Brain, Behavior, and Immunity最新文献

{"title":"Differences in inflammation among black and white individuals: A systematic review and meta-analysis","authors":"Cameron R. Wiley ,&nbsp;DeWayne P. Williams ,&nbsp;Christine Sigrist ,&nbsp;Briana N. Brownlow ,&nbsp;Anna Markser ,&nbsp;Suzi Hong ,&nbsp;Esther M. Sternberg ,&nbsp;Gaston Kapuku ,&nbsp;Julian Koenig ,&nbsp;Julian F. Thayer","doi":"10.1016/j.bbi.2025.03.019","DOIUrl":"10.1016/j.bbi.2025.03.019","url":null,"abstract":"<div><h3>Importance</h3><div>Despite persisting health disparities between Black and White individuals, racial differences in inflammation have yet to be comprehensively examined.</div></div><div><h3>Objective</h3><div>To determine if significant differences in circulating levels of inflammatory markers between Black and White populations exist.</div></div><div><h3>Data sources</h3><div>Studies were identified through systematic searches of four electronic databases in January 2022. Additional studies were identified via reference lists and e-mail contact.</div></div><div><h3>Study selection</h3><div>Eligible studies included full-text empirical articles that consisted of Black and White individuals and reported statistics for inflammatory markers for each racial group. Of the 1368 potentially eligible studies, 84 (6.6 %) representing more than one million participants met study selection criteria.</div></div><div><h3>Data extraction and synthesis</h3><div>Risk of bias was assessed via meta regressions that considered relevant covariates. Data heterogeneity was tested using both the Cochrane Q-statistic and the standard <em>I²</em> index. Random effects models were used to calculate estimates of effect size from standardized mean differences.</div></div><div><h3>Main outcomes and measures</h3><div>Outcome measures included 12 inflammatory markers, including C-reactive protein (CRP), Fibrinogen, Interleukin-6 (IL-6), Tumor necrosis factor-alpha (TNF-α), and soluble intercellular adhesion molecule 1 (sICAM-1).</div></div><div><h3>Results</h3><div>Several markers had robust sample sizes for analysis, including CRP (White <em>N</em> = 934,594; Black <em>N</em> = 55,234), Fibrinogen (White <em>N</em> = 80,880; Black <em>N</em> = 18,001), and IL-6 (White <em>N</em> = 20,269; Black <em>N</em> = 14,675). Initial results indicated significant effects on CRP (<em>k</em> = 56, pooled Hedges’ <em>g</em> = 0.24), IL-6 (<em>k</em> = 33, <em>g</em> = 0.15), and Fibrinogen (<em>k</em> = 19, <em>g</em> = 0.49), with Black individuals showing higher levels. Results also indicated significant effects on sICAM-1 (<em>k</em> = 6, <em>g</em> = −0.46), and Interleukin-10 (<em>k</em> = 4, <em>g</em> = −0.18), with White individuals showing higher levels. Sensitivity analyses confirmed robust effects for CRP, IL-6, Fibrinogen, and sICAM-1 while also revealing significant effects on TNF-α (<em>k</em> = 18, <em>g</em> = −0.17) and Interleukin-8 (<em>k</em> = 5, <em>g</em> = −0.19), with White individuals showing higher levels of both.</div></div><div><h3>Conclusions and relevance</h3><div>Current <em>meta</em>-analytic results provide evidence for marked racial differences in common circulating inflammatory markers and illustrate the complexity of the inflammatory profile differences between Black and White individuals.</div><div><strong>Review Pre-Registration:</strong> PROSPERO Identifier – CRD42022312352.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 269-286"},"PeriodicalIF":8.8,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656143","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":"Astrocyte elevated gene-1 (AEG-1) in myeloid cells is a key driver for the development of chemotherapy-induced peripheral neuropathy","authors":"Bryan D. Mckiver ,&nbsp;Sara M. Herz ,&nbsp;Shivani Patel ,&nbsp;Tayla Bryan ,&nbsp;Jared Mann ,&nbsp;Justin L. Poklis ,&nbsp;John W. Bigbee ,&nbsp;Jolene J. Windle ,&nbsp;Aliasger K. Salem ,&nbsp;Devanand Sarkar ,&nbsp;M.Imad Damaj","doi":"10.1016/j.bbi.2025.03.020","DOIUrl":"10.1016/j.bbi.2025.03.020","url":null,"abstract":"<div><div>Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect of chemotherapy treatment, often resulting in the discontinuation of treatment. Paclitaxel activates peripheral macrophages, generating a neuroinflammatory response that contributes to CIPN development and maintenance.