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The role of social support on change in C-reactive Protein and BMI among youth with and without child maltreatment history 社会支持对有和无儿童虐待史青少年c反应蛋白和BMI变化的影响
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-28 DOI: 10.1016/j.bbi.2025.106250
Savannah A. Girod , Aishwarya Ganguli , Yo Jackson , Christine Heim , Idan Shalev , Eric Claus , Zachary Fisher , Jennie Noll , Chad Shenk , Hannah M.C. Schreier
Child maltreatment (CM) has long-term consequences for metabolic and inflammatory processes, but it is unclear when these associations emerge and whether other psychosocial resources (e.g., social support), can moderate these associations. This study examined (1) the extent to which a history of CM investigation was associated with changes in youth high-sensitivity C-reactive protein (hs-CRP) and body mass index (BMI) across a two-year period, and (2) the moderating role of social support from different sources (caregivers, siblings, and peers) on this association. Participants included 318 youth (ages 8–13, 49.7 % female, 72 % white, 82.7 % with past CM investigation) who completed baseline (Time 1) and two-year follow up (Time 2) visits. CM history, hs-CRP and BMI were assessed at T1. Caregiver, peer, and sibling support, hs-CRP, and BMI were assessed at T2. Adjusting for youth age, sex, race/ethnicity, household income, and hs-CRP and BMI at Time 1, no main effects of CM history on Time 2 hs-CRP or BMI were found (ps > 0.28). However, independent of CM history, greater peer support was associated with lower BMI at Time 2 (β = -0.10, p = 0.005). Peer support further moderated the association between CM history and Time 2 BMI (β = -0.16, p = 0.007), such that CM history was associated with higher BMI only when peer support was relatively lower. Additionally, independent of CM history, greater sibling support was associated with lower hs-CRP at Time 2 (β = -0.09, p = 0.03). Post-hoc sensitivity analyses suggested unique effects when considering the number of types of CM experienced. Experiencing more types of CM was associated with greater Time 2 hs-CRP only when peer support was relatively lower (β = 0.07, p = 0.048). Additionally, youth who experienced more types of CM and who had higher levels of sibling support showed lower Time 2 hs-CRP (β = -0.15, p = 0.03). Overall, findings suggest that independent of CM history, greater sibling and peer support were associated with lower hs-CRP and BMI across a two-year period. Although there were no main effects of CM, greater peer support buffered the longitudinal effects of CM history on youth BMI. Additionally, in the context of experiencing multiple types of CM, greater levels of peer and sibling support functioned as protective factors.
儿童虐待(CM)对代谢和炎症过程具有长期影响,但尚不清楚这些关联何时出现,以及其他社会心理资源(如社会支持)是否可以调节这些关联。本研究考察了(1)CM调查史与青少年高敏感性c反应蛋白(hs-CRP)和体重指数(BMI)变化的关联程度,以及(2)不同来源的社会支持(照顾者、兄弟姐妹和同伴)在这种关联中的调节作用。参与者包括318名青少年(年龄8-13岁,49.7% %女性,72 %白人,82.7 %既往CM调查),他们完成了基线(时间1)和两年随访(时间2)。T1时评估CM病史、hs-CRP和BMI。T2时评估照顾者、同伴和兄弟姐妹支持、hs-CRP和BMI。调整了年龄、性别、种族/民族、家庭收入和时间1时的hs-CRP和BMI,没有发现CM病史对时间2时hs-CRP或BMI的主要影响(ps > 0.28)。然而,与CM病史无关,更多的同伴支持与时间2时较低的BMI相关(β = -0.10,p = 0.005)。同伴支持进一步调节CM病史与Time 2 BMI之间的关系(β = -0.16,p = 0.007),因此CM病史仅在同伴支持相对较低时才与较高的BMI相关。此外,与CM病史无关,兄弟姐妹的支持与时间2时hs-CRP降低相关(β = -0.09,p = 0.03)。事后敏感性分析表明,当考虑到所经历的CM类型的数量时,具有独特的效果。仅当同伴支持相对较低时,CM类型较多与Time 2 hs-CRP升高相关(β = 0.07,p = 0.048)。此外,经历更多类型CM和兄弟姐妹支持水平较高的青少年表现出较低的Time - 2 hs-CRP (β = -0.15,p = 0.03)。总的来说,研究结果表明,在两年的时间里,与CM病史无关,兄弟姐妹和同伴的支持与较低的hs-CRP和BMI有关。虽然CM没有主要影响,但更大的同伴支持缓冲了CM史对青少年BMI的纵向影响。此外,在经历多种类型CM的情况下,更高水平的同伴和兄弟姐妹支持是保护因素。
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引用次数: 0
Dissecting the genetic relationship between severe mental disorders and autoimmune diseases 剖析严重精神障碍与自身免疫性疾病之间的遗传关系。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-28 DOI: 10.1016/j.bbi.2025.106249
Erik D. Wiström , Julian Fuhrer , Alexey Shadrin , Vera Fominykh , Kevin S. O’Connell , Piotr Jaholkowski , Nils Eiel Steen , Sara E. Stinson , Pravesh Parekh , Oleksandr Frei , Linn Rødevand , Nadine Parker , Jan Haavik , Srdjan Djurovic , Anders M. Dale , Ole A. Andreassen , Olav B. Smeland
Severe mental disorders have been linked to immune system dysfunction. While a genetic association between mental disorders and autoimmune diseases has been suggested, their genetic relationship remains incompletely understood. Utilizing a complementary set of statistical analyses, we conducted a comprehensive investigation of the genetic architecture between severe mental disorders (major depression (MD), bipolar disorder (BD), and schizophrenia (SCZ)) and seven autoimmune diseases (autoimmune thyroiditis, celiac disease, inflammatory bowel disease (IBD), multiple sclerosis, psoriasis, rheumatoid arthritis, and type 1 diabetes), involving a total of 667,518 cases from 10 genome-wide association studies. While MD was positively genetically correlated with five autoimmune diseases, BD and SCZ were only positively correlated with IBD, suggesting differences in the genetic signal shared with autoimmunity across these mental disorders. A considerable fraction of genetic variants influencing autoimmune diseases (range 17.1–88.4 %) was estimated to overlap with mental disorders; however, this constitutes only a minor part of genetic variants influencing the more polygenic mental disorders. Finally, we identified 172 genetic loci jointly affecting mental disorders and autoimmune diseases, implicating both lipid metabolism and TNF signaling. In conclusion, MD, BD, and SCZ have a small but distinct genetic overlap with autoimmune diseases, which may inform new possible immune targets for treatment in mental illness.
