Brain, Behavior, and Immunity最新文献

{"title":"Pathogen-specific exposure is associated with multisite chronic pain: A prospective cohort study","authors":"Jialiu Fang ,&nbsp;Zemene Demelash Kifle ,&nbsp;Jing Tian ,&nbsp;Silvana Bettiol ,&nbsp;Flavia Cicuttini ,&nbsp;Graeme Jones ,&nbsp;Feng Pan","doi":"10.1016/j.bbi.2025.05.028","DOIUrl":"10.1016/j.bbi.2025.05.028","url":null,"abstract":"<div><div>Evidence suggests that pathogens may influence pain perception and regulation; however, no study has explored the relationship between serological evidence of infection and multisite chronic musculoskeletal pain. Therefore, this study aimed to investigate the association between serological evidence of infection and multisite chronic musculoskeletal pain. Participants (n = 6,814; mean [SD]age, 56.5[8.2] years; females [52.9 %]) in the UK Biobank were included. Multiplex serology panel measuring serum immunoglobulin G antibody levels against 20 infectious agents was performed at baseline. Chronic pain (≥3 months) in the knee, neck/shoulder, hip, back, or ‘all over the body’ was assessed at baseline and follow-up. Participants were grouped by number of chronic pain sites: no chronic pain, chronic pain in 1–2 sites, or ≥3 sites. Multinomial logistic regression and mixed-effect multinomial logistic regression models were used for the analyses. The seroprevalences of serologically detected infections across the 20 agents ranged from 0.2 % to 95.4 %. In multivariable analyses, serological evidence of infection with Epstein-Barr Virus (EBV), Human T-Cell Lymphotropic Virus Type-1 (HTLV-1), and <em>Chlamydia Trachomatis</em> was cross-sectionally associated with chronic pain in ≥3 sites compared to those without chronic pain. In longitudinal analyses, EBV [relative risk ratio (RRR) = 2.18, 95 %CI:1.17 − 4.05] and <em>Chlamydia Trachomatis</em> [RRR = 1.38, 95 %CI:1.09 − 1.74] were also associated with chronic pain in ≥3 sites. Additionally, serological evidence of single and multiple infections was associated with chronic pain in ≥3 sites, but not in 1–2 sites. Collectively, serological evidence of infection with EBV and <em>Chlamydia Trachomatis</em> is associated with multisite chronic musculoskeletal pain. These findings suggest that infectious agents may play a role in the pathogenesis of widespread chronic pain.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 157-164"},"PeriodicalIF":8.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144231355","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":"Nod2 deficiency exacerbates schizophrenia-related alterations in offspring of maternal immune activation in a sex-dependent manner","authors":"Fengjie Gao ,&nbsp;Chuyao Wang ,&nbsp;Zhen Cao ,&nbsp;Xinyu Zhang ,&nbsp;Wenyu Xi ,&nbsp;Yixin Liu ,&nbsp;Xianyan Zhan ,&nbsp;Min Jia ,&nbsp;Ningzhi Gou ,&nbsp;Lu Yu ,&nbsp;Yudan Zhang ,&nbsp;Yijie Guo ,&nbsp;Wei Wang ,&nbsp;Feng Zhu ,&nbsp;Xiancang Ma ,&nbsp;Yuan Gao","doi":"10.1016/j.bbi.2025.05.030","DOIUrl":"10.1016/j.bbi.2025.05.030","url":null,"abstract":"<div><h3>Introduction</h3><div>Schizophrenia is a severe mental disorder with a complex etiopathogenesis involving both genetic and environmental risk factors. Evidence suggests that immune dysregulation plays a key role in its development, with maternal immune activation (MIA) during pregnancy identified as a significant environmental contributor. However, not all maternal infections result in schizophrenia-like outcomes, indicating that genetic susceptibility may render some individuals more vulnerable to MIA. Nucleotide-binding oligomerization domain-containing protein 2 (NOD2), an intracellular receptor, plays a crucial role in maintaining the balance between intestinal microbiota and immune responses, but its precise role in gut-brain interactions during neurodevelopment remain unclear.</div></div><div><h3>Methods</h3><div>To investigate the interaction between MIA and <em>Nod2</em> deficiency, we evaluated behavioral and physiological phenotypes in <em>Nod2</em>^-/- mice exposed to poly(I:C)-induced MIA. In addition to immune responses, we analyzed maternal gut microbiota and the transmission of microbiota between mothers and offspring. Given the role of the gut-brain axis in schizophrenia, we conducted intestinal immunofluorescence staining, organoid cultures, and RNA sequencing of fetal brains to assess gut injury and neuroimmune changes in the brain. Male and female offspring were analyzed separately.