Brain, Behavior, and Immunity最新文献

{"title":"The role of social support on change in C-reactive Protein and BMI among youth with and without child maltreatment history","authors":"Savannah A. Girod ,&nbsp;Aishwarya Ganguli ,&nbsp;Yo Jackson ,&nbsp;Christine Heim ,&nbsp;Idan Shalev ,&nbsp;Eric Claus ,&nbsp;Zachary Fisher ,&nbsp;Jennie Noll ,&nbsp;Chad Shenk ,&nbsp;Hannah M.C. Schreier","doi":"10.1016/j.bbi.2025.106250","DOIUrl":"10.1016/j.bbi.2025.106250","url":null,"abstract":"<div><div>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 (<em>p</em>s &gt; 0.28). However, independent of CM history, greater peer support was associated with lower BMI at Time 2 (β = -0.10, <em>p</em> = 0.005). Peer support further moderated the association between CM history and Time 2 BMI (β = -0.16, <em>p</em> = 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, <em>p</em> = 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, <em>p</em> = 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, <em>p</em> = 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.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106250"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862088","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}

{"title":"Adverse childhood experiences and physiological wear-and-tear in adolescence: Findings from the Generation XXI cohort","authors":"Armine Abrahamyan ,&nbsp;Milton Severo ,&nbsp;Michelle Kelly-Irving ,&nbsp;Liane Correia-Costa ,&nbsp;Mariana Amorim ,&nbsp;Sara Soares ,&nbsp;Sílvia Fraga","doi":"10.1016/j.bbi.2026.106260","DOIUrl":"10.1016/j.bbi.2026.106260","url":null,"abstract":"<div><h3>Background</h3><div>Adversity-induced stress may increase vulnerability to biological risk and contribute to cumulative physiological dysregulation, as reflected by elevated allostatic load (AL). We aimed to estimate the association between adverse childhood experiences (ACEs) and AL at two different time points in a pediatric population from the population-based Generation XXI birth cohort.</div></div><div><h3>Methods</h3><div>Total ACE scores were derived from prospectively collected data at ages 10 and 13. AL was assessed using nine biomarkers across four physiological systems: cardiovascular, metabolic, immune/inflammatory, and renal. We analyzed a sample of 3787 participants with data collected at baseline and two subsequent follow-up waves. Adjusted odds ratios (aOR) and 95% confidence intervals (CI) were obtained from linear and logistic regression analyses to estimate the associations between ACEs measured at ages 10 and 13and the AL index at age 13.</div></div><div><h3>Results</h3><div>We found a significant association between exposure to ACE at age 13 and an elevated AL index at the same age (β = 0.004; 95 % CI [0.001; 0.006]), but not at age 10 (β = 0.001; 95 %CI [-0.002; 0.004]). In the analysis of individual ACEs, we found that when ACEs occurred before age 10, parental separation or divorce (β = 0.024; 95 %CI [0.007; 0.042]) emerged as a significant factor contributing to increased AL index. When adversity occurred between ages 10 and 13, parental separation or divorce (β = 0.023; 95 %CI [0.007; 0.039]), difficulties in school (β = 0.021; 95 %CI [0.007; 0.035]), and household alcohol/drug use (β = 0.058; 95 %CI [0.011; 0.106]) during this period were associated with increased AL burden at age 13, after adjusting for adolescents’ age, sex, height, and maternal education. Biomarker-level analyses showed that, among the four physiological systems comprising AL, metabolic and immune systems appeared most responsive to ACEs.</div></div><div><h3>Conclusions</h3><div>These findings suggest that adolescents exposed to selected ACEs at age 10 showed increased AL burden, with cumulative ACEs by age 13 further amplifying this association.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106260"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932098","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}

