首页 > 最新文献

Brain, behavior, & immunity - health最新文献

英文 中文
Perceived stress precedes declines in Well-being: A prospective study of stress, well-being, hair cortisol, and low-grade inflammation in hospital employees 感知压力先于幸福感的下降:一项关于医院员工压力、幸福感、毛发皮质醇和低度炎症的前瞻性研究
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-11 DOI: 10.1016/j.bbih.2025.101158
Monica T. Jones , Rachael A. Cronin , Mathew D. Marques , Matthias Weigl , Nicolas Rohleder , Linda Becker , Helena C. Kaltenegger , Bradley J. Wright

Objective

Chronic low-grade inflammation may help explain the relationship between stress, well-being, and disease, but the pathway and temporal order have not yet been tested prospectively. To understand the pathways between perceived stress, well-being, C-reactive protein, and hair cortisol, we investigated the temporal ordering of these variables in a sample of hospital employees.

Methods

Random-intercepts cross-lagged panel models were conducted using three 6-monthly waves of data collected from new employees at a German hospital (N = 296, 77.7 % female, M age = 28.59) in a prospective cohort study. Self-reported data on perceived stress and well-being, hair strands for hair cortisol concentration, and capillary blood samples for C-reactive protein were collected for analysis.

Results

While our study did not support a causal relationship between changes in stress levels and later changes in either hair cortisol or low-grade inflammation, we provide evidence to suggest that increases in perceived stress led to later decreases in well-being. In contrast, changes in well-being did not predict changes in perceived stress levels.

Conclusion

This is the first prospective repeated-measure study to examine the temporal associations between stress, well-being, hair cortisol concentrations, and chronic low-grade inflammation. Our analyses suggest that perceived stress in this sample precedes changes in well-being, highlighting the importance of prevention and early intervention.
目的慢性低度炎症可能有助于解释压力、健康和疾病之间的关系,但其途径和时间顺序尚未得到前瞻性的检验。为了了解感知压力、幸福感、c反应蛋白和毛发皮质醇之间的关系,我们在医院员工样本中调查了这些变量的时间顺序。方法采用随机截距交叉滞后面板模型,采用前瞻性队列研究,收集德国某医院新员工(N = 296, 77.7%为女性,年龄28.59岁)的3个6个月数据波。收集自我报告的感知压力和幸福感数据、头发皮质醇浓度和毛细管血液c反应蛋白样本进行分析。虽然我们的研究不支持压力水平的变化与后来毛发皮质醇或低度炎症的变化之间的因果关系,但我们提供的证据表明,感知压力的增加导致后来幸福感的下降。相比之下,幸福感的变化并不能预测感知压力水平的变化。结论:这是第一项前瞻性重复测量研究,旨在研究压力、幸福感、毛发皮质醇浓度和慢性低度炎症之间的时间相关性。我们的分析表明,在这个样本中,感知到的压力先于幸福感的变化,强调了预防和早期干预的重要性。
{"title":"Perceived stress precedes declines in Well-being: A prospective study of stress, well-being, hair cortisol, and low-grade inflammation in hospital employees","authors":"Monica T. Jones ,&nbsp;Rachael A. Cronin ,&nbsp;Mathew D. Marques ,&nbsp;Matthias Weigl ,&nbsp;Nicolas Rohleder ,&nbsp;Linda Becker ,&nbsp;Helena C. Kaltenegger ,&nbsp;Bradley J. Wright","doi":"10.1016/j.bbih.2025.101158","DOIUrl":"10.1016/j.bbih.2025.101158","url":null,"abstract":"<div><h3>Objective</h3><div>Chronic low-grade inflammation may help explain the relationship between stress, well-being, and disease, but the pathway and temporal order have not yet been tested prospectively. To understand the pathways between perceived stress, well-being, C-reactive protein, and hair cortisol, we investigated the temporal ordering of these variables in a sample of hospital employees.</div></div><div><h3>Methods</h3><div>Random-intercepts cross-lagged panel models were conducted using three 6-monthly waves of data collected from new employees at a German hospital (<em>N</em> = 296, 77.7 % female, M age = 28.59) in a prospective cohort study. Self-reported data on perceived stress and well-being, hair strands for hair cortisol concentration, and capillary blood samples for C-reactive protein were collected for analysis.</div></div><div><h3>Results</h3><div>While our study did not support a causal relationship between changes in stress levels and later changes in either hair cortisol or low-grade inflammation, we provide evidence to suggest that increases in perceived stress led to later decreases in well-being. In contrast, changes in well-being did not predict changes in perceived stress levels.</div></div><div><h3>Conclusion</h3><div>This is the first prospective repeated-measure study to examine the temporal associations between stress, well-being, hair cortisol concentrations, and chronic low-grade inflammation. Our analyses suggest that perceived stress in this sample precedes changes in well-being, highlighting the importance of prevention and early intervention.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101158"},"PeriodicalIF":3.5,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Accelerated Theta Burst Stimulation Transcranial Magnetic Stimulation (iTBS-TMS) Pururauka program for severe depressive episode and suicide ideation 经颅磁刺激(iTBS-TMS)重度抑郁发作和自杀意念的Pururauka方案
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-05 DOI: 10.1016/j.bbih.2025.101154
Hesed Virto-Farfan , Carlos Virto , Gustavo E. Tafet

Introduction

The Pururauka protocol is an accelerated intermittent theta burst stimulation (iTBS) paradigm designed to rapidly reduce depressive symptoms and suicidal ideation in individuals with severe major depressive episodes. This study evaluated its clinical effects in patients presenting with insufficient response to at least two prior pharmacological treatments, current suicidal ideation, and more than two previous suicide attempts.

Methods

Thirty-six adults with non-psychotic major depressive disorder (ICD-11) and HAM-D-17 scores >20 received a five-day accelerated iTBS intervention (180,000 pulses total) targeting the left dorsolateral prefrontal cortex. Depressive symptoms were assessed using the HAM-D and MADRS at baseline, daily during treatment, and at 1-, 3-, and 6-month follow-ups. Suicidal ideation was evaluated with HAM-D item 3 across the same time points. Satisfaction was measured with a visual analogue scale (VAS). Safety assessments included EEG screening and neuropsychiatric evaluations. Ethical approval was obtained from the Andean University of Cusco Ethics Committee (INFORME 023-2024-CIEI-UAC).