严重的精神障碍与免疫系统功能障碍有关。虽然已经提出了精神障碍和自身免疫性疾病之间的遗传关联,但它们的遗传关系仍然不完全清楚。利用一组互补的统计分析,我们对严重精神障碍(重度抑郁症(MD)、双相情感障碍(BD)和精神分裂症(SCZ))与7种自身免疫性疾病(自身免疫性甲状腺炎、乳糜泻、炎症性肠病(IBD)、多发性硬化症、牛皮癣、类风湿性关节炎和1型糖尿病)之间的遗传结构进行了全面调查,涉及来自10项全基因组关联研究的667,518例病例。虽然MD与5种自身免疫性疾病呈正相关,但BD和SCZ仅与IBD呈正相关,这表明这些精神障碍与自身免疫共有的遗传信号存在差异。据估计,影响自身免疫性疾病的相当一部分遗传变异(范围17.1- 88.4%)与精神障碍重叠;然而,这只是影响多基因精神障碍的遗传变异的一小部分。最后,我们确定了172个共同影响精神障碍和自身免疫性疾病的遗传位点,涉及脂质代谢和TNF信号。总之,MD、BD和SCZ与自身免疫性疾病有微小但明显的遗传重叠,这可能为精神疾病治疗提供新的可能的免疫靶点。
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引用次数: 0
Deletion of the microglial phagocytic receptor MerTK mimics early-life adversity-induced changes in synapses and behavior in male mice 小胶质吞噬受体MerTK的缺失模拟了雄性小鼠早期逆境诱导的突触和行为变化。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-25 DOI: 10.1016/j.bbi.2025.106246
Madison M. Garvin , Urjoshi Kar , Cassandra L. Kooiker , Jessica L. Bolton
<div><div>Early-life adversity (ELA) is a significant risk factor for emotional disorders like depression, likely due to changes in stress-related circuit development. We have previously shown that ELA increases the number of excitatory synapses onto corticotropin-releasing hormone (CRH)-expressing neurons in the paraventricular nucleus (PVN) by decreasing microglial synapse engulfment. Here, we hypothesize that ELA induces microglial dysfunction via inhibition of the microglial phagocytic receptor, MerTK, thus resulting in the observed changes in synapses and stress-related behavior. To determine whether deleting MerTK in microglia phenocopies the effects of ELA, microglia-specific conditional knockout (m)MerTK-KO (CX3CR1-Cre<sup>+</sup>::MerTK<sup>fl/fl</sup>) mice were crossed with ‘wild-type’ (CX3CR1-Cre<sup>-</sup>::MerTK<sup>fl/fl</sup>) mice, and their litters were reared in either a control or ELA (induced by limited bedding and nesting) environment, from postnatal days (P)2–10. Excitatory synapses in the PVN were assessed at P10, microglial engulfment was assessed at P8, and adult offspring were tested in a behavioral battery to measure threat-response (known to be dependent on PVN-CRH+ neurons) and anxiety-like behavior, followed by acute restraint stress to measure the neuroendocrine stress response. Following ELA at P10, we find that excitatory, but not inhibitory, synapses in the PVN are increased in males, which is mimicked by mMerTK-KO in control males, but causes no further increase in ELA males. Correspondingly, ELA and mMerTK-KO decrease microglial engulfment of excitatory presynaptic terminals at P8 in males. In contrast, females already have higher numbers of excitatory synapses at baseline, and exhibit no further increase with ELA or mMerTK-KO. Remarkably, the pattern of threat-response behavior in males closely matches the excitatory synapses, with mMerTK-KO control males escaping more from the simulated predator threat in the looming-shadow threat task, similar to ELA males. Again, females do not show any significant changes due to ELA or mMerTK-KO in the threat-response, although they do exhibit ELA-induced changes in anxiety-like behavior. ELA provokes a greater corticosterone response to acute stress in males, but not females, although females were again already higher at baseline. In sum, our results demonstrate that ELA provokes decreased microglial engulfment during development, leading to increased excitatory synapses in the PVN and an increased active response to threat in the looming-shadow test in males only. Deleting MerTK specifically from microglia recapitulates both the synaptic and behavioral effects in control males, but does not have an effect in ELA males or control females, suggesting that the MerTK pathway is already inhibited by ELA in males and less active in females at baseline. Our work is the first to elucidate the mechanisms underlying the male-biased microglial dysfunction caused by ELA, with prom
早期生活逆境(ELA)是抑郁症等情绪障碍的重要风险因素,可能会引发与压力相关的神经回路发育的变化。我们之前的研究表明,ELA通过减少小胶质突触的吞噬,增加了室旁核(PVN)中表达促肾上腺皮质激素释放激素(CRH)的神经元上的兴奋性突触的数量。在这里,我们假设ELA通过抑制小胶质吞噬受体MerTK诱导小胶质功能障碍,从而导致观察到的突触和应激相关行为的变化。为了确定在小胶质细胞中删除MerTK是否会影响ELA的作用,将小胶质细胞特异性条件敲除(m)MerTK- ko (CX3CR1-Cre+::MerTKfl/fl)小鼠与“野生型”(CX3CR1-Cre-::MerTKfl/fl)小鼠杂交,并将它们的窝仔从出生后2-10天(P)开始饲养在对照或ELA(由有限的床上和筑巢诱导)环境中。在P10时评估PVN中的兴奋性突触,在P8时评估小胶质吞噬,并在行为电池中测试成年后代以测量威胁反应(已知依赖PVN- crh + 神经元)和焦虑样行为,随后进行急性约束应激以测量神经内分泌应激反应。在P10发生ELA后,我们发现雄性PVN中的兴奋性突触增加,而不是抑制性突触增加,这在对照雄性中被mMerTK-KO模仿,但ELA雄性没有进一步增加。相应地,ELA和mMerTK-KO减少雄性P8兴奋性突触前末端的小胶质吞噬。相比之下,雌性在基线时已经有更多的兴奋性突触,并且在ELA或mMerTK-KO组中没有进一步增加。值得注意的是,雄性的威胁-反应行为模式与兴奋性突触密切匹配,mMerTK-KO控制的雄性在隐现阴影威胁任务中更多地逃避模拟捕食者的威胁,与ELA雄性相似。同样,女性在威胁反应中没有表现出ELA或mMerTK-KO的显著变化,尽管她们确实表现出ELA引起的焦虑样行为的变化。ELA在男性中对急性应激的皮质酮反应更强,而在女性中没有,尽管女性在基线时已经更高了。总之,我们的研究结果表明,ELA在发育过程中引起小胶质细胞吞噬减少,导致PVN中兴奋性突触增加,并且在阴影测试中对威胁的积极反应增加。从小胶质细胞中特异性删除MerTK在对照雄性小鼠中具有突触和行为效应,但对ELA雄性小鼠和对照组雌性小鼠均无影响,这表明MerTK通路在雄性小鼠中已被ELA抑制,而雌性小鼠在基线时活性较低。我们的研究首次阐明了由ELA引起的男性偏向性小胶质细胞功能障碍的机制,有望为高危儿童开发更好的预防和治疗策略。
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引用次数: 0
Neural oscillations serving abstract reasoning are differentially associated with inflammatory markers in people with HIV 在艾滋病毒感染者中,服务于抽象推理的神经振荡与炎症标志物存在差异。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-24 DOI: 10.1016/j.bbi.2025.106236
Tony W. Wilson , Mikki Schantell , Sarah M. Dietz , Samantha H. Penhale , Kellen M. McDonald , Kyla R. De Luca , Molly E. Voller , Lan D. Volberding , Olivia R. Carusi , Lucy K. Horne , Yasra Arif , Ryan Glesinger , Jason A. John , Hannah J. Okelberry , Pamela E. May-Weeks , Adam J. Case , Matthew C. Zimmerman , Rachel K. Spooner

