Brain, Behavior, and Immunity最新文献

{"title":"Interactions between sex hormones and the gut microbiome","authors":"Linnea R. Freeman","doi":"10.1016/j.bbi.2025.02.025","DOIUrl":"10.1016/j.bbi.2025.02.025","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages 313-314"},"PeriodicalIF":8.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487408","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":"Altered monocyte subpopulations and their association with autism spectrum disorder risk in children","authors":"Wenhua Li ,&nbsp;Lingling Zhang ,&nbsp;Yiran Xu ,&nbsp;Hongwei Li ,&nbsp;Bingbing Li ,&nbsp;Shuang Sun ,&nbsp;Xiaoli Zhang ,&nbsp;Guiqin Duan ,&nbsp;Yiwen Chen ,&nbsp;Jie Zhang ,&nbsp;Yangyang Cao ,&nbsp;Xiaoping Li ,&nbsp;Qianqian Liu ,&nbsp;Yanan Wu ,&nbsp;Shan Zhang ,&nbsp;Jianmei W. Leavenworth ,&nbsp;Xiaoyang Wang ,&nbsp;Changlian Zhu","doi":"10.1016/j.bbi.2025.02.028","DOIUrl":"10.1016/j.bbi.2025.02.028","url":null,"abstract":"<div><h3>Objective</h3><div>Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficits in social communication, restricted interests, and repetitive behaviors. Emerging evidence suggests a link between immune dysregulation and ASD. This study investigates alterations in monocyte subpopulations and cytokine production in children with ASD and their potential associations with ASD risk and severity.</div></div><div><h3>Methods</h3><div>Initially, the immune status of peripheral blood mononuclear cells was assessed in cohort-I of 96 typically developing (TD) children and 92 children diagnosed with ASD using flow cytometry. Subsequently, the secretion of cytokines IL-6 and IL-10 by monocytes was evaluated following stimulation with a leukocyte activation mixture and intracellular protein staining technique in cohort-II.</div></div><div><h3>Results</h3><div>Children with ASD exhibited significantly higher levels of total monocytes, classical monocytes (CD14^hi/CD16^–), and non-classical monocytes (CD14^low/CD16⁺) compared to TD children (<em>p</em> &lt; 0.001). Elevated levels of classical monocytes (β: 0.395; 95 %CI: 0.260–0.530; <em>p</em> &lt; 0.001) and non-classical monocytes (β: 0.629; 95 %CI: 0.516–0.742; <em>p</em> &lt; 0.001) were significantly associated with ASD after adjusting for age, sex and body mass index. Furthermore, increased production of IL-6 by monocytes was observed in children with ASD (<em>p</em> = 0.001). Logistic regression analysis revealed that classical monocytes (OR: 1.104; 95 %CI: 1.062–1.147; <em>p</em> &lt; 0.001), non-classical monocytes (OR: 2.913; 95 %CI: 2.130–3.986; <em>p</em> &lt; 0.001) and IL-6 production by monocytes (OR: 1.306; 95 %CI: 1.096–1.557; <em>p</em> = 0.003) are risk factors for ASD. Spearman correlation analysis revealed a negative correlation between classical monocyte levels and adaptive behavior developmental quotient (DQ) (r = − 0.377; <em>p</em> = 0.001), fine motor DQ (r = − 0.329; <em>p</em> = 0.003) and personal-social DQ (r = − 0.247; <em>p</em> = 0.029) in children with ASD.</div></div><div><h3>Conclusion</h3><div>Elevated classical and non-classical monocytes are potential risk factors for ASD and may influence neurodevelopmental outcomes. Further research is needed to elucidate the precise mechanisms and therapeutic implications.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages 315-326"},"PeriodicalIF":8.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487407","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":"Further insights and suggestions for improving the study of infections and neurodegenerative disease risk in diabetes","authors":"E Zhao ,&nbsp;Zhengting Duan ,&nbsp;Jingmei Li","doi":"10.1016/j.bbi.2025.02.026","DOIUrl":"10.1016/j.bbi.2025.02.026","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Page 274"},"PeriodicalIF":8.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143480338","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":"Under pressure: Stress and autoimmune diabetes in war","authors":"Daljeet Kaur,&nbsp;Tal-Talya Avitan,&nbsp;Ron Piran","doi":"10.1016/j.bbi.2025.02.033","DOIUrl":"10.1016/j.bbi.2025.02.033","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 1-3"},"PeriodicalIF":8.