</div><div>Astrocyte Elevated Gene-1 (AEG-1), also known as Metadherin or LYRIC, is a multifunctional protein that modulates macrophage activity and regulates inflammation through direct interaction with NF-κB, a transcriptional regulator of proinflammatory cytokine/chemokine (PIC) expression.</div><div>We aimed to determine whether AEG-1 contributes to the development and maintenance of CIPN pathologies by using both global (AEG-1 KO) and myelocyte-specific knockout (AEG-1ΔMAC) transgenic mouse strains in an animal model of CIPN that replicates specific human clinical phenotypes. We hypothesized that inhibition of AEG1 expression in myeloid cells, such as monocytes and macrophages, would prevent the development and maintenance of CIPN.</div><div>Our results showed that global AEG-1 deletion prevented the development of CIPN pathologies induced by PAC, as well as oxaliplatin (OHP). PAC treatment was found to increase AEG-1 and PIC expression in the DRGs of WT mice and in peritoneal macrophages isolated from C57BL/6J mice. However, in the absence of AEG-1 expression, PAC-induced neuroinflammation was completely halted in the DRGs of AEG-1 KO mice. This preventative phenotype and PIC expression profile was mirrored in AEG-1ΔMAC mice, which also displayed reduced NF-κB protein levels and F4/80+ macrophages trafficked to the lumbar DRGs following PAC treatment.</div><div>In summary, our results are the first to demonstrate the biological role AEG-1, particularly in myeloid cells, in development of CIPN.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 329-340"},"PeriodicalIF":8.8,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656141","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":"Chronic stress leads to earlier cognitive decline in an Alzheimer’s mouse model: The role of neuroinflammation and TrkB","authors":"Shir Shlomi-Loubaton ,&nbsp;Keren Nitzan ,&nbsp;Maria Rivkin-Natan ,&nbsp;Salomé Sabbah ,&nbsp;Roni Toledano ,&nbsp;Motty Franko ,&nbsp;Ziv Bentulila ,&nbsp;Dekel David ,&nbsp;Dan Frenkel ,&nbsp;Ravid Doron","doi":"10.1016/j.bbi.2025.03.021","DOIUrl":"10.1016/j.bbi.2025.03.021","url":null,"abstract":"<div><div>While most Alzheimer’s disease (AD) studies focus on the cognitive aspects of the disease, less focus is given to affective symptoms. In this study, we investigated the long-term consequences of exposure to chronic stress. 5xFAD AD model mice were exposed to unpredictable chronic mild stress, and cognitive and emotional aspects were examined at 3-time points (up to 4 months after exposure to stress). We found that exposure to chronic stress accelerates neuropathology outcomes in the 5xFAD mouse model in adulthood, accompanied by changes in the neurotrophic system. Specifically, we found that chronic stress accelerated the appearance of short-term spatial memory deficits in the 5xFAD mice and decreased tyrosine kinase B full receptor (TrkB.FL) expression levels. In vitro, we showed that corticosterone impairs the ability of microglia to uptake Aβ and reduces microglial activation. To conclude, our study may shed light on the mechanisms through which mild chronic stress might contribute to the onset and progression of Alzheimer’s disease symptoms.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 303-314"},"PeriodicalIF":8.8,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Financial stress and sleep duration in immune and neuroendocrine patterning. An analytical triangulation in ELSA","authors":"Odessa S. Hamilton,&nbsp;Andrew Steptoe","doi":"10.1016/j.bbi.2025.03.006","DOIUrl":"10.1016/j.bbi.2025.03.006","url":null,"abstract":"<div><h3>Background</h3><div>Proinflammatory and neuroendocrine mediators are implicated in disease aetiopathogenesis. Stress increases concentrations of immune-neuroendocrine biomarkers through a complex network of brain-body signalling pathways. Suboptimal sleep further modulates these processes by altering major effector systems that sensitise the brain to stress. Given the ubiquitous, impactful nature of material deprivation, we tested for a synergistic association of financial stress and suboptimal sleep with these molecular processes.