Introduction

Despite living a normal lifespan, people with HIV (PWH) are at a much greater risk of developing cognitive impairment. While the precise mechanisms are not fully understood, persistently high inflammation levels are thought to be a key contributor, as multiple studies have linked cognitive impairment and elevated inflammation. In contrast, evidence of a relationship between neural function and inflammatory activity is extremely limited in PWH and/or controls. Thus, in the current study, we integrate state-of-the-art dynamic functional brain mapping with measures of three inflammatory markers that have been widely reported as elevated in PWH.

Methods

A total of 142 participants (range: 20–66 years old; 64 PWH and 78 controls) completed a validated abstract reasoning task during magnetoencephalographic (MEG) imaging, underwent comprehensive neuropsychological testing, and provided a blood sample for plasma-based inflammatory marker analysis of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interferon γ-induced protein 10 (IP-10). The two groups were matched on age, sex, race/ethnicity, body-mass index (BMI), handedness, anxiety, substance use, and common medical conditions such as diabetes. Oscillatory neural responses supporting abstract reasoning were imaged by applying a beamformer to the processed MEG data, and whole-brain, voxel-wise analyses were conducted using each individual’s CRP, TNF-α and IP-10 concentrations, controlling for age and BMI, to identify the differential impact of inflammation on oscillatory neural dynamics in PWH.

Results

PWH exhibited significantly higher levels on each of the three inflammatory markers and performed more poorly on the abstract reasoning task than matched controls, with CRP levels being significantly related to performance across all participants. Critically, TNF-α levels were significantly related to the strength of theta oscillations during abstract reasoning in the left inferior frontal gyrus, with higher TNF-α scaling with weaker theta and the strength of this relationship differing by group. A similar relationship among increasing CRP levels and decreasing gamma oscillations was found in the left inferior parietal cortices, while increasing CRP was also associated with decreasing gamma in the right dorsolateral prefrontal cortex across both groups, with the latter being coupled to behavioral performance in controls.