Results

Mean HAM-D scores decreased from 38.89 at baseline to 13.61 at day 5 and 12.36 at six months (p < 0.001). Suicidal ideation resolved in most participants by day 3 and remained minimal or absent during follow-up. MADRS scores showed similar patterns, with 68 % of participants presenting no depressive symptoms immediately after treatment. No serious adverse events occurred, and satisfaction scores remained high throughout the protocol.

Conclusion

The Pururauka accelerated iTBS protocol was associated with rapid and sustained reductions in depressive symptoms and suicidal ideation in individuals with severe depressive episodes and insufficient response to previous medications. These preliminary findings warrant confirmation in future randomized controlled trials.
Pururauka方案是一种加速间歇性θ波爆发刺激(iTBS)模式,旨在快速减少重度抑郁症患者的抑郁症状和自杀意念。本研究评估了其在对至少两种药物治疗反应不足、当前有自杀意念和两次以上自杀企图的患者中的临床效果。方法36例非精神病性重度抑郁症(ICD-11)和HAM-D-17评分为20分的成年人接受了为期5天的加速iTBS干预(共180,000次脉冲),目标是左背外侧前额皮质。在基线、治疗期间每日以及1、3和6个月随访时,使用HAM-D和MADRS评估抑郁症状。在同一时间点用HAM-D项目3评估自杀意念。满意度采用视觉模拟量表(VAS)测量。安全性评估包括脑电图筛查和神经精神评估。获得了库斯科安第斯大学伦理委员会(inform 023-2024-CIEI-UAC)的伦理批准。结果HAM-D平均评分从基线时的38.89下降到第5天和第6个月时的13.61和12.36 (p < 0.001)。大多数参与者的自杀意念在第3天消失,在随访期间保持最小或不存在。MADRS评分显示了类似的模式,68%的参与者在治疗后没有立即出现抑郁症状。没有发生严重的不良事件,在整个治疗过程中,满意度得分仍然很高。结论Pururauka加速iTBS方案与严重抑郁发作且对既往药物反应不足的个体的抑郁症状和自杀意念的快速和持续减少有关。这些初步发现有必要在未来的随机对照试验中得到证实。
{"title":"Accelerated Theta Burst Stimulation Transcranial Magnetic Stimulation (iTBS-TMS) Pururauka program for severe depressive episode and suicide ideation","authors":"Hesed Virto-Farfan ,&nbsp;Carlos Virto ,&nbsp;Gustavo E. Tafet","doi":"10.1016/j.bbih.2025.101154","DOIUrl":"10.1016/j.bbih.2025.101154","url":null,"abstract":"<div><h3>Introduction</h3><div>The <em>Pururauka</em> protocol is an accelerated intermittent theta burst stimulation (iTBS) paradigm designed to rapidly reduce depressive symptoms and suicidal ideation in individuals with severe major depressive episodes. This study evaluated its clinical effects in patients presenting with insufficient response to at least two prior pharmacological treatments, current suicidal ideation, and more than two previous suicide attempts.</div></div><div><h3>Methods</h3><div>Thirty-six adults with non-psychotic major depressive disorder (ICD-11) and HAM-D-17 scores &gt;20 received a five-day accelerated iTBS intervention (180,000 pulses total) targeting the left dorsolateral prefrontal cortex. Depressive symptoms were assessed using the HAM-D and MADRS at baseline, daily during treatment, and at 1-, 3-, and 6-month follow-ups. Suicidal ideation was evaluated with HAM-D item 3 across the same time points. Satisfaction was measured with a visual analogue scale (VAS). Safety assessments included EEG screening and neuropsychiatric evaluations. Ethical approval was obtained from the Andean University of Cusco Ethics Committee (INFORME 023-2024-CIEI-UAC).</div></div><div><h3>Results</h3><div>Mean HAM-D scores decreased from 38.89 at baseline to 13.61 at day 5 and 12.36 at six months (p &lt; 0.001). Suicidal ideation resolved in most participants by day 3 and remained minimal or absent during follow-up. MADRS scores showed similar patterns, with 68 % of participants presenting no depressive symptoms immediately after treatment. No serious adverse events occurred, and satisfaction scores remained high throughout the protocol.</div></div><div><h3>Conclusion</h3><div>The <em>Pururauka</em> accelerated iTBS protocol was associated with rapid and sustained reductions in depressive symptoms and suicidal ideation in individuals with severe depressive episodes and insufficient response to previous medications. These preliminary findings warrant confirmation in future randomized controlled trials.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101154"},"PeriodicalIF":3.5,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Peripheral immune system activity in young psychiatry patients 年轻精神病患者的外周免疫系统活动
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-03 DOI: 10.1016/j.bbih.2025.101143
Lennart Seizer , Johanna Löchner , Tobias J. Renner
The interaction between the immune system and the central nervous system has been implicated in the development of psychiatric disorders in adult patients. However, comprehensive data regarding pediatric psychiatry are still lacking. This study aims to describe the distributions of various markers of immune system activity in a large clinical sample of children and adolescents and summarize the immunological profiles associated with different psychiatric disorders. We analyzed blood samples from 1543 patients aged 6–18 years (62 % female), admitted to the Child and Adolescent Psychiatry at the University Hospital of Tübingen between 2014 and 2024. Immune markers such as C-reactive protein and various cell counts and ratios were measured and regressed on psychiatric diagnoses according to the ICD-10 classification. Our findings revealed several distinct immunological profiles linked to specific psychiatric conditions in youth, such as higher CRP levels in patients with severe stress and adjustment disorders. The study underscores the potential role that immune system aberrations may play in mental health disorders and highlights the importance of investigating this link in this age group. However, some inconsistencies with the existing literature were found, such as the lack of association between depression and immune activity, which calls for further research to elucidate these relationships. Future studies should include longitudinal designs to better understand the causal pathways and potential for immune-targeted therapies in pediatric psychiatry.
免疫系统和中枢神经系统之间的相互作用与成人精神疾病的发展有关。然而,关于儿童精神病学的综合数据仍然缺乏。本研究旨在描述大量儿童和青少年临床样本中各种免疫系统活性标记物的分布,并总结与不同精神疾病相关的免疫学概况。我们分析了2014年至2024年期间在宾根大学医院儿童和青少年精神病学收治的1543名6-18岁患者(62%为女性)的血液样本。根据ICD-10分类,测定免疫标志物如c反应蛋白和各种细胞计数及比值,并对精神病诊断进行回归。我们的研究结果揭示了几种不同的免疫特征与青少年特定的精神状况有关,例如患有严重压力和适应障碍的患者的CRP水平较高。该研究强调了免疫系统异常可能在精神健康障碍中发挥的潜在作用,并强调了在这一年龄组调查这种联系的重要性。然而,也发现了一些与现有文献不一致的地方,比如抑郁症和免疫活动之间缺乏联系,这需要进一步的研究来阐明这些关系。未来的研究应包括纵向设计,以更好地了解儿童精神病学的因果途径和免疫靶向治疗的潜力。
{"title":"Peripheral immune system activity in young psychiatry patients","authors":"Lennart Seizer ,&nbsp;Johanna Löchner ,&nbsp;Tobias J. Renner","doi":"10.1016/j.bbih.2025.101143","DOIUrl":"10.1016/j.bbih.2025.101143","url":null,"abstract":"<div><div>The interaction between the immune system and the central nervous system has been implicated in the development of psychiatric disorders in adult patients. However, comprehensive data regarding pediatric psychiatry are still lacking. This study aims to describe the distributions of various markers of immune system activity in a large clinical sample of children and adolescents and summarize the immunological profiles associated with different psychiatric disorders. We analyzed blood samples from 1543 patients aged 6–18 years (62 % female), admitted to the Child and Adolescent Psychiatry at the University Hospital of Tübingen between 2014 and 2024. Immune markers such as C-reactive protein and various cell counts and ratios were measured and regressed on psychiatric diagnoses according to the ICD-10 classification. Our findings revealed several distinct immunological profiles linked to specific psychiatric conditions in youth, such as higher CRP levels in patients with severe stress and adjustment disorders. The study underscores the potential role that immune system aberrations may play in mental health disorders and highlights the importance of investigating this link in this age group. However, some inconsistencies with the existing literature were found, such as the lack of association between depression and immune activity, which calls for further research to elucidate these relationships. Future studies should include longitudinal designs to better understand the causal pathways and potential for immune-targeted therapies in pediatric psychiatry.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101143"},"PeriodicalIF":3.5,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145941060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Psychological distress predicts disease activity in inflammatory bowel disease: Results from the mind-body IBD longitudinal study 心理困扰预测炎症性肠病的疾病活动:来自身心IBD纵向研究的结果
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-03 DOI: 10.1016/j.bbih.2025.101147
Natasha Seaton , Joanna L. Hudson , Valeria Mondelli , Leah Raymond , Pooja Schmill , Ailsa Hart , Rona Moss-Morris