</div></div><div><h3>Results</h3><div>Dual exposure led to schizophrenia-like behaviors in a sex-specific manner, as well as brain development disruptions, compromised gut integrity, reduced intestinal organoid-forming capacity, and altered gut microbiota composition. Importantly, maternal gut microbiota disturbances, coupled with microbial transmission to offspring, appear to increase schizophrenia risk with potential long-term behavioral consequences.</div></div><div><h3>Conclusion</h3><div>This study underscores the intricate interplay of genetic, environmental, and microbiome factors, offering a valuable model for investigating the complex pathophysiology of neurodevelopmental disorders.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 126-142"},"PeriodicalIF":8.8,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207728","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":"Commentary to the article: “Differences in inflammation among black and white individuals: A systematic review and meta-analysis”","authors":"Aura Maria Ramírez ,&nbsp;Laura Manuela Olarte Bermúdez ,&nbsp;Nelson Bedoya","doi":"10.1016/j.bbi.2025.05.029","DOIUrl":"10.1016/j.bbi.2025.05.029","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 124-125"},"PeriodicalIF":8.8,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207727","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":"HDAC inhibitors engage MITF and the disease-associated microglia signature to enhance amyloid β uptake","authors":"Verena Haage ,&nbsp;John F. Tuddenham ,&nbsp;Alex Bautista ,&nbsp;Frankie Garcia G. ,&nbsp;Charles C. White ,&nbsp;Ronak Patel ,&nbsp;Natacha Comandante-Lou ,&nbsp;Victoria Marshe ,&nbsp;Jennifer Griffin ,&nbsp;Ye Zhou ,&nbsp;Deniz Ghaffari ,&nbsp;Beatrice Acheson ,&nbsp;Mariko Taga ,&nbsp;Peter H. St George-Hyslop ,&nbsp;Rajesh Kumar Soni ,&nbsp;Peter A. Sims ,&nbsp;Vilas Menon ,&nbsp;Andrew A. Sproul ,&nbsp;Philip L. De Jager","doi":"10.1016/j.bbi.2025.05.027","DOIUrl":"10.1016/j.bbi.2025.05.027","url":null,"abstract":"<div><div>Disease-associated microglia (DAM), initially described in mouse models of neurodegenerative diseases, have been classified into two related states; starting from a TREM2-independent DAM1 state to a TREM2dependent state termed DAM2, with each state being characterized by the expression of specific marker genes (Keren-Shaul, 2017). Recently, single-cell (sc)RNA-Seq studies have reported the existence of DAM in humans (Pettas, 2022; Jauregui, 2023; Friedman, 2018; Mathys, 2019; Tuddenham, 2024); however, whether DAM play beneficial or detrimental roles in the context of neurodegeneration is still under debate (Butovsky and Weiner, 2018; Wang and Colonna, 2019). Here, we present a pharmacological approach to mimic human DAM <em>in vitro</em>: we validated <em>in silico</em> predictions that two different histone deacetylase (HDAC) inhibitors, Entinostat and Vorinostat, recapitulate aspects of the DAM signature in two human microglia-like model systems. HDAC inhibition increases RNA expression of <em>MITF</em>, a transcription factor previously described as a regulator of the DAM signature (Dolan, 2023). This engagement of <em>MITF</em> appears to be associated with one part of the DAM signature, refining our understanding of the DAM signature as a combination of at least two transcriptional programs that appear to be correlated <em>in vivo</em>. Further, we functionally characterized our DAM-like model system, showing that the upregulation of this transcriptional program by HDAC inhibitors leads to an upregulation of amyloid β and pHrodo Dextran uptake – while E.coli uptake is reduced – and a specific reduction of MCP1 secretion in response to IFN-γ and TNF-α. Enhanced amyloid β uptake was confirmed in iPSC-derived microglia. Overall, our strategy for compound-driven microglial polarization offers potential for exploring the function of human DAM and for an immunomodulatory strategy around HDAC inhibition.