophil-to-lymphocyte ratio and monocyte-to-lymphocyte ratio), and SV did not show any significantly association with PSD status.…”

Section: Characteristics Of Psd and Non-psd Patientsmentioning

confidence: 84%

“…The available data have shown that immuno-inflammatory responses are activated immediately after acute stroke, both centrally and peripherally, followed by impressive increased expression of pro-inflammatory cytokines (such as interleukin [IL]-1, IL-6 and tumor necrosis factor [TNF]-a) to initiate and/ or amplify inflammatory response (5), causing dysfunction of noradrenergic system, hyperactivity of the hypothalamic pituitary adrenal (HPA) axis and extensive activation of indoleamine 2,3-dioxygenase enzyme that accelerates serotonin depletion in physiological regions such as paralimbic areas of left frontal and temporal cortex, which may ultimately lead to depression (6)(7)(8)(9). Although there is a large amount of evidence that inflammatory molecules are involved in the formation of PSD (10)(11)(12)(13), but genetic factors underlying the association remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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The potential risk factors of early-onset post-stroke depression from immuno-inflammatory perspective

et al. 2022

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BackgroundMounting evidence strongly uncovered that peripheral immuno-inflammatory response induced by acute stroke is associated with the appearance of post-stroke depression (PSD), but the mechanism remains unclear.Methods103 stroke patients were assessed at 2 weeks after onset using Diagnostic and Statistical Manual of Mental Disorders, 5th edition and then divided into PSD and non-PSD groups. Polymorphisms of inflammatory molecules (interleukin [IL]-1β, IL-6, IL-10, IL-18, tumor necrosis factor-α [TNF-α], interferon-γ [IFN-γ] and C-reactive protein [CRP]), complete blood count parameters, splenic attenuation (SA) and splenic volume (SV) on unenhanced chest computed tomography, demographic and other clinical characteristics were obtained. Binary logistic regression model was used to analyze the associations between inflammation-related factors and the occurrence of PSD at 2 weeks after stroke.Results49 patients were diagnosed with PSD at 2 weeks after onset (early-onset PSD). The C/T genotypes of CRP rs2794520 and rs1205 were less in PSD group than non-PSD group (both adjusted odds ratio = 3.364; 95%CI: 1.039-10.898; p = 0.043). For CRP rs3091244, the frequency of G allele was higher (80.61% vs. 13.89%) while the frequency of A allele was lower (6.12% vs. 71.30%) in PSD patients than non-PSD patients (χ2 = 104.380; p<0.001). SA of PSD patients was lower than that of non-PSD patients in the presence of CRP rs2794520 C/T genotype and rs1205 C/T genotype (both t = 2.122; p = 0.039). Peripheral monocyte count was less in PSD group than non-PSD group (adjusted odds ratio = 0.057; 95%CI: 0.005-0.686; p = 0.024).ConclusionsCRP polymorphisms, SA based on CRP genotype, and peripheral monocytes are associated with the risk of early-onset PSD, suggesting peripheral immuno-inflammatory activities elicited by stroke in its aetiology.

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Section: Characteristics Of Psd and Non-psd Patientsmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

The potential risk factors of early-onset post-stroke depression from immuno-inflammatory perspective

et al. 2022

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“…Moreover, low IL-10 levels were related to poor stroke outcomes and a delayed, exacerbated inflammatory response that was alleviated by IL-10 administration after pMCAO ( 76 ). Lower levels of IL-10 and IL-33 may also be used to predict post stroke depression ( 77 , 78 ). The IL-10 expression in the brain tissue increases with pathological changes of the central nervous system, promotes the survival of gliocyte and neurons, and inhibits inflammatory responses through multiple signaling pathways.…”

Section: Il-10mentioning

confidence: 99%

Interleukins and Ischemic Stroke

et al. 2022

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Ischemic stroke after cerebral artery occlusion is one of the major causes of chronic disability worldwide. Interleukins (ILs) play a bidirectional role in ischemic stroke through information transmission, activation and regulation of immune cells, mediating the activation, multiplication and differentiation of T and B cells and in the inflammatory reaction. Crosstalk between different ILs in different immune cells also impact the outcome of ischemic stroke. This overview is aimed to roughly discuss the multiple roles of ILs after ischemic stroke. The roles of IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-9, IL-10, IL-12, IL-13, IL-15, IL-16, IL-17, IL-18, IL-19, IL-21, IL-22, IL-23, IL-32, IL-33, IL-34, IL-37, and IL-38 in ischemic stroke were discussed in this review.

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“…17-item Hamilton Depression Scale (HAMD-17) was adopted at 14 ± 2 days after the onset of AIS to evaluate mental disorders of the patients. HAMD-17 points <7 means normal condition; mild depression for 7–17 points; moderate depression for 18–24 points; more than 24 points for severe depression (Zhu et al, 2016 ; He et al, 2017 ; Luan et al, 2020 ; Chi et al, 2021 ). The diagnosis was made according to the American Diagnostic and Statistical Manual of Mental Disorders Version 5 (DSM-5).…”

Section: Methodsmentioning

confidence: 99%

A new nomogram including total cerebral small vessel disease burden for individualized prediction of early-onset depression in patients with acute ischemic stroke

Zhou

Chen

et al. 2022

Front. Aging Neurosci.

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ObjectivesThe present study was designed to evaluate the effects of total cerebral small vessel disease (CSVD) on early-onset depression after acute ischemic stroke (AIS), and to develop a new nomogram including total CSVD burden to predict early-onset post-stroke depression (PSD).MethodsWe continuously enrolled patients with AIS who were hospitalized at the First Affiliated Hospital of Soochow University between October 2017 and June 2019. All patients were assessed for depressive symptoms using the 17-item Hamilton Depression Scale (HAMD-17) at 14 ± 2 days after the onset of AIS. The diagnosis for depression was made according to the American Diagnostic and Statistical Manual of Mental Disorders Version 5 (DSM-5). The demographic and clinical data were collected including total CSVD burden. On the basis of a multivariate logistic model, the independent factors of early-onset PSD were identified and the predictive nomogram was generated. The performance of the nomogram was evaluated by Harrell's concordance index (C-index) and calibration plot.ResultsA total of 346 patients were enrolled. When contrasted to a 0 score of total CSVD burden, the score ≥2 (moderate to severe total CSVD burden) was an independent risk factor for early-onset PSD. Besides, gender, cognitive impairments, baseline Barthel Index (BI), and plasma fibrinogen were independently associated with early-onset PSD. The nomogram based on all these five independent risk factors was developed and validated with an Area Under Curve (AUC) of 0.780. In addition, the calibration plot revealed an adequate fit of the nomogram in predicting the risk of early-onset depression in patients with AIS.ConclusionsOur study found the total CSVD burden score of 2–4 points was an independent risk factor of early-onset PSD. The proposed nomogram based on total CSVD burden, gender, cognitive impairments, baseline BI, and plasma fibrinogen concentration gave rise to a more accurate and more comprehensive prediction for early-onset PSD.

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Interleukin-10 level is associated with post-stroke depression in acute ischaemic stroke patients

Cited by 25 publications

References 44 publications

The potential risk factors of early-onset post-stroke depression from immuno-inflammatory perspective

The potential risk factors of early-onset post-stroke depression from immuno-inflammatory perspective

Interleukins and Ischemic Stroke

A new nomogram including total cerebral small vessel disease burden for individualized prediction of early-onset depression in patients with acute ischemic stroke

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