Background & aims

Psychological distress (depression, anxiety, stress) is common in inflammatory bowel disease (IBD) and is linked to poorer outcomes, yet behavioural pathways and economic consequences remain unclear. This study tested a gut-brain-behaviour-outcome (GBBO) framework, testing: 1) reciprocal links between distress and disease activity; 2) whether health behaviours mediate distress-disease activity relationships; 3) if distress and self-reported disease activity (SRDA) predict adverse disease outcomes, controlling for inflammation and 4) whether disease activity mediates relationships between distress and adverse outcomes.

Methods

IBD patients (n = 157) reported distress, health behaviours, SRDA, healthcare use and disease-related outcomes at 3 waves at 6-month intervals. Faecal calprotectin (FCP) was assayed at baseline and 6 months. Analyses were conducted using structural equation modelling and mixed-effects models.

Results

Baseline distress predicted higher SRDA six months later (β = 0.16, p=.03) but did not predict FCP; reverse pathways were nonsignificant. Impaired sleep quality mediated 55 % of the effect of distress on future SRDA (β = 0.09, p=.04). Other behaviours were nonsignificant. Controlling for FCP, distress and SRDA independently predicted secondary healthcare usage (primary/secondary care) and disease-related outcomes (flare frequency/severity, absenteeism and productivity loss). FCP was positively related to flare frequency/severity and allied health practitioner visits only. Mediation analysis showed that SRDA partially mediated absenteeism.