Discussion

These findings provide the first evidence linking elevated inflammatory levels to altered brain dynamics and performance in PWH. Such data provides crucial empirical evidence supporting the long-held view that elevated inflammation may be central to the higher rates of cognitive decline in PWH. Future work should examine whether decreasing these inflammatory levels leads to improvements in cognitive function in PWH.
导读:尽管过着正常的生活,但艾滋病毒感染者(PWH)发生认知障碍的风险要大得多。虽然确切的机制尚不完全清楚,但持续的高炎症水平被认为是一个关键因素,因为多项研究已将认知障碍和炎症升高联系起来。相比之下,在PWH和/或对照组中,神经功能和炎症活动之间关系的证据极为有限。因此,在当前的研究中,我们将最先进的动态功能脑测绘与三种炎症标志物的测量相结合,这三种炎症标志物已被广泛报道在PWH中升高。方法:共有142名参与者(年龄范围:20-66岁 ;64名PWH和78名对照组)在脑磁图(MEG)成像期间完成了一项经过验证的抽象推理任务,进行了全面的神经心理测试,并提供了血液样本用于基于血浆的炎症标志物分析c反应蛋白(CRP)、肿瘤坏死因子α (TNF-α)和干扰素γ诱导蛋白10 (IP-10)。这两组在年龄、性别、种族/民族、身体质量指数(BMI)、用手习惯、焦虑、物质使用和糖尿病等常见疾病方面进行了匹配。通过将波束形成器应用于处理后的MEG数据,对支持抽象推理的振荡神经反应进行成像,并使用每个个体的CRP, TNF-α和IP-10浓度进行全脑体素分析,控制年龄和BMI,以确定炎症对PWH中振荡神经动力学的差异影响。结果:PWH在三种炎症标志物上都表现出明显更高的水平,在抽象推理任务上的表现比匹配的对照组更差,CRP水平与所有参与者的表现显著相关。关键的是,TNF-α水平与左额下回抽象推理期间的θ波振荡强度显著相关,TNF-α水平越高θ波振荡强度越弱,且这种关系的强度因组而异。在左顶叶下皮层中,CRP水平的升高和伽马振荡的减少之间也存在类似的关系,而在两组中,CRP水平的升高也与右背外侧前额叶皮层中伽马的降低有关,后者与对照组的行为表现有关。讨论:这些发现提供了第一个将炎症水平升高与PWH患者脑动力学和表现改变联系起来的证据。这些数据提供了重要的经验证据,支持长期以来的观点,即炎症升高可能是PWH患者认知能力下降率较高的核心。未来的工作应该研究降低这些炎症水平是否会导致PWH患者认知功能的改善。
{"title":"Neural oscillations serving abstract reasoning are differentially associated with inflammatory markers in people with HIV","authors":"Tony W. Wilson ,&nbsp;Mikki Schantell ,&nbsp;Sarah M. Dietz ,&nbsp;Samantha H. Penhale ,&nbsp;Kellen M. McDonald ,&nbsp;Kyla R. De Luca ,&nbsp;Molly E. Voller ,&nbsp;Lan D. Volberding ,&nbsp;Olivia R. Carusi ,&nbsp;Lucy K. Horne ,&nbsp;Yasra Arif ,&nbsp;Ryan Glesinger ,&nbsp;Jason A. John ,&nbsp;Hannah J. Okelberry ,&nbsp;Pamela E. May-Weeks ,&nbsp;Adam J. Case ,&nbsp;Matthew C. Zimmerman ,&nbsp;Rachel K. Spooner","doi":"10.1016/j.bbi.2025.106236","DOIUrl":"10.1016/j.bbi.2025.106236","url":null,"abstract":"<div><h3>Introduction</h3><div>Despite living a normal lifespan, people with HIV (PWH) are at a much greater risk of developing cognitive impairment. While the precise mechanisms are not fully understood, persistently high inflammation levels are thought to be a key contributor, as multiple studies have linked cognitive impairment and elevated inflammation. In contrast, evidence of a relationship between neural function and inflammatory activity is extremely limited in PWH and/or controls. Thus, in the current study, we integrate state-of-the-art dynamic functional brain mapping with measures of three inflammatory markers that have been widely reported as elevated in PWH.</div></div><div><h3>Methods</h3><div>A total of 142 participants (range: 20–66 years old; 64 PWH and 78 controls) completed a validated abstract reasoning task during magnetoencephalographic (MEG) imaging, underwent comprehensive neuropsychological testing, and provided a blood sample for plasma-based inflammatory marker analysis of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interferon γ-induced protein 10 (IP-10). The two groups were matched on age, sex, race/ethnicity, body-mass index (BMI), handedness, anxiety, substance use, and common medical conditions such as diabetes. Oscillatory neural responses supporting abstract reasoning were imaged by applying a beamformer to the processed MEG data, and whole-brain, voxel-wise analyses were conducted using each individual’s CRP, TNF-α and IP-10 concentrations, controlling for age and BMI, to identify the differential impact of inflammation on oscillatory neural dynamics in PWH.</div></div><div><h3>Results</h3><div>PWH exhibited significantly higher levels on each of the three inflammatory markers and performed more poorly on the abstract reasoning task than matched controls, with CRP levels being significantly related to performance across all participants. Critically, TNF-α levels were significantly related to the strength of theta oscillations during abstract reasoning in the left inferior frontal gyrus, with higher TNF-α scaling with weaker theta and the strength of this relationship differing by group. A similar relationship among increasing CRP levels and decreasing gamma oscillations was found in the left inferior parietal cortices, while increasing CRP was also associated with decreasing gamma in the right dorsolateral prefrontal cortex across both groups, with the latter being coupled to behavioral performance in controls.</div></div><div><h3>Discussion</h3><div>These findings provide the first evidence linking elevated inflammatory levels to altered brain dynamics and performance in PWH. Such data provides crucial empirical evidence supporting the long-held view that elevated inflammation may be central to the higher rates of cognitive decline in PWH. Future work should examine whether decreasing these inflammatory levels leads to improvements in cognitive function in PWH.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106236"},"PeriodicalIF":7.6,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Acute ischaemic stroke alters the composition and function of circulating B cells 急性缺血性中风改变循环B细胞的组成和功能。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-24 DOI: 10.1016/j.bbi.2025.106244
Mehwish Younas , Harry R. Deijnen , Ruth Stephens , Alison Harris , Thomas O. Williams , Sabrina Tamburrano , Ian E. Prise , Craig J. Smith , Stuart M. Allan , Laura McCulloch , John R. Grainger , Barry W. McColl
Distinct B cell populations are found in circulation, including those with innate-like properties, that have varied functions in pathogen protection, vaccination and immunoregulation. The effects of tissue injury on circulating B cell populations are poorly explored. Here we show that, following acute ischaemic stroke (AIS), a common cause of neurological disability associated with systemic immune dysfunction, the circulating B cell compartment has altered functionality, alongside marked reductions in marginal zone (MZ)-like B cells, an innate-like B cell subset. Of note, release of Immunoglobulin (Ig) M, a key innate-like B cell-derived factor important in anti-bacterial responses, and regulatory cytokines including IL-6 and IL-10, was impaired upon stimulation of sorted B cells from AIS patients. B cells express adrenergic receptors (ARs), in both control and AIS patients, and release of the β2-AR agonist noradrenaline (NA) is elevated acutely following stroke. In vitro exposure of B cells from healthy individuals to NA recapitulated some of the functional modulation observed in AIS patients. Moreover, increased cell death of MZ-like B cells was observed in response to NA. Secondary infection is a common post-stroke complication that could be responsible for altered B cell characteristics. However, in line with the impact of NA on B cell populations, alterations were largely driven by stroke rather than secondary infection. Taken together, these findings demonstrate that neuroimmune factors are an important signal that could rapidly modify defined B cell populations early after tissue injury and highlight altered innate-like B cell function as a previously unappreciated characteristic of the systemic immunological response to acute stroke.
在循环中发现不同的B细胞群,包括那些具有先天样特性的B细胞群,它们在病原体保护、疫苗接种和免疫调节方面具有不同的功能。组织损伤对循环B细胞群的影响尚不清楚。在这里,我们表明,急性缺血性中风(AIS)是与全身免疫功能障碍相关的神经功能障碍的常见原因,在急性缺血性中风(AIS)之后,循环B细胞区室的功能发生了改变,同时边缘区(MZ)样B细胞(先天样B细胞亚群)也显著减少。值得注意的是,免疫球蛋白(Ig) M是一种关键的先天样B细胞衍生因子,在抗菌反应中起重要作用,以及包括IL-6和IL-10在内的调节性细胞因子的释放在AIS患者分选B细胞的刺激下受损。B细胞表达肾上腺素能受体,在对照组和AIS患者中,β2-AR激动剂去甲肾上腺素(NA)的释放在卒中后急剧升高。健康个体的B细胞在体外暴露于NA,再现了在AIS患者中观察到的一些功能调节。此外,NA对mz样B细胞的反应增加了细胞死亡。继发性感染是卒中后常见的并发症,可导致B细胞特征改变。然而,与NA对B细胞群的影响一致,改变主要是由中风而不是继发感染引起的。综上所述,这些发现表明,神经免疫因子是一个重要的信号,可以在组织损伤后早期迅速改变确定的B细胞群,并强调先天样B细胞功能的改变是急性卒中全身免疫反应的一个以前未被认识的特征。
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引用次数: 0
Social factors as buffers for the adverse impact of adverse childhood experiences on biological age acceleration among adults in Hispanic Community Health Study / Study of Latinos 社会因素缓冲不良童年经历对西班牙裔社区健康研究/拉丁裔研究中成年人生理年龄加速的不利影响
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-22 DOI: 10.1016/j.bbi.2025.106241
Yinxian Chen , Sarina Abrishamcar , Jasmine K. Aqua , Christian Dye , Linda C. Gallo , Maria M. Llabre , Frank J. Penedo , Carmen R. Isasi , Krista M. Perreira , Bharat Thyagarajan , Martha Daviglus , Amber Pirzada , Andrea Baccarelli , Karen N. Conneely , Rebecca Jones-Antwi , Shakira F. Suglia