{"title":"Contribution of proneurotrophin-3 to nerve trauma-induced neuropathic pain through promoting TrkC-mediated increase of CCL2 in primary sensory neurons","authors":"Huijie Shang ,&nbsp;Xianglei Meng ,&nbsp;Bing Wang ,&nbsp;Xiaozhou Feng ,&nbsp;Ruining Ma ,&nbsp;Huijuan Hu ,&nbsp;Alex Bekker ,&nbsp;Yuan-Xiang Tao","doi":"10.1016/j.bbi.2026.106256","DOIUrl":"10.1016/j.bbi.2026.106256","url":null,"abstract":"<div><div>Neuropathic pain induced by nerve trauma remains a substantial and unresolved clinical challenge. Despite ongoing research, therapeutic options for this disorder remain inadequate. Here, we report that neurotrophin-3 (<em>Nt3</em>) mRNA and its encoded proneurotrophin-3 (proNT3) protein are upregulated in neurons of the injured dorsal root ganglion (DRG), but not in the spinal cord, following peripheral nerve trauma. Mature neurotrophin-3 (NT3) protein is undetectable in the DRG under both normal and nerve trauma conditions. Genetic blockage of <em>Nt3</em> mRNA/proNT3 protein upregulation in the injured DRG attenuates the development and maintenance of nerve trauma-induced neuropathic pain, without impacting acute/basal pain responses or locomotor function. Conversely, mimicking nerve trauma-induced upregulation of DRG <em>Nt3</em> mRNA/pro-NT3 produces neuropathic pain-like symptoms. These symptoms are mitigated by intrathecal injection of NT3 protein or by selective knockdown of tropomyosin receptor kinase C (TrkC), but not TrkA or TrkB, in the DRG. Notably, intrathecal injection of NT3 also alleviates nerve trauma-induced neuropathic pain. Mechanistically, upregulated proNT3 contributes to the nerve trauma-induced increases of C-C chemokine ligand 2 (<em>Ccl2</em>) mRNA and CCL2 protein through activating TrkC in the injured DRG. Given that CCL2 is a key driver in neuropathic pain genesis and that <em>Nt3</em> mRNA co-expresses with <em>TrkC</em> and <em>Ccl2</em> mRNA in DRG neurons, proNT3 likely participates in nerve trauma-induced neuropathic pain through promoting TrkC-mediated increase of CCL2 in DRG neurons, highlighting a potential therapeutic target for the treatment of this disorder.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106256"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932109","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}

{"title":"Fructose malabsorption induces dysbiosis and increases anxiety in male human and animal models","authors":"Adeline Coursan ,&nbsp;Delphine Polve ,&nbsp;Anne-Marie Leroi ,&nbsp;Magali Monnoye ,&nbsp;Lea Roussin ,&nbsp;Clara Benatar ,&nbsp;Marie-Pierre Tavolacci ,&nbsp;Muriel Quillard Muraine ,&nbsp;Mathilde Maccarone ,&nbsp;Olivia Guérin ,&nbsp;Estelle Houivet ,&nbsp;Charlène Guérin ,&nbsp;Valery Brunel ,&nbsp;Jérôme Bellenger ,&nbsp;Jean-Paul Pais de Barros ,&nbsp;Guillaume Gourcerol ,&nbsp;Laurent Naudon ,&nbsp;Sophie Layé ,&nbsp;Charlotte Madore ,&nbsp;Xavier Fioramonti ,&nbsp;Véronique Douard","doi":"10.1016/j.bbi.2025.106221","DOIUrl":"10.1016/j.bbi.2025.106221","url":null,"abstract":"<div><div>Excessive fructose intake is a growing public health concern, yet many individuals have a limited capacity to absorb typical dietary levels, leading to chronic fructose malabsorption and intestinal spillover. In animal models, this spillover disrupts the gut microbiota, but its impact in humans remains unexplored. We hypothesized that fructose malabsorption–induced dysbiosis contributes to peripheral inflammation, which, together with neuroinflammation, plays a role in mood disorders. This study investigates the link between fructose malabsorption, gut microbiota, and mood disorders in a human cohort, and explores their association with neuroinflammation in a <em>Glut5</em> knockout (GLUT5_KO) mouse model of fructose-malabsorption.