Conclusions

Psychological distress exacerbates symptoms and economic cost. Poor sleep partially mediates the relationship between distress and SRDA, but not inflammation. Psychological interventions that focus on improving sleep could be cost-effective ways to improve mental health and symptom burden, with downstream impact on healthcare utilisation and productivity losses.
背景和目的心理困扰(抑郁、焦虑、压力)在炎症性肠病(IBD)中很常见,并与较差的预后有关,但行为途径和经济后果尚不清楚。本研究测试了肠道-大脑-行为-结果(GBBO)框架,测试:1)痛苦和疾病活动之间的相互联系;2)健康行为是否介导痛苦与疾病活动的关系;3)是否焦虑和自我报告疾病活动性(SRDA)预测疾病不良结局,控制炎症;4)疾病活动性是否介导焦虑和不良结局之间的关系。方法157例sibd患者每隔6个月分3次报告抑郁、健康行为、SRDA、医疗保健使用和疾病相关结局。在基线和6个月时测定粪便钙保护蛋白(FCP)。采用结构方程模型和混合效应模型进行分析。结果基线焦虑可预测6个月后较高的SRDA (β = 0.16, p= 0.03),但不能预测FCP;反向通路不显著。睡眠质量受损介导了焦虑对未来SRDA影响的55% (β = 0.09, p= 0.04)。其他行为不显著。控制FCP,窘迫和SRDA独立预测二级医疗保健使用(初级/二级医疗)和疾病相关结果(突发频率/严重程度、缺勤和生产力损失)。FCP仅与耀斑频率/严重程度和联合保健医生就诊呈正相关。中介分析表明,SRDA对旷工有部分中介作用。结论心理困扰加重了症状和经济成本。睡眠不足在一定程度上介导了焦虑和SRDA之间的关系,但不是炎症。以改善睡眠为重点的心理干预可能是改善心理健康和减轻症状负担的经济有效方法,对医疗保健利用和生产力损失具有下游影响。
{"title":"Psychological distress predicts disease activity in inflammatory bowel disease: Results from the mind-body IBD longitudinal study","authors":"Natasha Seaton ,&nbsp;Joanna L. Hudson ,&nbsp;Valeria Mondelli ,&nbsp;Leah Raymond ,&nbsp;Pooja Schmill ,&nbsp;Ailsa Hart ,&nbsp;Rona Moss-Morris","doi":"10.1016/j.bbih.2025.101147","DOIUrl":"10.1016/j.bbih.2025.101147","url":null,"abstract":"<div><h3>Background &amp; aims</h3><div>Psychological distress (depression, anxiety, stress) is common in inflammatory bowel disease (IBD) and is linked to poorer outcomes, yet behavioural pathways and economic consequences remain unclear. This study tested a gut-brain-behaviour-outcome (GBBO) framework, testing: 1) reciprocal links between distress and disease activity; 2) whether health behaviours mediate distress-disease activity relationships; 3) if distress and self-reported disease activity (SRDA) predict adverse disease outcomes, controlling for inflammation and 4) whether disease activity mediates relationships between distress and adverse outcomes.</div></div><div><h3>Methods</h3><div>IBD patients (n = 157) reported distress, health behaviours, SRDA, healthcare use and disease-related outcomes at 3 waves at 6-month intervals. Faecal calprotectin (FCP) was assayed at baseline and 6 months. Analyses were conducted using structural equation modelling and mixed-effects models.</div></div><div><h3>Results</h3><div>Baseline distress predicted higher SRDA six months later (β = 0.16, <em>p=.</em>03) but did not predict FCP; reverse pathways were nonsignificant. Impaired sleep quality mediated 55 % of the effect of distress on future SRDA (β = 0.09, <em>p=.</em>04). Other behaviours were nonsignificant. Controlling for FCP, distress and SRDA independently predicted secondary healthcare usage (primary/secondary care) and disease-related outcomes (flare frequency/severity, absenteeism and productivity loss). FCP was positively related to flare frequency/severity and allied health practitioner visits only. Mediation analysis showed that SRDA partially mediated absenteeism.</div></div><div><h3>Conclusions</h3><div>Psychological distress exacerbates symptoms and economic cost. Poor sleep partially mediates the relationship between distress and SRDA, but not inflammation. Psychological interventions that focus on improving sleep could be cost-effective ways to improve mental health and symptom burden, with downstream impact on healthcare utilisation and productivity losses.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101147"},"PeriodicalIF":3.5,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inflammatory profiles of transdiagnostic symptom dimensions in healthy females 健康女性的炎症特征的跨诊断症状维度
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-01 DOI: 10.1016/j.bbih.2025.101146
Alicia J. Smith , Stacey Kigar , Quentin Dercon , Mary-Ellen Lynall , Konstantinos Ioannidis , Muzaffer Kaser , Caitlin Hitchcock , Tim Dalgleish , Camilla L. Nord
<div><h3>Background</h3><div>Psychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression.</div></div><div><h3>Methods</h3><div>A modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N = 26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data).</div></div><div><h3>Results</h3><div>We identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a ‘social withdrawal’ factor were associated with greater baseline neutrophil (95 % highest density interval (HDI) = [0.06, 1.32]; BF<sub>10</sub> = 2.92) and monocyte counts (95 % HDI = [0.29, 1.46]; BF<sub>10</sub> = 19.08), whereas higher ‘anxious-depression’ scores were associated with a lower baseline monocyte count (95 % HDI = [-0.96, −0.02]; BF<sub>10</sub> = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre-to post stress induction: (95 % HDI = [0.18, 2.14]); BF<sub>10</sub> = 5.66). We also found evidence for an association between the ‘social withdrawal’ factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95 % HDI = [-1.14, −0.01]; BF<sub>10</sub> = 1.88).</div></div><div><h3>Conclusions</h3><div>We find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of
精神疾病越来越多地被定义为具有跨诊断潜在机制的异质类别,这些机制跨越多种诊断并在单一诊断中有所不同。由心理社会压力引起的炎症是一个特别有力的例子:先前的研究表明,炎症特征可能对应于症状亚组,而不是传统的诊断类别。然而,与特定炎症特征相关的跨诊断症状的可靠鉴定仍然很少。在这项研究中,我们研究了炎症特征(在基线和应激诱导后)与女性的跨诊断症状维度之间的关系,女性表现出更高的焦虑和抑郁等压力相关疾病的患病率。方法选取年龄在18 ~ 35岁的健康女性(N = 26)为研究对象。我们获得静脉血样本,在基线和综合生理和社会应激诱导后,测量全血细胞计数、血浆细胞因子和外周血单个核细胞(PBMCs;用于细胞刺激和细胞内流式细胞术分析)。参与者完成了一系列精神病学自我报告问题,从中我们建立了三个跨诊断因素评分模型。最后,我们使用贝叶斯回归来评估跨诊断因素对炎症标志物(基线和应激诱导)的预测贡献,以及炎症措施的主成分(来自炎症数据的主成分分析(PCA))。结果我们确定了炎症特征与跨诊断症状维度之间的特定关系。“社会退缩”因子得分越高,基线中性粒细胞越高(95%最高密度区间(HDI) = [0.06, 1.32];BF10 = 2.92)和单核细胞计数(95% HDI = [0.29, 1.46]; BF10 = 19.08),而较高的“焦虑-抑郁”评分与较低的基线单核细胞计数(95% HDI = [-0.96, - 0.02]; BF10 = 1.81)和更大的应激炎症反应(例如,中性粒细胞评分从应激诱导前到应激诱导后的变化:(95% HDI =[0.18, 2.14])相关;bf10 = 5.66)。我们还发现了“社交退缩”因素与单核细胞、嗜碱性粒细胞和白细胞介素-6 (95% HDI = [-1.14, - 0.01]; BF10 = 1.88)权重最大的免疫主成分之间存在关联的证据。结论:我们发现了初步证据,不同的跨诊断精神症状维度映射到特定的炎症谱,无论是在基线还是应激诱导后。这代表了使用数据驱动和假设驱动的方法来识别和联系跨诊断因素与炎症变化的原理证明,这可能用于未来更大规模的临床人群研究,或用于分层干预背景下的测试。