Background

This study examined whether social factors, including social support, social networks, and familism, modify the longitudinal association between ACEs and epigenetic age acceleration (EAA).

Methods

We analyzed DNA methylation (DNAm) profile data from two visits (approximately six years apart) among 960 Hispanic/Latino adults in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). GrimAge epigenetic age and DunedinPACE pace of aging were used. Linear mixed models examined effect modification of social support, social networks (network diversity and the number of embedded networks), and familism (family obligation, support, and as referents) on the association between high vs. low-to-moderate ACEs (i.e., ≥ 4 vs. < 4 ACEs) and repeatedly measured EAA. Models adjusted for age, sex, parental education, childhood economic hardship, nativity, and cell-type proportions. We also dichotomized the levels of social support and both subscales of social networks to low (≤ 75th percentile) and high (> 75th percentile), and assessed joint effect modification by social support and networks.

Results

The mean difference in GrimAge acceleration (AgeAccelGrim) between high and low-to-moderate ACEs was statistically significantly attenuated when social support levels were higher (β for interaction = -0.73 years; 95 % CI: −1.23, −0.24; p = 0.003). No evidence of effect modification was found for social networks or familism. Having only high social support (β for interaction = -1.40 years; 95 % CI: −2.79, −0.01; p = 0.049) or both high social support and network diversity (β for interaction = -1.57 years; 95 % CI: −2.72, −0.42; p = 0.008) significantly decreased the mean difference in AgeAccelGrim between high and low-to-moderate ACEs.

Conclusion

Social support may independently buffer the adverse impact of ACEs on biological age acceleration among Hispanic/Latino adults, and the buffering effect may be stronger when accompanied by diverse social networks.
背景:本研究探讨了社会支持、社会网络和家族主义等社会因素是否改变了ace与表观遗传年龄加速(EAA)之间的纵向关联。方法:我们分析了西班牙裔社区健康研究/拉丁裔研究(HCHS/SOL)中960名西班牙裔/拉丁裔成年人两次访问(间隔约6年)的DNA甲基化(DNAm)数据。采用GrimAge表观遗传年龄和DunedinPACE衰老速度。线性混合模型检验了社会支持、社会网络(网络多样性和嵌入网络的数量)和家庭主义(家庭义务、支持和作为参考)对高与低至中度ace(即≥4 vs 第75百分位)之间关联的效应修正,并评估了社会支持和网络的联合效应修正。结果:当社会支持水平较高时,高、低中度ace之间的平均grage加速(AgeAccelGrim)差异有统计学意义(β交互作用 = -0.73 年;95 % CI: -1.23, -0.24; p = 0.003)。没有证据表明社会网络或家庭主义的影响会改变。只有高社会支持(β互动 = -1.40 年;95年 % CI: -2.79, -0.01; p = 0.049)或高社会支持和网络多样性(β互动 = -1.57 年;95年 % CI: -2.72, -0.42; p = 0.008)显著下降的平均差AgeAccelGrim高和中度ace之间。结论:社会支持可以独立地缓冲ace对西班牙/拉丁裔成人生理年龄加速的不利影响,并且当社会网络多样化时,缓冲作用可能更强。
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引用次数: 0
Inflammation, metabolic dysregulation, and depression profiles related to anhedonia and atypical, energy-related symptoms 与快感缺乏和非典型能量相关症状相关的炎症、代谢失调和抑郁概况。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-22 DOI: 10.1016/j.bbi.2025.106240
J.C. Zwiep , F. Lamers , C.H. Vinkers , N.J.A. van der Wee , B.W.J.H. Penninx , L. Nawijn , Y. Milaneschi

Introduction

Depression manifests heterogenous bio-clinical profiles. Anhedonia has been previously linked to inflammation. Other research has associated inflammation and metabolic dysregulations with atypical, energy-related depressive symptoms (AES). In the present study, we examined the associations of inflammation and metabolic dysregulations with anhedonia and compared these associations with those of inflammation and metabolic dysregulations with AES, and with a negative control symptom profile, previously shown unrelated to inflammation and metabolic dysregulation.