</div></div><div><h3>Methods</h3><div>With data drawn from the English Longitudinal Study of Ageing (ELSA), associations were tested on 4,940 participants (∼66 ± 9.4 years) across four-years (2008–2012). Through analytical triangulation, we tested whether financial stress (&gt;60% insufficient resources) and suboptimal sleep (≤5 / ≥9  h) were independently and interactively associated with immune-neuroendocrine profiles, derived from a latent profile analysis (LPA) of C-reactive protein, fibrinogen, white blood cell counts, hair cortisol, and insulin-like growth factor-1.</div></div><div><h3>Results</h3><div>A three-class LPA model offered the greatest parsimony. After adjustment for genetic predisposition, sociodemographics, lifestyle, and health, financial stress was associated with short-sleep cross-sectionally (RRR = 1.45; 95% CI = 1.18–1.79; <em>p</em> &lt; 0.001) and longitudinally (RRR = 1.31; 95% CI = 1.02–1.68; <em>p</em> = 0.035), and it increased risk of belonging to the <em>high-risk</em> inflammatory profile by 42% (95% CI = 1.12–1.80; <em>p</em> = 0.004). Suboptimal sleep was not related to future risk of <em>high-risk</em> profile membership, nor did it moderate financial stress-biomarker profile associations.</div></div><div><h3>Discussion</h3><div>Results advance psychoneuroimmunological knowledge by revealing how inflammation and neuroendocrine markers cluster in older cohorts and respond to financial stress over time. Financial stress associations with short-sleep are supported. The null role of suboptimal sleep, as exposure and mediator, in profile membership, provides valuable insight into the dynamic role of sleep in immune-neuroendocrine processes.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 396-408"},"PeriodicalIF":8.8,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroimmune and behavioral changes elicited by maternal immune activation in mice are ameliorated by early postnatal immune stimulation","authors":"Lourdes K. Davis ,&nbsp;Louise M. Ince ,&nbsp;Sriya Gullapalli ,&nbsp;Laura K. Fonken","doi":"10.1016/j.bbi.2025.03.005","DOIUrl":"10.1016/j.bbi.2025.03.005","url":null,"abstract":"<div><div>Though the etiology of autism spectrum disorder (ASD) is complex and not fully understood, it is believed that genetic risk factors, coupled with early life inflammation may predispose individuals to develop ASD. Maternal immune activation (MIA) is associated with increased incidence of ASD in offspring; however, not all mothers who experience inflammation during pregnancy have children with autism, suggesting that MIA may act as a disease primer that results in ASD pathology when paired with additional inflammatory insults. Here, we tested the hypothesis that MIA is a disease primer by using a two-hit model that combined MIA with a secondary immune stimulation in early life. C57BL/6J mouse dams were treated with polyinosinic-polycytidylic acid (Poly(I:C)) at embyronic day 12.5, and a subset of litters were then treated with the endotoxin lipopolysaccharide (LPS) four days after birth. Offspring were assessed in young adulthood for changes in behavior including sociability, repetitive-like behaviors, and anxiety-like behaviors. Flow cytometry was performed in adulthood to assess changes in immune cell populations in the periphery and in the brain. MIA increased repetitive-like behaviors in male mice and decreased sociability in both sexes. Unexpectedly, the secondary immune stimulation with LPS did not exacerbate changes in social and repetitive-like behaviors in either sex. MIA also altered distribution of cytotoxic CD8 + T cell populations in the periphery and brain of both sexes: CD8 + T cells were elevated in thymus but reduced in spleen, lymph, and brain. Additionally, MIA altered microglia activity in a region-specific manner in male mice, which was also not exacerbated but rather ameliorated when combined with LPS. Our results demonstrate that changes in repetitive-like and social behaviors that are induced by MIA in male mice are not exacerbated by subsequent inflammatory challenge and highlights the importance of considering the timing of stressors in the appearance of developmental pathology.