{"title":"Inflammatory profiles of transdiagnostic symptom dimensions in healthy females","authors":"Alicia J. Smith ,&nbsp;Stacey Kigar ,&nbsp;Quentin Dercon ,&nbsp;Mary-Ellen Lynall ,&nbsp;Konstantinos Ioannidis ,&nbsp;Muzaffer Kaser ,&nbsp;Caitlin Hitchcock ,&nbsp;Tim Dalgleish ,&nbsp;Camilla L. Nord","doi":"10.1016/j.bbih.2025.101146","DOIUrl":"10.1016/j.bbih.2025.101146","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Psychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;A modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N = 26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;We identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a ‘social withdrawal’ factor were associated with greater baseline neutrophil (95 % highest density interval (HDI) = [0.06, 1.32]; BF&lt;sub&gt;10&lt;/sub&gt; = 2.92) and monocyte counts (95 % HDI = [0.29, 1.46]; BF&lt;sub&gt;10&lt;/sub&gt; = 19.08), whereas higher ‘anxious-depression’ scores were associated with a lower baseline monocyte count (95 % HDI = [-0.96, −0.02]; BF&lt;sub&gt;10&lt;/sub&gt; = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre-to post stress induction: (95 % HDI = [0.18, 2.14]); BF&lt;sub&gt;10&lt;/sub&gt; = 5.66). We also found evidence for an association between the ‘social withdrawal’ factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95 % HDI = [-1.14, −0.01]; BF&lt;sub&gt;10&lt;/sub&gt; = 1.88).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;We find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of ","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101146"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Coordination of inflammatory and adrenocortical stress response during pregnancy and variation by mental health 妊娠期间炎症和肾上腺皮质应激反应的协调及心理健康的变化
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-01 DOI: 10.1016/j.bbih.2025.101145
Heidemarie K. Laurent , Sherryl H. Goodman , Douglas A. Granger , Penina M. Backer
Well-regulated coordination of a multi-system stress response is particularly consequential for intergenerational health during pregnancy, when maternal stress systems typically adapt to protect the fetus. However, little is known about patterns of combined immune/inflammatory mediator (IM) and hypothalamic-pituitary-adrenal (HPA) axis responding to acute stress in human pregnancy, let alone variations associated with maternal health risks. In this study we aimed to define normative perinatal stress response coordination and potential risk profiles by testing relations among pregnant women's salivary IM's and cortisol in response to psychosocial stress, as well as both concurrent affective distress symptomatology and lifetime diagnoses of affective disorders. A community sample of pregnant women (n = 158) participating in the first timepoint of a longitudinal study completed the Trier Social Stress Task and contributed five saliva samples assayed for cortisol; pro-inflammatory cytokines IL1β, IL6, TNFα; and CRP. They self-reported symptoms reflecting common (general distress) and distinct (anhedonic depression, anxious arousal) components of affective distress, and were interviewed about mental health history with a structured clinical interview. Multilevel modeling of IM and cortisol trajectories revealed IM and cortisol responses were positively coordinated on average, but varied across women. Greater affective distress predicted higher/increasing IM stress responses that diverged from cortisol recovery; history of mood disorder specifically related to increasing post-stress IM's, while current general distress related to non-coordination/divergence of IM from cortisol response. These findings highlight a novel stress response pathway characterizing both previous and current affective distress that may help efforts to ameliorate intergenerational impacts of perinatal stress.
多系统应激反应的良好调节协调对怀孕期间的代际健康尤其重要,此时母亲的应激系统通常会适应以保护胎儿。然而,关于免疫/炎症介质(IM)和下丘脑-垂体-肾上腺(HPA)轴对人类妊娠急性应激反应的模式知之甚少,更不用说与孕产妇健康风险相关的变异了。在这项研究中,我们旨在通过检测孕妇在社会心理应激反应中的唾液IM和皮质醇的关系,以及并发的情感困扰症状和情感障碍的终生诊断,来定义规范的围产期应激反应协调和潜在的风险概况。一个社区孕妇样本(n = 158)参与了纵向研究的第一个时间点,完成了Trier社会压力任务,并提供了5个唾液样本用于检测皮质醇;促炎因子il - 1β、il - 6、tnf - α;和c反应蛋白。他们自我报告的症状反映了情感痛苦的常见(一般痛苦)和独特(快感缺乏性抑郁,焦虑唤醒)成分,并通过结构化的临床访谈对他们进行了精神健康史采访。IM和皮质醇轨迹的多层次建模显示,IM和皮质醇反应平均是正协调的,但在女性中有所不同。更大的情感困扰预示着更高/增加的应激反应偏离皮质醇恢复;情绪障碍史特别与应激后IM增加有关,而当前的普遍痛苦与IM与皮质醇反应的不协调/偏离有关。这些发现强调了一种新的应激反应途径,可以描述以前和现在的情感困扰,这可能有助于改善围产期应激的代际影响。
{"title":"Coordination of inflammatory and adrenocortical stress response during pregnancy and variation by mental health","authors":"Heidemarie K. Laurent ,&nbsp;Sherryl H. Goodman ,&nbsp;Douglas A. Granger ,&nbsp;Penina M. Backer","doi":"10.1016/j.bbih.2025.101145","DOIUrl":"10.1016/j.bbih.2025.101145","url":null,"abstract":"<div><div>Well-regulated coordination of a multi-system stress response is particularly consequential for intergenerational health during pregnancy, when maternal stress systems typically adapt to protect the fetus. However, little is known about patterns of combined immune/inflammatory mediator (IM) and hypothalamic-pituitary-adrenal (HPA) axis responding to acute stress in human pregnancy, let alone variations associated with maternal health risks. In this study we aimed to define normative perinatal stress response coordination and potential risk profiles by testing relations among pregnant women's salivary IM's and cortisol in response to psychosocial stress, as well as both concurrent affective distress symptomatology and lifetime diagnoses of affective disorders. A community sample of pregnant women (<em>n</em> = 158) participating in the first timepoint of a longitudinal study completed the Trier Social Stress Task and contributed five saliva samples assayed for cortisol; pro-inflammatory cytokines IL1β, IL6, TNFα; and CRP. They self-reported symptoms reflecting common (general distress) and distinct (anhedonic depression, anxious arousal) components of affective distress, and were interviewed about mental health history with a structured clinical interview. Multilevel modeling of IM and cortisol trajectories revealed IM and cortisol responses were positively coordinated on average, but varied across women. Greater affective distress predicted higher/increasing IM stress responses that diverged from cortisol recovery; history of mood disorder specifically related to increasing post-stress IM's, while current general distress related to non-coordination/divergence of IM from cortisol response. These findings highlight a novel stress response pathway characterizing both previous and current affective distress that may help efforts to ameliorate intergenerational impacts of perinatal stress.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101145"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Early brain changes in Lyme disease are associated with clinical outcomes 莱姆病的早期大脑变化与临床结果相关
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-01 DOI: 10.1016/j.bbih.2025.101153
Cherie L. Marvel , Alison W. Rebman , Kylie H. Alm , Pegah Touradji , Arnold Bakker , Prianca A. Nadkarni , Deeya Bhattacharya , Owen P. Morgan , Amy Mistri , Christopher C. Sandino , Jonathan A. Ecker , Erica A. Kozero , Arun Venkatesan , Abhay Moghekar , Ashar A. Keeys , John N. Aucott