Methods

Data was from 2,981 persons of the Netherlands Study of Depression and Anxiety (NESDA). Inflammatory markers included C-reactive protein (CRP), Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), and glycoprotein acetyls. Metabolic markers were body mass index (BMI), waist circumference, triglycerides, high-density-lipoprotein cholesterol (HDL cholesterol), glucose and leptin. Anhedonia, AES and negative control symptom profiles were based on sum scores from different items from the Inventory of Depressive Symptomatology Self-Report (IDS-SR). The results were internally replicated in NESDA’s 6-year follow-up (N = 2,256).

Results

Anhedonia was positively associated with IL-6, glycoprotein acetyls, BMI, waist circumference, triglycerides, glucose, and leptin (β ranging from 0.063 to 0.122) and negatively associated with HDL cholesterol (β = -0.063). Associations were only partially explained by major lifestyle and health-related factors and confirmed at 6-year follow-up (r = 0.939 correlation between estimates at baseline and follow-up). AES showed highly consistent associations with the markers, with relatively larger effects as compared to anhedonia, while the negative control symptoms were linked only to higher glycoprotein acetyls.

Conclusion

Our results indicate consistent associations between several markers of inflammation and metabolic dysregulation with anhedonia and AES. Full characterization of depression profiles and their complex interrelations should be leveraged in future clinical research to select specific subgroup of depressed patients and develop more targeted treatment approaches.
简介:抑郁症表现出异质的生物临床特征。快感缺乏先前与炎症有关。其他研究将炎症和代谢失调与非典型能量相关抑郁症状(AES)联系起来。在本研究中,我们研究了炎症和代谢失调与快感缺乏症的关联,并将这些关联与炎症和代谢失调与AES的关联进行了比较,并与阴性对照症状进行了比较,这些症状之前被证明与炎症和代谢失调无关。方法:数据来自荷兰抑郁与焦虑研究(NESDA)的2981人。炎症标志物包括c反应蛋白(CRP)、白细胞介素-6 (IL-6)、肿瘤坏死因子α (TNF-α)和糖蛋白乙酰基。代谢指标为体重指数(BMI)、腰围、甘油三酯、高密度脂蛋白胆固醇(HDL胆固醇)、葡萄糖和瘦素。快感缺乏症、AES和阴性对照症状概况基于抑郁症状自我报告量表(IDS-SR)中不同项目的总得分。该结果在NESDA的6年随访中得到了内部重复(N = 2256)。结果:快乐缺乏症与IL-6、糖蛋白乙酰基、BMI、腰围、甘油三酯、葡萄糖和瘦素呈正相关(β范围为0.063 ~ 0.122),与高密度脂蛋白胆固醇呈负相关(β = -0.063)。主要生活方式和健康相关因素只能部分解释相关性,并在6年随访中得到证实(r = 基线和随访估计值之间的相关性为0.939)。AES与标记物高度一致,与快感缺乏症相比,其影响相对较大,而阴性对照症状仅与较高的糖蛋白乙酰基相关。结论:我们的研究结果表明,炎症和代谢失调与快感缺乏症和AES之间存在一致的关联。在未来的临床研究中,应充分了解抑郁症的特征及其复杂的相互关系,以选择特定的抑郁症患者亚组,并制定更有针对性的治疗方法。
{"title":"Inflammation, metabolic dysregulation, and depression profiles related to anhedonia and atypical, energy-related symptoms","authors":"J.C. Zwiep ,&nbsp;F. Lamers ,&nbsp;C.H. Vinkers ,&nbsp;N.J.A. van der Wee ,&nbsp;B.W.J.H. Penninx ,&nbsp;L. Nawijn ,&nbsp;Y. Milaneschi","doi":"10.1016/j.bbi.2025.106240","DOIUrl":"10.1016/j.bbi.2025.106240","url":null,"abstract":"<div><h3>Introduction</h3><div>Depression manifests heterogenous bio-clinical profiles. Anhedonia has been previously linked to inflammation. Other research has associated inflammation and metabolic dysregulations with atypical, energy-related depressive symptoms (AES). In the present study, we examined the associations of inflammation and metabolic dysregulations with anhedonia and compared these associations with those of inflammation and metabolic dysregulations with AES, and with a negative control symptom profile, previously shown unrelated to inflammation and metabolic dysregulation.</div></div><div><h3>Methods</h3><div>Data was from 2,981 persons of the Netherlands Study of Depression and Anxiety (NESDA). Inflammatory markers included C-reactive protein (CRP), Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), and glycoprotein acetyls. Metabolic markers were body mass index (BMI), waist circumference, triglycerides, high-density-lipoprotein cholesterol (HDL cholesterol), glucose and leptin. Anhedonia, AES and negative control symptom profiles were based on sum scores from different items from the Inventory of Depressive Symptomatology Self-Report (IDS-SR). The results were internally replicated in NESDA’s 6-year follow-up (N = 2,256).</div></div><div><h3>Results</h3><div>Anhedonia was positively associated with IL-6, glycoprotein acetyls, BMI, waist circumference, triglycerides, glucose, and leptin (β ranging from 0.063 to 0.122) and negatively associated with HDL cholesterol (β = -0.063). Associations were only partially explained by major lifestyle and health-related factors and confirmed at 6-year follow-up (<em>r</em> = 0.939 correlation between estimates at baseline and follow-up). AES showed highly consistent associations with the markers, with relatively larger effects as compared to anhedonia, while the negative control symptoms were linked only to higher glycoprotein acetyls.</div></div><div><h3>Conclusion</h3><div>Our results indicate consistent associations between several markers of inflammation and metabolic dysregulation with anhedonia and AES. Full characterization of depression profiles and their complex interrelations should be leveraged in future clinical research to select specific subgroup of depressed patients and develop more targeted treatment approaches.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"132 ","pages":"Article 106240"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Neural control of Immunotherapy: how Tumor-innervation shapes Anti-Tumor immune responses 免疫治疗的神经控制:肿瘤神经支配如何影响抗肿瘤免疫反应。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-22 DOI: 10.1016/j.bbi.2025.106239
Hatice Satilmis , Adrien Denis , Karin Vanderkerken , Elke De Bruyne , Eline Menu , Erica K Sloan , Kim De Veirman
The role of the sympathetic nervous system (SNS) in cancer biology has gained increasing attention, and its ability to affect immunotherapy is starting to become clearer. Extensive evidence shows that neuro-onco-immune interactions significantly influence tumor progression and the effectiveness of cancer treatments. Blocking SNS signaling, primarily through β-adrenergic receptors, enhances immune cell functions, by increasing CD8+ T-cell activation and cytokine production, while reducing immunosuppressive cell populations.
This review explores the relationship between SNS signaling and cancer immunotherapy, emphasizing how SNS activation affects the efficacy of various immunotherapies, including immune modulators, immune checkpoint inhibitors, oncolytic virus therapy, therapeutic vaccines, and CAR-T cell therapies. We summarize retrospective studies investigating the use of β-blockers during immunotherapy, suggesting potential benefits for treatment outcomes of blocking SNS signaling in the tumor microenvironment. We examine ongoing clinical trials that evaluate the use of beta-blockers with immune checkpoint inhibitors, which aim to improve patient outcomes. While translational and preclinical studies provide ample evidence for targeting SNS signaling in cancer immunotherapy, clinical studies are only beginning to emerge. Ultimately, this review underscores the need for further research to better understand how SNS signaling can be targeted to optimize immunotherapy, paving the way for more effective treatment strategies.