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 375-386"},"PeriodicalIF":8.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623653","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":"Immune dysregulation in psychiatric disorders with and without exposure to childhood maltreatment: A transdiagnostic stratified meta-analysis","authors":"Minne Van Den Noortgate ,&nbsp;Manuel Morrens ,&nbsp;Marianne Foiselle ,&nbsp;Livia De Picker","doi":"10.1016/j.bbi.2025.03.002","DOIUrl":"10.1016/j.bbi.2025.03.002","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;Childhood maltreatment (CM), i.e. physical, psychological, or sexual abuse and neglect, affects approximately one third of the general population and is an important risk factor for all major psychiatric disorders. Exposure to CM also has a profound impact on immune function, with both factors independently implicated in the development and prognosis of different mental disorders. This study aims to 1) assess differences in immune markers among adults diagnosed with psychiatric disorders with and without a history of CM and 2) explore the role of CM as a mediating factor in immune abnormalities among psychiatric patients compared to non-psychiatric controls.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;A PRISMA-compliant systematic search of PubMed, Web of Science and Embase databases was performed until October 24th, 2024 for original studies that assessed immune markers in trauma-stratified adult psychiatric patients (PROSPERO ID CRD42021273059). We modelled random-effects &lt;em&gt;meta&lt;/em&gt;-analyses to compare levels of pro-inflammatory (PIM), anti-inflammatory (AIM) and cellular immune markers (CIM) between traumatized (CM + ) and non-traumatized (CM-) individuals, and investigated exposure to CM as a mediating factor in the immune abnormalities among adult psychiatric patients compared to non-psychiatric controls. Secondary analyses were performed for diagnostic subgroups and individual immune markers. Study quality was assessed with the Newcastle Ottawa Scale.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;We included data from 53 studies on n = 12,141 patients with mood disorders (MD), schizophrenia spectrum disorders (SSD), substance use disorders (SUD), eating disorders (ED) and anxiety disorders (AD). We uncovered a consistent transdiagnostic impact of CM on blood-based pro-inflammatory molecules (OR = 1.186; 95 % CI 1.030–1.365, p = 0.018) among patients with psychiatric disorders. This effect was not observed in the non-psychiatric controls included in the same studies. We did not find evidence of specific trauma-induced abnormalities in immune composite scores for separate diagnostic subgroups, except for PIM in SUD patients (OR = 2.324, 95 % CI 1.043–5.182, p = 0.039). Interleukin 6 (IL-6) was identified as a significant mediator between CM exposure and a psychiatric diagnosis in adulthood (OR = 1.609; 95 % CI 1.100–2.353, p = 0.014), while increases in C-reactive protein (CRP) and Interleukin 10 (IL-10) did not appear to be trauma-specific.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Our findings confirm a transdiagnostic impact of exposure to CM on increased pro-inflammatory molecular and cellular immune levels in psychiatric patients. IL-6 emerged as a crucial mediator, suggesting that CM leads to specific immune alterations predisposing individuals to psychiatric conditions. This &lt;em&gt;meta&lt;/em&gt;-analysis highlights the role of trauma-induced immune abnormalities as a potentially crucial mechanism contributing to increased vuln","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 193-204"},"PeriodicalIF":8.