In Lyme disease (LD), 10–20 % of patients develop persistent symptoms following antibiotic treatment (i.e., post-treatment Lyme disease (PTLD)), which often includes neurological symptoms. This study tested the hypothesis that physiological brain changes occur early in LD and influence outcomes.
Task-based functional MRI (fMRI) and health surveys were administered to patients with acute LD (n = 20) after treatment and six months later. Demographically matched healthy controls (HC; n = 19) were also assessed six months apart. The LD group was categorized at six months into those who had returned to health (RTH, n = 11) or reported persistent symptoms (sPTLD, n = 9). FMRI data from both LD subgroups were compared to each other and HC at both time points. FMRI-guided regions of interest (ROI) values were compared to health surveys.
Baseline brain activity in RTH was elevated in fronto-parietal regions relative to sPTLD (p < .0025) and HC (p < .001). Notably, 64 % of activation clusters in RTH were in white matter, confirmed by segmentation analysis. FMRI-guided ROI values from RTH vs. HC correlated with higher health survey scores. At 6-months, few group differences remained. By contrast, sPTLD vs. HC fMRI comparisons yielded few activation differences at either time point or correlations with health survey scores.
Robust brain activity in early LD was associated with future RTH. By contrast, the absence of early brain activity was associated with persistent symptoms, suggesting that failure to mount an early response contributes to PTLD. Understanding how brain activity relates to recovery in LD can aid prognosis and guide treatment.
在莱姆病(LD)中,10 - 20%的患者在抗生素治疗后出现持续症状(即治疗后莱姆病(PTLD)),通常包括神经系统症状。本研究验证了脑生理变化发生在LD早期并影响预后的假设。对20例急性LD患者(n = 20)在治疗后和6个月后进行任务型功能磁共振成像(fMRI)和健康调查。人口统计学匹配的健康对照(HC, n = 19)也相隔6个月进行评估。LD组在6个月时被分为恢复健康(RTH, n = 11)和报告持续症状(sPTLD, n = 9)。两个LD亚组的FMRI数据相互比较,并在两个时间点对HC进行比较。将fmri引导的感兴趣区域(ROI)值与健康调查进行比较。与sPTLD和HC相比,RTH的额顶叶区基线脑活动升高(p < .001)。值得注意的是,通过分割分析,RTH中64%的激活簇位于白质中。fmri引导下RTH与HC的ROI值与较高的健康调查得分相关。6个月时,几乎没有组间差异。相比之下,sPTLD与HC的fMRI比较在任何时间点或与健康调查分数的相关性上都没有什么激活差异。LD早期活跃的大脑活动与未来的RTH相关。相比之下,早期大脑活动的缺乏与持续症状有关,这表明未能形成早期反应有助于PTLD的发生。了解脑活动与LD恢复的关系有助于预后和指导治疗。
{"title":"Early brain changes in Lyme disease are associated with clinical outcomes","authors":"Cherie L. Marvel ,&nbsp;Alison W. Rebman ,&nbsp;Kylie H. Alm ,&nbsp;Pegah Touradji ,&nbsp;Arnold Bakker ,&nbsp;Prianca A. Nadkarni ,&nbsp;Deeya Bhattacharya ,&nbsp;Owen P. Morgan ,&nbsp;Amy Mistri ,&nbsp;Christopher C. Sandino ,&nbsp;Jonathan A. Ecker ,&nbsp;Erica A. Kozero ,&nbsp;Arun Venkatesan ,&nbsp;Abhay Moghekar ,&nbsp;Ashar A. Keeys ,&nbsp;John N. Aucott","doi":"10.1016/j.bbih.2025.101153","DOIUrl":"10.1016/j.bbih.2025.101153","url":null,"abstract":"<div><div>In Lyme disease (LD), 10–20 % of patients develop persistent symptoms following antibiotic treatment (i.e., post-treatment Lyme disease (PTLD)), which often includes neurological symptoms. This study tested the hypothesis that physiological brain changes occur early in LD and influence outcomes.</div><div>Task-based functional MRI (fMRI) and health surveys were administered to patients with acute LD (n = 20) after treatment and six months later. Demographically matched healthy controls (HC; n = 19) were also assessed six months apart. The LD group was categorized at six months into those who had returned to health (RTH, n = 11) or reported persistent symptoms (sPTLD, n = 9). FMRI data from both LD subgroups were compared to each other and HC at both time points. FMRI-guided regions of interest (ROI) values were compared to health surveys.</div><div>Baseline brain activity in RTH was elevated in fronto-parietal regions relative to sPTLD (p &lt; .0025) and HC (p &lt; .001). Notably, 64 % of activation clusters in RTH were in white matter, confirmed by segmentation analysis. FMRI-guided ROI values from RTH vs. HC correlated with higher health survey scores. At 6-months, few group differences remained. By contrast, sPTLD vs. HC fMRI comparisons yielded few activation differences at either time point or correlations with health survey scores.</div><div>Robust brain activity in early LD was associated with future RTH. By contrast, the absence of early brain activity was associated with persistent symptoms, suggesting that failure to mount an early response contributes to PTLD. Understanding how brain activity relates to recovery in LD can aid prognosis and guide treatment.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101153"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Animal models of Huntington's disease. Pros and cons 亨廷顿舞蹈病的动物模型。利与弊
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-01 DOI: 10.1016/j.bbih.2025.101149
Polina Stepanova , Merja H. Voutilainen , Ove Eriksson , Dan Lindholm
Modelling of human neurological diseases uses a plethora of ever-more sophisticated methods and approaches. For Huntington's disease (HD), which affects specific neuronal types and circuits in the brain, this has meant the use of both neurotoxic compounds and various animal models of different complexity, ranging from rodents to non-primate ones. Genetic models are classified based on the use of specific constructs including gene including gene fragments, full-length, knock-out and knock-in models. In this review, we will discuss the available animal models for HD, highlighting their pros and cons in studying the neuropathology, behavioural alterations, and biological mechanisms that prevail in HD and during the disease progression. We also highlight present knowledge gaps and difficulties to fully recapitulate the human disease. At the end we will further elaborate on current outstanding questions in HD research that warrant further studies using both animal models and patient data. This may help to guide future research and increase the translational relevance of the models to solve key questions and pave the way for better treatment options and design of drugs to alleviate the course of HD.
人类神经系统疾病的建模使用了大量越来越复杂的方法和途径。亨廷顿舞蹈症(HD)影响大脑中特定的神经元类型和回路,这意味着要使用神经毒性化合物和各种不同复杂程度的动物模型,从啮齿动物到非灵长类动物。遗传模型的分类基于使用特定的结构,包括基因,包括基因片段,全长,敲除和敲入模型。在这篇综述中,我们将讨论现有的HD动物模型,强调它们在研究HD和疾病进展过程中普遍存在的神经病理学、行为改变和生物学机制方面的优缺点。我们还强调目前在全面概括人类疾病方面的知识差距和困难。最后,我们将进一步阐述当前HD研究中悬而未决的问题,这些问题需要进一步使用动物模型和患者数据进行研究。这可能有助于指导未来的研究,增加模型的翻译相关性,以解决关键问题,并为更好的治疗方案和药物设计铺平道路,以缓解HD的病程。