</div><div>In a human cohort of male healthy volunteers, fructose malabsorption was assessed using a breath hydrogen test, while plasma lipopolysaccharide (LPS), IL8 and TNFα levels and anxiety traits (measured using the State-Trait Anxiety Inventory, STAI) were analyzed. Gut microbiota composition was characterized through 16S rRNA sequencing, and dietary fructose intake was recorded. In the preclinical study, GLUT5_KO male mice, which lack intestinal fructose transport, were fed a 5% fructose diet for four weeks. Behavioral assays assessed anxiety- and depressive-like behaviors, while gut microbiota composition and microglia-associated gene expression were analyzed.</div><div>Sixty percent of volunteers exhibited fructose malabsorption, along with elevated plasma LPS, IL8 and TNFα levels, increased anxiety traits on the STAI, and distinct gut microbiota alterations, partially linked to fructose intake patterns. The average daily fructose intake was 30 g per individual, with significant variability in dietary sources. In the preclinical model, GLUT5_KO mice on a 5% fructose diet displayed increased anxiety- and depressive-like behaviors, pronounced gut microbiota shifts, and altered expression of microglia-associated genes.</div><div>These findings highlight the complex interplay between dietary fructose, gut microbiota, low grade inflammation and neuroinflammation in shaping mental health. Chronic fructose malabsorption may contribute to mood disorders through gut dysbiosis and microglia-dependent neuroinflammation, warranting further investigation into dietary interventions.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106221"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793369","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}

{"title":"TNF-mediated hilar interneuron loss and aberrant granule cell migration are associated with chronic cognitive deficits following TBI","authors":"Elizabeth A. Harris ,&nbsp;Sabrina Budianto ,&nbsp;Sreejita Arnab ,&nbsp;Caroline de Jager ,&nbsp;Georgia E. Hodes ,&nbsp;John R. Bethea ,&nbsp;Michelle H. Theus","doi":"10.1016/j.bbi.2025.106216","DOIUrl":"10.1016/j.bbi.2025.106216","url":null,"abstract":"<div><div>Chronic morbidities, including cognitive impairment, are a common consequence of traumatic brain injury (TBI), with millions currently living with permanent TBI-related disabilities. Recent work has indicated that altered cellular architecture in the dentate gyrus (DG) may play a significant role in the development of chronic cognitive impairment and excitotoxicity. However, current understanding of the temporal progression of these pathological changes in the context of neuroinflammation and chronic cognitive outcomes is limited. This study characterized temporospatial changes in the hilar region of the DG, showing that the population of reelin- and somatostatin-expressing inhibitory interneurons was significantly reduced as early as 7 days post-injury (dpi), and that aberrant migration of excitatory granule cells occurs gradually in the weeks to months following injury. These findings coincided with upregulation of monocyte/macrophage-associated inflammatory mediators, including MIP-1β, MIG, MCP-1, and TNF-α at 7 days dpi, with differential cytokine regulation persisting 120 dpi. Injury was associated with the development of chronic spatial memory impairment and reduced risk-assessment behavior, with a transient reduction in spontaneous anxiety. TNFR1 and TNFR2 were differentially expressed in inhibitory neurons, further implicating TNF-signaling as a driver of hilar neuron loss. Furthermore, systemic administration of anti-TNF-α monoclonal antibody induced significant neuroprotection, attenuated pro-inflammatory mediators, and hilar interneuron loss. These findings suggest that TNF-TNFR signaling plays a crucial role in driving hilar interneuron loss and aberrant granule cell migration, which, in turn, may contribute to the development of excitotoxicity and chronic cognitive deficits.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106216"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720852","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}