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting CB2 receptor with a novel antagonist reverses cognitive decline, neurodegeneration and pyroptosis in a TAU-dependent frontotemporal dementia mouse model","authors":"Ignacio Silva-Llanes ,&nbsp;Silvia Rodríguez-López ,&nbsp;Pedro González-Naranjo ,&nbsp;Eric del Sastre ,&nbsp;Manuela G. López ,&nbsp;Juan Antonio Páez ,&nbsp;Nuria Campillo ,&nbsp;Isabel Lastres-Becker","doi":"10.1016/j.bbi.2025.03.008","DOIUrl":"10.1016/j.bbi.2025.03.008","url":null,"abstract":"<div><div>Frontotemporal dementia (FTD) comprises a group of disorders characterized by a progressive decline in behavior or language linked to the degeneration of the frontal and anterior temporal lobes followed by hippocampal atrophy. There are no effective treatments for FTD and for this reason, novel pharmacological targets, such as the endocannabinoid system (ECS), are being explored. Previous results from our laboratory showed a TAU^P301L-dependent increase in CB₂ receptor expression in hippocampal neurons of a FTD mouse model, alongside the neuroprotective impact of CB₂ ablation. In this study, we evaluated the therapeutic potential of a new CB₂ antagonist (PGN36) in our TAU-dependent FTD mouse model. Six-month-old mice received stereotaxic injections of an adeno-associated virus expressing human TAU^P301L protein (AAV-TAU^P301L) into the right hippocampus and were treated daily with PGN36 (5 mg/kg, i.p.) or vehicle for three weeks. By integrating behavioral tests, RNA-seq, qPCR expression analysis, and immunofluorescence in the AAV expressing TAU mouse model, we found that PGN36 treatment reverses key features of the neurodegenerative process triggered by TAU^P301L overexpression. PGN36 treatment effectively countered TAU^P301L-induced cognitive decline by reducing TAU protein expression levels and restoring markers of synaptic plasticity. Notably, we observed neuroprotection in the dentate gyrus granular layer, which we attribute to the modulation of pyroptosis. This programmed cell death pathway, is triggered by TAU^P301L overexpression. PGN36 appears to modulate the pyroptotic cascade, thereby preventing the pyroptosis-induced neuronal loss. These findings collectively underscore the neuroprotective potential of this novel CB₂ antagonist treatment against TAU-associated FTD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 251-268"},"PeriodicalIF":8.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623654","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":"Psychological correlates of antibody response to mRNA SARS-CoV-2 vaccination: A prospective observational cohort study","authors":"Kieran Ayling ,&nbsp;Hannah Jackson ,&nbsp;Ru Jia ,&nbsp;Simon Royal ,&nbsp;Lucy Fairclough ,&nbsp;Kavita Vedhara","doi":"10.1016/j.bbi.2025.03.011","DOIUrl":"10.1016/j.bbi.2025.03.011","url":null,"abstract":"<div><h3>Background</h3><div>Vaccines fundamentally changed the course of the COVID-19 pandemic, saving &gt; 14 million lives within a year. However, vaccine-conferred protection showed inter-individual variability, with many identified correlates of protection (e.g., age) not amenable to change. This prospective observational cohort study examined whether modifiable psychological factors (depressive symptoms, anxiety, perceived stress and positive mood), which predict antibody responses to other vaccines, also influenced the effectiveness of COVID-19 vaccines. We focussed on novel mRNA vaccines as these conferred greater clinical protection and psychological correlates have not been investigated in these vaccines previously.</div></div><div><h3>Methods</h3><div>One-hundred and eighty-four adults attending a mass-vaccination centre in the UK received a two-dose BNT162b2 mRNA SARS-CoV-2 vaccine course, completed validated psychological measures, and provided blood samples prior to vaccination and 4 weeks following the second vaccine dose.</div></div><div><h3>Results</h3><div>In separate linear regression models controlling for pre-vaccination antibody levels, demographic and clinical factors, higher levels of depressive symptoms (β = -0.15 [95 % CI: −0.30, −0.01], <em>p</em> = 0.041, partial <em>f</em>² = 0.009) and lower levels of positive mood (β = 0.16 [95 % CI: 0.01, 0.30], <em>p</em> = 0.036, partial <em>f</em>² = 0.011) were significantly associated with lower SARS-CoV-2 spike-specific antibody levels following vaccination. No significant relationships were observed between measures of anxiety or perceived stress and antibody responses.