{"title":"Animal models of Huntington's disease. Pros and cons","authors":"Polina Stepanova ,&nbsp;Merja H. Voutilainen ,&nbsp;Ove Eriksson ,&nbsp;Dan Lindholm","doi":"10.1016/j.bbih.2025.101149","DOIUrl":"10.1016/j.bbih.2025.101149","url":null,"abstract":"<div><div>Modelling of human neurological diseases uses a plethora of ever-more sophisticated methods and approaches. For Huntington's disease (HD), which affects specific neuronal types and circuits in the brain, this has meant the use of both neurotoxic compounds and various animal models of different complexity, ranging from rodents to non-primate ones. Genetic models are classified based on the use of specific constructs including gene including gene fragments, full-length, knock-out and knock-in models. In this review, we will discuss the available animal models for HD, highlighting their pros and cons in studying the neuropathology, behavioural alterations, and biological mechanisms that prevail in HD and during the disease progression. We also highlight present knowledge gaps and difficulties to fully recapitulate the human disease. At the end we will further elaborate on current outstanding questions in HD research that warrant further studies using both animal models and patient data. This may help to guide future research and increase the translational relevance of the models to solve key questions and pave the way for better treatment options and design of drugs to alleviate the course of HD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101149"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gut microbiota–neuroinflammation axis: A new mechanism and therapeutic target for comorbid depression in epilepsy 肠道微生物群-神经炎症轴:癫痫共病抑郁的新机制和治疗靶点
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-01 DOI: 10.1016/j.bbih.2025.101150
Xiujuan wang , Mu Liu , Liuzhao Cao , Hao Huang , Juan Yang , Haiqing Zhang , chengyu pan , Zucai Xu
This review systematically summarizes the key pathological mechanisms and therapeutic potential of the gut microbiota–neuroinflammation axis in comorbid depression in epilepsy. Approximately 30–50 % of epilepsy patients suffer from depression, which leads to poor treatment adherence and significantly increases the risk of mortality and suicide. Studies have shown that dysbiosis of the gut microbiota and central nervous system inflammation interact through multiple pathways—including microbial metabolites, immune modulation, and the vagus nerve—to form a “gut–brain–emotion” regulatory network. Epilepsy patients often exhibit reduced diversity and abnormal composition of gut microbiota, most notably dysregulation of Firmicutes, which promotes systemic inflammation and activation of local central nervous system inflammation. Neuroinflammation, by affecting neurotransmitter metabolism, blood-brain barrier function, and neuroplasticity, exacerbates abnormal neuronal discharges and depressive symptoms, thereby creating a vicious cycle. Intervention strategies targeting this axis have shown promising prospects, including supplementation with probiotics or prebiotics, modulation of microbial metabolites, anti-inflammatory therapies, and dietary regulation, all of which can significantly improve both the frequency of epileptic seizures and emotional states. Multi-omics analysis and precise subtyping are advancing the development of individualized treatment plans, bridging the gaps among neuroscience, immunology, and microbiology. Although challenges remain in standardized sampling, causal mechanism validation, and long-term follow-up studies, the gut microbiota–neuroinflammation axis has emerged as a new frontier in the precise prevention and treatment of comorbid depression in epilepsy, providing a tangible theoretical foundation and practical strategies for improving patient outcomes.
本文系统地综述了肠道微生物群-神经炎症轴在癫痫共病抑郁中的主要病理机制和治疗潜力。大约30 - 50%的癫痫患者患有抑郁症,这导致治疗依从性差,并大大增加了死亡和自杀的风险。研究表明,肠道菌群失调和中枢神经系统炎症通过多种途径相互作用,包括微生物代谢物、免疫调节和迷走神经,形成“肠-脑-情绪”调节网络。癫痫患者通常表现出肠道微生物群多样性减少和组成异常,最明显的是厚壁菌门失调,这促进了全身炎症和局部中枢神经系统炎症的激活。神经炎症通过影响神经递质代谢、血脑屏障功能和神经可塑性,加剧异常神经元放电和抑郁症状,从而形成恶性循环。针对该轴的干预策略显示出良好的前景,包括补充益生菌或益生元,调节微生物代谢物,抗炎治疗和饮食调节,所有这些都可以显着改善癫痫发作的频率和情绪状态。多组学分析和精确分型正在推进个体化治疗计划的发展,弥合神经科学、免疫学和微生物学之间的差距。尽管在标准化采样、因果机制验证和长期随访研究方面仍存在挑战,但肠道微生物群-神经炎症轴已成为精准预防和治疗癫痫共病抑郁的新前沿,为改善患者预后提供了切实的理论基础和实践策略。
{"title":"Gut microbiota–neuroinflammation axis: A new mechanism and therapeutic target for comorbid depression in epilepsy","authors":"Xiujuan wang ,&nbsp;Mu Liu ,&nbsp;Liuzhao Cao ,&nbsp;Hao Huang ,&nbsp;Juan Yang ,&nbsp;Haiqing Zhang ,&nbsp;chengyu pan ,&nbsp;Zucai Xu","doi":"10.1016/j.bbih.2025.101150","DOIUrl":"10.1016/j.bbih.2025.101150","url":null,"abstract":"<div><div>This review systematically summarizes the key pathological mechanisms and therapeutic potential of the gut microbiota–neuroinflammation axis in comorbid depression in epilepsy. Approximately 30–50 % of epilepsy patients suffer from depression, which leads to poor treatment adherence and significantly increases the risk of mortality and suicide. Studies have shown that dysbiosis of the gut microbiota and central nervous system inflammation interact through multiple pathways—including microbial metabolites, immune modulation, and the vagus nerve—to form a “gut–brain–emotion” regulatory network. Epilepsy patients often exhibit reduced diversity and abnormal composition of gut microbiota, most notably dysregulation of Firmicutes, which promotes systemic inflammation and activation of local central nervous system inflammation. Neuroinflammation, by affecting neurotransmitter metabolism, blood-brain barrier function, and neuroplasticity, exacerbates abnormal neuronal discharges and depressive symptoms, thereby creating a vicious cycle. Intervention strategies targeting this axis have shown promising prospects, including supplementation with probiotics or prebiotics, modulation of microbial metabolites, anti-inflammatory therapies, and dietary regulation, all of which can significantly improve both the frequency of epileptic seizures and emotional states. Multi-omics analysis and precise subtyping are advancing the development of individualized treatment plans, bridging the gaps among neuroscience, immunology, and microbiology. Although challenges remain in standardized sampling, causal mechanism validation, and long-term follow-up studies, the gut microbiota–neuroinflammation axis has emerged as a new frontier in the precise prevention and treatment of comorbid depression in epilepsy, providing a tangible theoretical foundation and practical strategies for improving patient outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101150"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145736233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PPARγ as a predictive biomarker for antidepressant response in major depressive disorder: Insights from TNIP1 transcriptional regulation PPARγ作为重度抑郁症抗抑郁反应的预测性生物标志物:来自TNIP1转录调控的见解
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-12-01 DOI: 10.1016/j.bbih.2025.101151
Yu-Wei Lin , Daw-Yang Hwang , Yi-Yung Hung