交感神经系统(SNS)在癌症生物学中的作用越来越受到关注,其影响免疫治疗的能力也开始变得更加清晰。大量证据表明,神经-肿瘤-免疫相互作用显著影响肿瘤进展和癌症治疗的有效性。主要通过β-肾上腺素能受体阻断SNS信号,通过增加CD8+ t细胞的活化和细胞因子的产生,同时减少免疫抑制细胞群,从而增强免疫细胞功能。本文探讨了SNS信号与癌症免疫治疗之间的关系,强调了SNS激活如何影响各种免疫疗法的疗效,包括免疫调节剂、免疫检查点抑制剂、溶瘤病毒疗法、治疗性疫苗和CAR-T细胞疗法。我们总结了在免疫治疗中使用β受体阻滞剂的回顾性研究,提示阻断肿瘤微环境中SNS信号传导对治疗结果的潜在益处。我们研究了正在进行的临床试验,这些试验评估了β受体阻滞剂与免疫检查点抑制剂的使用,目的是改善患者的预后。虽然转化和临床前研究为靶向SNS信号用于癌症免疫治疗提供了充足的证据,但临床研究才刚刚开始出现。最后,这篇综述强调了进一步研究的必要性,以更好地了解如何靶向SNS信号来优化免疫治疗,为更有效的治疗策略铺平道路。
{"title":"Neural control of Immunotherapy: how Tumor-innervation shapes Anti-Tumor immune responses","authors":"Hatice Satilmis ,&nbsp;Adrien Denis ,&nbsp;Karin Vanderkerken ,&nbsp;Elke De Bruyne ,&nbsp;Eline Menu ,&nbsp;Erica K Sloan ,&nbsp;Kim De Veirman","doi":"10.1016/j.bbi.2025.106239","DOIUrl":"10.1016/j.bbi.2025.106239","url":null,"abstract":"<div><div>The role of the sympathetic nervous system (SNS) in cancer biology has gained increasing attention, and its ability to affect immunotherapy is starting to become clearer. Extensive evidence shows that neuro-onco-immune interactions significantly influence tumor progression and the effectiveness of cancer treatments. Blocking SNS signaling, primarily through β-adrenergic receptors, enhances immune cell functions, by increasing CD8<sup>+</sup> T-cell activation and cytokine production, while reducing immunosuppressive cell populations.</div><div>This review explores the relationship between SNS signaling and cancer immunotherapy, emphasizing how SNS activation affects the efficacy of various immunotherapies, including immune modulators, immune checkpoint inhibitors, oncolytic virus therapy, therapeutic vaccines, and CAR-T cell therapies. We summarize retrospective studies investigating the use of β-blockers during immunotherapy, suggesting potential benefits for treatment outcomes of blocking SNS signaling in the tumor microenvironment. We examine ongoing clinical trials that evaluate the use of beta-blockers with immune checkpoint inhibitors, which aim to improve patient outcomes. While translational and preclinical studies provide ample evidence for targeting SNS signaling in cancer immunotherapy, clinical studies are only beginning to emerge. Ultimately, this review underscores the need for further research to better understand how SNS signaling can be targeted to optimize immunotherapy, paving the way for more effective treatment strategies.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"132 ","pages":"Article 106239"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Increases in inflammation are associated with decreased trust of racial out-group members 炎症的增加与种族外群体成员信任度的下降有关。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-22 DOI: 10.1016/j.bbi.2025.106242
Natalie M. Antenucci , Mallory J. Feldman , Tatum A. Jolink , Taylor N. West , Megan N. Cardenas , Gabriella M. Alvarez , Keely A. Muscatell
While social group divisions occur naturally, inauspicious contexts like pathogen threat may exacerbate divides, driving in-group favoritism and out-group derogation. Minimal work has examined biological underpinnings of intergroup dynamics, particularly immune changes likely to accompany pathogen threat. To address this, we administered the influenza vaccine to 44 young adult participants. Before and after receiving the vaccine, participants completed a modified affect misattribution procedure, wherein they rated the trustworthiness of racial in-group and out-group faces. Participants also provided pre- and post-vaccine blood samples which were assayed for the inflammatory cytokine interleukin-6 (IL-6). Results showed a negative association between inflammatory reactivity and ratings of out-group faces: those who experienced greater increases in IL-6 rated racial out-group faces as less trustworthy than those with less IL-6 reactivity. This work begins exploring the role of inflammation in intergroup processes and findings, while preliminary, suggest a novel biological process that is associated with intergroup perception.
虽然社会群体分裂是自然发生的,但病原体威胁等不利环境可能会加剧分裂,导致群体内偏爱和群体外贬损。很少有人研究群体间动态的生物学基础,特别是可能伴随病原体威胁的免疫变化。为了解决这个问题,我们对44名年轻成年参与者进行了流感疫苗接种。在接种疫苗之前和之后,参与者完成了一项修改后的影响错误归因程序,其中他们对种族群体内和群体外面孔的可信度进行了评级。参与者还提供了疫苗接种前和疫苗接种后的血液样本,用于检测炎症细胞因子白介素-6 (IL-6)。结果显示炎症反应性与外群体面孔评分之间存在负相关关系:那些经历了IL-6较大增加的人认为种族外群体面孔比那些IL-6反应性较低的人更不值得信赖。这项工作开始探索炎症在群体间过程中的作用,研究结果虽然初步,但表明了一种与群体间感知相关的新型生物学过程。
{"title":"Increases in inflammation are associated with decreased trust of racial out-group members","authors":"Natalie M. Antenucci ,&nbsp;Mallory J. Feldman ,&nbsp;Tatum A. Jolink ,&nbsp;Taylor N. West ,&nbsp;Megan N. Cardenas ,&nbsp;Gabriella M. Alvarez ,&nbsp;Keely A. Muscatell","doi":"10.1016/j.bbi.2025.106242","DOIUrl":"10.1016/j.bbi.2025.106242","url":null,"abstract":"<div><div>While social group divisions occur naturally, inauspicious contexts like pathogen threat may exacerbate divides, driving in-group favoritism and out-group derogation. Minimal work has examined biological underpinnings of intergroup dynamics, particularly immune changes likely to accompany pathogen threat. To address this, we administered the influenza vaccine to 44 young adult participants. Before and after receiving the vaccine, participants completed a modified affect misattribution procedure, wherein they rated the trustworthiness of racial in-group and out-group faces. Participants also provided pre- and post-vaccine blood samples which were assayed for the inflammatory cytokine interleukin-6 (IL-6). Results showed a negative association between inflammatory reactivity and ratings of out-group faces: those who experienced greater increases in IL-6 rated racial out-group faces as less trustworthy than those with less IL-6 reactivity. This work begins exploring the role of inflammation in intergroup processes and findings, while preliminary, suggest a novel biological process that is associated with intergroup perception.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106242"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Using social risk factors to predict allostatic biotypes of depression: A latent profile and multinomial regression analysis 使用社会风险因素预测抑郁症的适应型:潜在特征和多项回归分析。
IF 7.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-22 DOI: 10.1016/j.bbi.2025.106243
Jay O’Shields , Helisha Soni , Orion Mowbray