</div></div><div><h3>Conclusions</h3><div>Lower levels of depressive symptoms and greater positive mood were associated with larger antibody responses following mRNA SARS-CoV-2 vaccination in a community sample attending for their first course of COVID-19 vaccinations. As both are amenable to change, they could offer mechanisms for enhancing vaccine effectiveness particularly among populations at greater risk of vaccine failure.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 103-109"},"PeriodicalIF":8.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143611655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of macrophage efferocytosis by the CLCF1/NF-κB pathway improves neurological and cognitive impairment following CO poisoning","authors":"Xudong Zhou ,&nbsp;Jingjing He ,&nbsp;Huiping Song ,&nbsp;Weiwei Zhao ,&nbsp;Rui Li ,&nbsp;Wei Han ,&nbsp;Qin Li","doi":"10.1016/j.bbi.2025.03.003","DOIUrl":"10.1016/j.bbi.2025.03.003","url":null,"abstract":"<div><div>Severe carbon monoxide (CO) poisoning can induce structural and functional damage to the nervous system, resulting in persistent cognitive impairments. Properly terminating inflammation caused by neuronal damage is essential for tissue repair. Macrophages clear cell corpses and fragments through efferocytosis and produce cytokines to coordinate the immune response, thus promoting neuronal repair and regeneration. However, within the microenvironment of the CO-affected nervous system, macrophage efferocytosis is disrupted. Our study found that macrophages regulate efferocytosis by releasing Cardiotrophin-like cytokine factor 1 (CLCF1), which modulates the NF-κB pathway in both macrophages and microglia, thereby controlling inflammation and promoting nervous system repair. Furthermore, efferocytosis regulates the secretion of cytokines such as TNF-α, IL-1β, and IL-10, promoting M2 polarization of macrophages, which aids in neuronal repair and regeneration. Regulating macrophage CLCF1 expression also leads to improvements in the memory, learning, and motor abilities of rats poisoned with CO.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 126-146"},"PeriodicalIF":8.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143621530","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":"CX3CL1-CX3CR1 pathway mediates hyperthermia-induced microglial processes retraction","authors":"Ru Song ,&nbsp;Chunhua Liu ,&nbsp;Minqi Peng ,&nbsp;Zhengjiang Qian ,&nbsp;Mingyu Wei ,&nbsp;Fangmei Yu ,&nbsp;Mingchen Yao ,&nbsp;Xiang Li ,&nbsp;Bo Feng","doi":"10.1016/j.bbi.2025.03.007","DOIUrl":"10.1016/j.bbi.2025.03.007","url":null,"abstract":"<div><div>In infants, high fever is associated with robust microglial morphological changes, including process retraction and soma enlargement, which contribute to fever-induced seizures. The molecular mechanisms underlying dynamic process retraction during hyperthermia remain poorly understood. Using a hyperthermia-induced microglial activation model in postnatal day 8 mice, we identified the CX₃CL1-CX₃CR1 interaction as a key regulator of process retraction. The CX₃CL1 is mainly cleaved by metalloproteases ADAM10 under hyperthermia stimulation. Pharmacological inhibition or genetic knockdown of ADAM10 prevented microglial process retraction. Hyperthermia is known to induce the release of glutamate and activation of the NMDA receptor. We found that NMDA mimicked the effects of hyperthermia on microglia, while the NMDA blocker MK801 attenuated hyperthermia-induced process retraction. Collectively, our findings suggest that the CX₃CL1-CX₃CR1 pathway plays a critical role in mediating dynamic microglial process retraction in response to hyperthermia.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 205-216"},"PeriodicalIF":8.8,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}