Introduction

Major depressive disorder (MDD) is a debilitating disease possibly linked to immune defense mechanisms. TNIP1, a key anti-inflammatory regulator in NF-κB and TLR pathways, is implicated in MDD, but its transcriptional regulation and role in treatment response are unclear.

Methods

We analyzed mRNA expression of TNIP1 and 13 transcription factors in monocytes from pre- and post-treatment (4–6 weeks) MDD patients and healthy controls. Peripheral blood mononuclear cells were isolated, tagged by CD14, and mRNA was extracted and analyzed. Participants were recruited at Kaohsiung Chang Gung Memorial Hospital (2014–2025). ANCOVA, paired t-tests, and multiple linear regression adjusted for age, gender, BMI, and smoking were used to compare groups and predict treatment outcomes.

Results

This study encompassed 62 MDD patients and 52 healthy controls. Pre-treatment HAMD-17 averaged 23.90 ± 4.60, and post-treatment HAMD-17 averaged 8.43 ± 4.24. MDD patients showed higher PPAR-γ (p < 0.001), FOS (p = 0.023), and lower JUN (p = 0.029) expression than controls. Post-treatment, TNIP1 expression increased (p = 0.031). Lower pre-treatment PPAR-γ predicted greater symptom improvement (p = 0.016).

Conclusion

This study highlights the differential expression of PPAR-γ, FOS, and JUN in MDD patients, underscoring their potential roles in immune regulation. The association between lower pre-treatment PPAR-γ expression and improved treatment outcomes suggests its utility as a biomarker for predicting therapeutic response.
重度抑郁症(MDD)是一种衰弱性疾病,可能与免疫防御机制有关。TNIP1是NF-κB和TLR通路中的关键抗炎调节因子,与MDD有关,但其转录调控及其在治疗反应中的作用尚不清楚。方法分析治疗前、治疗后(4-6周)MDD患者和健康对照组单核细胞中TNIP1和13个转录因子的mRNA表达。分离外周血单个核细胞,用CD14标记,提取mRNA进行分析。参与者在高雄长工纪念医院招募(2014-2025)。采用ANCOVA、配对t检验和调整年龄、性别、BMI和吸烟的多元线性回归进行组间比较和预测治疗结果。结果本研究纳入了62例重度抑郁症患者和52例健康对照。预处理HAMD-17平均23.90±4.60,处理后HAMD-17平均8.43±4.24。MDD患者PPAR-γ (p < 0.001)、FOS (p = 0.023)和JUN (p = 0.029)表达均高于对照组。治疗后,TNIP1表达升高(p = 0.031)。较低的治疗前PPAR-γ预测更大的症状改善(p = 0.016)。结论本研究提示PPAR-γ、FOS和JUN在MDD患者中的差异表达,提示其在免疫调节中的潜在作用。治疗前较低的PPAR-γ表达与改善的治疗结果之间的关联表明其作为预测治疗反应的生物标志物的实用性。
{"title":"PPARγ as a predictive biomarker for antidepressant response in major depressive disorder: Insights from TNIP1 transcriptional regulation","authors":"Yu-Wei Lin ,&nbsp;Daw-Yang Hwang ,&nbsp;Yi-Yung Hung","doi":"10.1016/j.bbih.2025.101151","DOIUrl":"10.1016/j.bbih.2025.101151","url":null,"abstract":"<div><h3>Introduction</h3><div>Major depressive disorder (MDD) is a debilitating disease possibly linked to immune defense mechanisms. TNIP1, a key anti-inflammatory regulator in NF-κB and TLR pathways, is implicated in MDD, but its transcriptional regulation and role in treatment response are unclear.</div></div><div><h3>Methods</h3><div>We analyzed mRNA expression of TNIP1 and 13 transcription factors in monocytes from pre- and post-treatment (4–6 weeks) MDD patients and healthy controls. Peripheral blood mononuclear cells were isolated, tagged by CD14, and mRNA was extracted and analyzed. Participants were recruited at Kaohsiung Chang Gung Memorial Hospital (2014–2025). ANCOVA, paired t-tests, and multiple linear regression adjusted for age, gender, BMI, and smoking were used to compare groups and predict treatment outcomes.</div></div><div><h3>Results</h3><div>This study encompassed 62 MDD patients and 52 healthy controls. Pre-treatment HAMD-17 averaged 23.90 ± 4.60, and post-treatment HAMD-17 averaged 8.43 ± 4.24. MDD patients showed higher PPAR-γ (<em>p</em> &lt; 0.001), FOS (<em>p</em> = 0.023), and lower JUN (<em>p</em> = 0.029) expression than controls. Post-treatment, TNIP1 expression increased (<em>p</em> = 0.031). Lower pre-treatment PPAR-γ predicted greater symptom improvement (<em>p</em> = 0.016).</div></div><div><h3>Conclusion</h3><div>This study highlights the differential expression of PPAR-γ, FOS, and JUN in MDD patients, underscoring their potential roles in immune regulation. The association between lower pre-treatment PPAR-γ expression and improved treatment outcomes suggests its utility as a biomarker for predicting therapeutic response.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101151"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Brain, behavior, & immunity - health
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1