{"title":"LRRC4 enhances synaptic function and alleviates neuronal injury in high-fat diet mice","authors":"Suping Qin ,&nbsp;Jiaxin Deng ,&nbsp;Bin Hu ,&nbsp;Xuejiao Zhang ,&nbsp;Yi Ding ,&nbsp;Tianxin Zhang ,&nbsp;Bohui Yuan ,&nbsp;Dexu Sun ,&nbsp;Xiaotian Wang ,&nbsp;Feng Zhou ,&nbsp;Xiaomei Liu","doi":"10.1016/j.bbi.2026.106254","DOIUrl":"10.1016/j.bbi.2026.106254","url":null,"abstract":"<div><div>Obesity, a chronic metabolic disease, increases the risk of neurodegenerative disorders and cognitive impairments. Cumulative evidence reveal obesity impairs hippocampal synaptic plasticity and induces neuronal apoptosis. Leucine rich repeat containing 4 (LRRC4) is a member of the Netrin G ligand (NGL) family, and plays a crucial role in maintaining neuronal morphology, function, and structure of synapses. However, it remains unclear whether LRRC4 affects obesity-induced cognitive impairment or its underlying mechanism. Herein, we showed that a high-fat diet (HFD) led to cognitive deficits in obese mice, as assessed by the Morris water maze and Nest building tests. The expression of LRRC4 and postsynaptic dense protein 95 (PSD-95) was downregulated in the hippocampus of mice with HFD-fed obesity. Furthermore, the effects of LRRC4 overexpression (AAV-LRRC4) and knockout (<em>Lrrc4^−/−</em>, deletion location: 28,831,753–28,828,926) on neurological function and synapses were investigated. Data from behavioral and electrophysiological studies demonstrated that LRRC4 knockout impaired synaptic plasticity and resulted in cognitive impairment in mice. Moreover, the expression level of PSD-95 was further decreased in <em>Lrrc4^−/−</em>mice fed by HFD. Meanwhile, the expression of the anti-apoptotic protein Bcl-2 was decreased, whereas the levels of the pro-apoptotic proteins cleaved-caspase 3 and BAX were increased in the hippocampus of HFD <em>Lrrc4^−/−</em> mice. This indicated that <em>Lrrc4</em> knockout exacerbated neuronal injury and apoptosis. Overexpression of LRRC4 in the hippocampus of HFD mice, ameliorated the behavioral abnormalities of HFD mice and strengthened synaptic transmission. In parallel, Golgi staining displayed a significant increase in the length and number of dendritic branches of neurons. Additionally, LRRC4 overexpression promoted PSD-95 expression and exerted an anti-apoptotic effect, as evidenced by the upregulation of Bcl-2 and downregulation of cleaved caspase-3 and BAX in the hippocampus. These findings suggest that LRRC4 enhances synaptic function and alleviates neuronal injury in HFD mice. Targeting LRRC4 may have therapeutic potentiality for neurodegenerative disorders and cognitive deficits.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106254"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145910616","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}

{"title":"Epigenetic biomarkers of inflammation in studies on mental health: Current applications, limitations, and future directions","authors":"Winni Schalkwijk ,&nbsp;Lot D. de Witte ,&nbsp;Frederieke A.J. Gigase ,&nbsp;Charlotte A.M. Cecil ,&nbsp;Matthew Suderman ,&nbsp;Sinan Gülöksüz ,&nbsp;Bart P.F. Rutten ,&nbsp;Marco P. Boks","doi":"10.1016/j.bbi.2025.106245","DOIUrl":"10.1016/j.bbi.2025.106245","url":null,"abstract":"<div><h3>Background</h3><div>Inflammation has emerged as a potentially modifiable risk factor for mental illness, warranting further research. Epidemiological studies have primarily relied on measuring blood levels of single inflammatory proteins, but these have proven limited in detecting robust long-term associations with mental health. DNA methylation (DNAm)-based epigenetic biomarkers of inflammation have demonstrated greater predictive performance than protein markers for several physical health outcomes and hold potential to increase understanding of the immune-mental health link.