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 279-293"},"PeriodicalIF":8.8,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198276","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":"Plasma kynurenine pathway metabolite levels increase in depressed patients after antidepressant treatment","authors":"Romain Colle ,&nbsp;Kenneth Chappell ,&nbsp;Khalil El Asmar ,&nbsp;Bruno Fève ,&nbsp;Philippe Chanson ,&nbsp;Denis J. David ,&nbsp;Céline Verstuyft ,&nbsp;Laurent Becquemont ,&nbsp;Emmanuelle Corruble","doi":"10.1016/j.bbi.2025.05.025","DOIUrl":"10.1016/j.bbi.2025.05.025","url":null,"abstract":"<div><div>The kynurenine (KYN) pathway helps regulate physiological systems implicated in major depressive disorder (MDD). We showed that plasma levels of KYN, kynurenic acid (KA), xanthurenic acid (XA), 3-hydroxyanthranilic acid (3-HAA), and picolinic acid (PA) are lower in depressed individuals. However, whether these levels are restored following treatment with antidepressant drugs (AD) and if this restoration is associated with clinical improvement remains unclear. Fasting plasma levels of tryptophan (TRP) and these metabolites, as well as the KYN/TRP ratio, were investigated in 173 depressed patients of the METADAP cohort and 214 healthy controls of VARIETE. Measures were obtained at baseline and 3 and 6 months after beginning AD treatment. Post-treatment changes in metabolites and their associations with changes in the 17-item Hamilton Depression Rating Scale (HDRS) score were analyzed using linear mixed-effects models. Plasma metabolite levels increased following AD treatment, with significant increases in KA (<em>P_FDR</em> = 0.00014), 3-HAA (<em>P_FDR</em> = 0.034), and PA (<em>P_FDR</em> = 0.0097). The KYN/TRP ratio and KA failed to return to healthy control levels. Increases in the KYN/TRP ratio (coef = -1.08, 95 %CI [-1.92–-0.23], <em>P_FDR</em> = 0.045) and KYN levels (coef = -2.37, 95 %CI [-3.83–-0.91], <em>P_FDR</em> = 0.0011) were significantly associated with HDRS score reductions, indicating depressive symptom improvement. Altogether, we observed increases in plasma KYN pathway metabolite levels in depressed patients following 6 months of AD treatment that, for some, was significantly associated with clinical improvement. Our findings suggest increases in these metabolites may be relevant to treating depression.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 92-99"},"PeriodicalIF":8.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166989","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":"Long-term dynamics of the spinal cord injury neuroinflammatory response and sensory dysfunction in female mice","authors":"Neal J. Wrobel ,&nbsp;Quan Shen ,&nbsp;Dustin H. Kim ,&nbsp;Bahar Adavoody ,&nbsp;Daniela Garcia Prada ,&nbsp;Richard G. Fessler ,&nbsp;Brian T. David","doi":"10.1016/j.bbi.2025.05.024","DOIUrl":"10.1016/j.bbi.2025.05.024","url":null,"abstract":"<div><div>The neuroinflammatory response which takes place within the spinal cord following a traumatic spinal cord injury (SCI) is widely recognized as a major influencer of the progression and severity of the secondary tissue damage which occurs after injury onset. Immunomodulatory therapies aimed at reducing secondary injury are, therefore, a notable point of focus in SCI research. To inform future studies aimed at development of such therapies, we present a detailed characterization of the dynamics of the spinal cord neuroimmune response in mice throughout the first 6 months after contusive SCI.</div><div>Female wild type (C57BL/6) mice received moderate spinal cord contusions at T9 (<em>n</em> = 8/cohort) while control mice remained naïve (<em>n</em> = 6/cohort). Nine terminal assessment time points were included, ranging from 1 day to 6 months post-injury (each timepoint was replicated between one and four times). At each terminal time point, levels of T cells, helper T cells, cytotoxic T cells, regulatory T cells, macrophages, and microglia within the spinal cord were assessed via flow cytometry. Measures of locomotor (open-field task) and sensory (tail flick) function were used to assess behavioral recovery.</div><div>The spinal cord neuroimmune response in mice exhibited a biphasic pattern, with one peak of peripheral immune cell infiltration within the first 2 weeks post-injury, followed by a second peak at 2 months post-injury. Both T cells and macrophages remained elevated in injured spinal cords, relative to controls, at 6 months post-injury. Spinal cord inflammation correlated with exacerbated sensory impairment acutely but correlated with greater normalization of sensory function at 6 months post-injury. Higher inflammation at 6 months post-injury was also associated with an increase in spleen to body mass ratio.