Objective

Major depression is often difficult to treat, particularly among individuals exposed to psychosocial risks like childhood maltreatment, loneliness, and recent stress. These experiences may lead to biological dysregulation consistent with allostatic load theory. This study explored whether distinct biological profiles among adults with depression are associated with specific psychosocial and health-related factors.

Method

Data were drawn from the Midlife in the United States study (MIDUS), including 367 participants with clinically significant depressive symptoms (CES-D ≥ 16). Latent profile analysis identified biological profiles based on 23 biomarkers across seven systems: inflammation, glucose, sympathetic and parasympathetic nervous systems, HPA-axis, cardiovascular, and lipids. Multinomial regression models examined associations between profile membership and psychosocial (childhood maltreatment, loneliness, recent stress), health (alcohol use, smoking, exercise), and demographic variables (sex, race/ethnicity, age, education).

Results

A five-profile solution best fit the data: High Inflammation & Glucose (n = 74), Low PNS (n = 83), High PNS (n = 73), Healthy Depression (n = 67), and High HPA-Axis (n = 70). Childhood maltreatment significantly predicted membership in the High Inflammation & Glucose and Low PNS profiles compared to the Healthy Depression group, even after controlling for health behaviors and demographics. Loneliness and recent stress were not significant predictors.

Conclusion

Childhood maltreatment is a predictor of biological dysregulation in depression, differentially predicting profiles characterized by inflammatory and metabolic vs parasympathetic functioning. These may represent different vulnerability pathways from social experiences to depressive illness. Incorporating measurement strategies specific to these pathways may aide in selecting treatment options for people who have depression and a history of childhood maltreatment.
目的:重度抑郁症通常很难治疗,特别是那些暴露于心理社会风险的个体,如童年虐待、孤独和最近的压力。这些经历可能导致与适应负荷理论一致的生物失调。这项研究探讨了成人抑郁症患者的不同生物学特征是否与特定的社会心理和健康相关因素有关。方法:数据来自Midlife in the United States研究(MIDUS),包括367名具有临床显著抑郁症状(CES-D ≥ 16)的参与者。潜在特征分析确定了基于七个系统的23个生物标志物的生物特征:炎症、葡萄糖、交感和副交感神经系统、hpa轴、心血管和脂质。多项回归模型检验了档案成员与社会心理(童年虐待、孤独、最近的压力)、健康(饮酒、吸烟、锻炼)和人口统计变量(性别、种族/民族、年龄、教育)之间的关联。结果:five-profile解决方案最适合的数据:高炎症和葡萄糖(n = 74),低pn (n = 83),高pn (n = 73),健康的抑郁症(n = 67),和高hpa轴(n = 70)。与健康抑郁组相比,童年虐待显著预测了高炎症、高血糖和低PNS特征的成员,即使在控制了健康行为和人口统计学之后也是如此。孤独和最近的压力并不是显著的预测因子。结论:童年虐待是抑郁症生物学失调的预测因子,预测炎症和代谢与副交感神经功能的差异。这些可能代表了从社会经历到抑郁症的不同脆弱性途径。结合特定于这些途径的测量策略可能有助于为患有抑郁症和童年虐待史的人选择治疗方案。
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引用次数: 0
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