</div></div><div><h3>Methods</h3><div>We conducted a comprehensive literature review of mental health studies using DNAm markers of inflammation. First, PubMed and EMBASE were searched for epigenome-wide association studies (EWAS) of inflammation, providing source data for deriving DNAm biomarkers. Second, we identified studies that used DNAm markers of inflammation to study mental health-related outcomes. We address technical considerations, biological implications, and future research directions.</div></div><div><h3>Results</h3><div>We identified 29 EWAS studies of circulating inflammatory proteins, of which C-reactive protein (CRP) was the most frequently studied. In addition, 14 studies examined epigenetic biomarkers of inflammation in relation to mental health, cognition or neuroimaging outcomes, where higher levels of DNA methylation (DNAm) markers of CRP and interleukin-6 (IL-6) were consistently associated with reduced cognitive function, lower brain volumes, and reduced white matter integrity. In contrast, findings for mental health (mostly depression) were less conclusive, with studies reporting either positive or null associations.</div></div><div><h3>Conclusion</h3><div>Epigenetic biomarkers of inflammation are emerging as valuable tools in mental health research. Further study on the value of these markers for mental health prediction is warranted, evaluating shared and distinct relations across mental illnesses. Advances may also come from developing novel epigenetic biomarkers that capture inflammatory processes with greater resolution, and from examining altered inflammatory states in relation to mental health risk exposures across the lifecourse.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106245"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877721","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}

{"title":"Symptomatology of depression and onset of cardiometabolic diseases − A 7-year follow-up study","authors":"Tahani Alshehri ,&nbsp;Yumeng Tian ,&nbsp;Ruifang Li-Gao ,&nbsp;Jeroen van der Velde ,&nbsp;Saskia le Cessie ,&nbsp;Frits R. Rosendaal ,&nbsp;Brenda W.J.H. Penninx ,&nbsp;Yuri Milaneschi ,&nbsp;Dennis O. Mook-Kanamori","doi":"10.1016/j.bbi.2026.106285","DOIUrl":"10.1016/j.bbi.2026.106285","url":null,"abstract":"<div><h3>Background</h3><div>Our study aimed to investigate the association of depressive mood and two depressive symptom profiles with the risk of cardiometabolic diseases (CMD) and to explore the underlying mechanisms of these associations through CMD-related metabolites and proteins.</div></div><div><h3>Methods</h3><div>In the Netherlands Epidemiology of Obesity study, depressive mood was measured with the Inventory of Depressive Symptomatology questionnaire, and two depressive symptom profiles, namely atypical energy-related symptom (AES) and melancholic, were created. The AES profile was derived by summing the score of five items: increased sleepiness, increased appetite, weight gain, low energy level and leaden paralysis. The melancholic symptom profile was used as another clinically established symptom profile for comparison with AES. The incidence of CMD (defined as development of cardiovascular diseases or type 2 diabetes (T2D)) was identified during a median follow-up of 6.7 years. Cox proportional hazards models assessed the association between depressive symptom profiles and CMD incidence, adjusted for confounders, while linear regression models examined associations with CMD-related proteins and metabolites identified in the UK Biobank.</div></div><div><h3>Results</h3><div>Compared to participants without depressive mood, those in the severe depressive mood group had the highest risk of developing CMD, with a hazard ratio (HR) of 1.65 (95% CI: 1.22–2.22). Regarding depressive symptom profiles, individuals with a severe AES profile showed a significantly increased risk of T2D (HR: 2.87, 95% CI: 1.92–4.30) compared to those without symptoms, whereas no significant association was observed for the melancholic symptom profile. The AES profile was more strongly associated with CMD-related metabolites, including glycoprotein acetyls, isoleucine and lipoproteins, and proteins predominantly enriched in the cytokine-cytokine receptor interaction pathway.</div></div><div><h3>Conclusion</h3><div>The AES profile is specifically associated with the incidence of T2D, and some specific metabolites and proteins were suggested to influence such association. Acknowledging the heterogeneity of depression may aid in tailoring CMD prevention.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106285"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973186","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}