</div><div>Together, the results of this investigation highlight the persistent nature of the SCI neuroinflammatory response and indicate that its relationship to other bodily systems continues to evolve even in the late-chronic stage of injury.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 143-156"},"PeriodicalIF":8.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180251","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":"Serum antineuronal antibodies in patients with post-COVID-19 condition − association to intensive care","authors":"Tatiana Posharina ,&nbsp;Mikko Varonen ,&nbsp;Hanna Jarva ,&nbsp;Mari Kanerva ,&nbsp;Helena Liira ,&nbsp;Sini M Laakso","doi":"10.1016/j.bbi.2025.05.026","DOIUrl":"10.1016/j.bbi.2025.05.026","url":null,"abstract":"<div><div>Post-COVID-19 condition (PCC), characterized by persistent symptoms following SARS-CoV-2 infection, is a global health challenge. Neurological symptoms are common in PCC, and immune-mediated mechanisms have been proposed as potential contributors. We set out to systematically explore serum antineuronal antibodies in patients with PCC and clinical factors associated with seropositivity.</div><div>Our prospective, single-center cohort study included adult patients with a confirmed SARS-CoV-2 infection at least three months prior and a diagnosis of PCC. Serum and cerebrospinal fluid (CSF) samples were analyzed for the presence of antineuronal antibodies. A control group with confirmed SARS-CoV-2 infection but without PCC symptoms was included, age-, sex- and time from acute infection to sampling −matched to seropositive cases of PCC.</div><div>Among 314 consecutive patients with PCC, 38 (12.1 %) tested positive for serum antineuronal antibodies. CSF analysis was performed for a subset; however, no intrathecal autoantibodies were detected. The most prevalent serum autoantibodies targeted CASPR-2 (n = 7, 18.9 %), neurofascin-186 (n = 5, 13.2 %), and glycine receptor (n = 4, 10.8 %). Multinomial logistic regression identified intensive care unit (ICU) admission during acute COVID-19 as the only significant predictor of autoantibody positivity (OR 3.4; 95 % CI: 1.0–10.4). Of the 35 control subjects, two (5.7 %) tested seropositive: one with low titer myelin oligodendrocyte glycoprotein antibodies and another with borderline myelin antibody levels. None of the patients met criteria for autoimmune encephalitis, and neurological assessments and brain magnetic resonance imaging were unremarkable. Neuropsychological testing showed a trend toward impairments in attention and executive functions among seropositive individuals.</div><div>Thus, there was no significant difference in the prevalence of serum antineuronal antibodies in PCC compared to post-infection controls, and the association between seropositivity and ICU admission suggested systemic immune activation rather than a specific autoantibody-mediated mechanism. It remains unclear whether observed neuropsychological deficits are attributable to autoantibodies or the effects of critical illness.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 87-91"},"PeriodicalIF":8.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155191","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":"Multimodal markers of immune activation predict cognitive outcomes in Parkinson’s disease","authors":"K.M. Scott ,&nbsp;L.R.B. Spindler ,&nbsp;A.R.D. Peattie ,&nbsp;A. Kouli ,&nbsp;T.D. Fryer ,&nbsp;Y.T. Hong ,&nbsp;M. Camacho ,&nbsp;I. Solim ,&nbsp;L. Kahanawita ,&nbsp;C.H. Williams-Gray","doi":"10.1016/j.bbi.2025.05.020","DOIUrl":"10.1016/j.bbi.2025.05.020","url":null,"abstract":"<div><h3>Background</h3><div>Inflammation is well described in the central nervous system (CNS) and the periphery in Parkinson’s disease (PD) and has been implicated in dementia risk. Longitudinal studies to identify immune/inflammatory biomarkers predicting cognitive decline are lacking.