{"title":"Sexual minority adults exhibit greater inflammation than heterosexual adults in the context of depressive symptoms and anxiety: Pathways to health disparities","authors":"Lisa M. Christian ,&nbsp;Rebecca R. Andridge ,&nbsp;Juan Peng ,&nbsp;Nithya P. Kasibhatla ,&nbsp;Thomas W. McDade ,&nbsp;Tessa Blevins ,&nbsp;Steve W. Cole ,&nbsp;Wendy D. Manning ,&nbsp;Claire M. Kamp Dush","doi":"10.1016/j.bbi.2025.106202","DOIUrl":"10.1016/j.bbi.2025.106202","url":null,"abstract":"<div><h3>Background</h3><div>Sexual minority individuals, including lesbian, gay, bisexual, and other non-heterosexual (LGB + ) adults have significantly greater risk for mental and physical health conditions, disparities linked with minority stress exposure.</div></div><div><h3>Methods</h3><div>Utilizing a Biopsychosocial Minority Stress Framework, this study examined depressive symptoms, anxiety, and inflammatory markers [interleukin(IL)-6 and C-reactive protein (CRP)] in a diverse sample of 661 adults (388 heterosexual; 273 LGB + ).</div></div><div><h3>Results</h3><div>LGB + adults reported greater anxiety and depressive symptoms (ps &lt; 0.01). This effect was partially mediated by greater exposure to adverse childhood experiences (ACES) among LGB + respondents. Compared to heterosexual adults, controlling for key potential confounds, LGB + adults exhibited greater elevations in CRP in relation to depressive symptoms (B_SM = 0.029, SE = 0.013 vs. B_HETERO = −0.0050, SE = 0.012; interaction p = 0.042). A similar pattern was observed in relation to IL-6, however the interaction effect was not statistically significant (p = 0.015). LGB + adults also showed greater increases in CRP in the context of anxiety (B_SM = 0.033, SE = 0.016 vs B_HETERO = −0.012, SE = 0.014; interaction p = 0.028). These effects were not accounted for by differences in body mass index (BMI) or tobacco use.</div></div><div><h3>Conclusions</h3><div>LGB + adults may experience greater inflammatory burden due to both 1) greater prevalence of anxiety and depression, and 2) sensitization to negative inflammatory sequalae in the context of anxiety and depression. Greater ACES contributed to the greater prevalence of anxiety and depressive symptoms among LGB + as compared to heterosexual participants. Ultimately, differential prevalence of, and physiological responses, to anxiety and depressive symptoms may contribute to physical and mental health disparities among sexual minority adults.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106202"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660406","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}

{"title":"Corrigendum to “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” [Brain Behav. Immun. 132 (2026) 106241]","authors":"Yinxian Chen ,&nbsp;Sarina Abrishamcar ,&nbsp;Jasmine K. Aqua ,&nbsp;Christian Dye ,&nbsp;Linda C. Gallo ,&nbsp;Maria M. Llabre ,&nbsp;Frank J. Penedo ,&nbsp;Carmen R. Isasi ,&nbsp;Krista M. Perreira ,&nbsp;Bharat Thyagarajan ,&nbsp;Martha Daviglus ,&nbsp;Amber Pirzada ,&nbsp;Andrea Baccarelli ,&nbsp;Karen N. Conneely ,&nbsp;Rebecca Jones-Antwi ,&nbsp;Shakira F. Suglia","doi":"10.1016/j.bbi.2026.106289","DOIUrl":"10.1016/j.bbi.2026.106289","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106289"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017340","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}