</div></div><div><h3>Methods</h3><div>Peripheral blood mononuclear cells and cerebrospinal fluid (CSF)-derived immune cells were obtained from newly-diagnosed PD cases and healthy controls as part of the NET-PDD study. Immunophenotyping was performed using flow cytometry. CSF:blood ratios were calculated as a index of cell ingress to the CNS. Neuroinflammation was evaluated using ¹¹C-PK11195 positron emission tomography (PET) MRI scanning. Participants were then followed-up clinically for 3 years to determine cognitive outcomes.</div></div><div><h3>Results</h3><div>Bivariate comparisons between PD cases who were cognitively impaired at 3 years (PD-CI N = 10), PD non cognitively impaired (PD-NCI, N = 25) and controls (N = 36) identified 22 blood/CSF immune variables that differed between groups. The differences with the largest effect sizes (Cliff’s d) were a higher proportion of activated CD4 T cells in the blood (CD4 + CD28+, d = 0.63) and a higher CSF:blood ratio of memory B cells (d = 0.63) in PD-CI versus controls. The substantia nigra was the only brain region in which PD-CI versus controls showed a higher ¹¹C-PK11195 non-displaceable binding potential (BP_ND) (d = 0.45). In a multivariate regression model including age and gender, the CSF:blood memory B cell ratio and substantia nigra ¹¹C-PK11195 BP_ND at baseline predicted cognitive decline over 3 years. ROC analysis demonstrated that the lead blood, CSF and imaging markers individually predicted cognitive status at 3 years with good accuracy (AUC 0.79–0.85).</div></div><div><h3>Conclusions</h3><div>An increase in activated CD4 cells in the blood, transition of B cells to the CNS and inflammation in the substantia nigra were predictive of longitudinal cognitive outcomes in PD. These markers warrant further validation as biomarkers for immune/inflammatory stratification and add to the evidence supporting development of therapeutic strategies to reduce microglial inflammation or the recruitment of lymphocytes to the CNS in early PD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 165-178"},"PeriodicalIF":8.8,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144156961","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":"Telomere-mitochondrial dynamics differ depending on childhood maltreatment history, catabolic postpartum state, and developmental period","authors":"R. Nehir Mavioglu ,&nbsp;Anja M. Gumpp ,&nbsp;Elisabeth M. Hummel ,&nbsp;Dirk A. Moser ,&nbsp;Ole Ammerpohl ,&nbsp;Alexander Behnke ,&nbsp;Matthias Mack ,&nbsp;Iris-Tatjana Kolassa","doi":"10.1016/j.bbi.2025.05.022","DOIUrl":"10.1016/j.bbi.2025.05.022","url":null,"abstract":"<div><div>Telomere attrition, a hallmark of aging, is linked to high-energy demand states like early development and biological or psychological stress. Metabolic regulation of telomere length (TL) may occur in these states as part of an energetic trade-off, prioritizing immediate needs over long-term requirements such as telomere maintenance, though this has not been observed in healthy humans. We examined associations between TL and mitochondrial bioenergetics, density, and DNA markers in immune cells of women at 1-week (<em>n</em> = 175) and 1-year postpartum (<em>n</em> = 106), depending on their history of childhood maltreatment (CM), and in their newborns (<em>n</em> = 132). At 1-week postpartum, a catabolic state of high energy demand, women with lower mitochondrial energy production efficiency exhibited shorter TL. One year later, these dynamics appeared only in women with a history of CM. In newborns, TL was shorter when mitochondrial density-normalized routine and ATP production-related respiration was higher. Mitochondrial DNA copy number was associated with TL in both mothers and newborns, regardless of the energetic state. Our findings suggest that telomere-mitochondrial dynamics can adapt to the body’s energetic needs.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 267-278"},"PeriodicalIF":8.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149118","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":"BBI commentary: Breaking barriers: How maternal bacteria influences foetal neurodevelopment","authors":"Philip W.J. Burnet","doi":"10.1016/j.bbi.2025.05.019","DOIUrl":"10.1016/j.bbi.2025.05.019","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"Pages 52-53"},"PeriodicalIF":8.8,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107642","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}