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514686","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":"Gut microbiome-derived lipopolysaccharides aggravate cognitive impairment via TLR4-mediated inflammatory signaling in neonatal rats following hypoxic-ischemic brain damage","authors":"Jianjie Wei ,&nbsp;Andi Chen ,&nbsp;Dongqin Huang ,&nbsp;Chengqian Teng ,&nbsp;Dingliang Cai ,&nbsp;Xuyang Wu ,&nbsp;Tianwei Wang ,&nbsp;Weibin Hu ,&nbsp;Zhibin Huang ,&nbsp;Peiyu Wang ,&nbsp;Xin Guan ,&nbsp;Xiaochun Zheng ,&nbsp;Xiaohui Chen","doi":"10.1016/j.bbi.2025.02.029","DOIUrl":"10.1016/j.bbi.2025.02.029","url":null,"abstract":"<div><div>Hypoxic-ischemic brain damage (HIBD) is a leading cause of infant mortality and neurological disabilities in children. Recent evidence indicates that gut microbiota significantly contributes to the development of inflammation and cognitive impairments following brain injury. However, the mechanisms by which gut microbiota influence inflammation and cognitive function in the neonates after HIBD are not well understood. This study established a neonatal rat model of HIBD by the classic Rice-Vannucci technique to investigate gut dysbiosis following hypoxic-ischemic (HI) insult and to elucidate the causal relationship between gut dysbiosis and cognitive impairments. Our results demonstrated that HI insult resulted in significant gut microbial dysbiosis, characterized by an expansion of <em>Enterobacteriaceae</em>. This dysbiosis was associated with intestinal barrier damage, lipopolysaccharides (LPS) leakage, and systemic inflammation. Conversely, administration of aminoguanidine (AG) to inhibit <em>Enterobacteriaceae</em> overgrowth restored intestinal barrier integrity and reduced systemic inflammation. Importantly, AG treatment effectively suppressed microglial activation, neuronal damage, and cognitive impairments in the neonatal rats subjected to HI insult. Additionally, RNA sequencing analysis revealed that differentially expressed genes in both colonic and hippocampal tissues were primarily associated with inflammation and neuronal apoptosis after HI insult. Further mechanistic exploration revealed that AG treatment mitigated intestinal LPS leakage, thereby reducing the activation of the TLR4/MyD88/NF-κB signaling pathway and production of the downstream inflammatory cytokines in both the colon and hippocampus. Notably, fecal microbiota transplantation (FMT) from the HIBD rats to the antibiotic cocktail-treated recipient rats resulted in microglial activation, neuronal damage, and cognitive impairments in the recipients. However, these adverse effects were effectively mitigated in the recipient rats that received FMT from the AG-treated donors, as well as in those undergoing hippocampal TLR4 knockdown. In conclusion, our findings indicate that LPS derived from gut <em>Enterobacteriaceae</em> overgrowth plays a critical role in the TLR4-mediated inflammatory signaling, providing a novel microbiota-based therapeutic approach for cognitive impairments following neonatal HIBD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 4-24"},"PeriodicalIF":8.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514684","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":"LGBTQ+ identity and its association with inflammation and cellular immune function","authors":"Ethan Morgan ,&nbsp;Claire M. Kamp Dush ,&nbsp;Thomas W. McDade ,&nbsp;Juan Peng ,&nbsp;Rebecca R. Andridge ,&nbsp;Steve W. Cole ,&nbsp;Wendy Manning ,&nbsp;Lisa M. Christian","doi":"10.1016/j.bbi.2025.02.032","DOIUrl":"10.1016/j.bbi.2025.02.032","url":null,"abstract":"<div><div>Self-identification among lesbian, gay, transgender, queer, and other sexual minorities (LGBTQ+) is complex and multifaceted, yet few studies have examined its impact on immune parameters. The National Couples’ Health and Time Study (NCHAT) is a nationally-representative cohort of 3,642 adult main respondents, ages 20 to 60 years, who are married or cohabiting, among whom 45 % self-identify as a non-heterosexual identity. Biological data were collected from a subset in the NCHAT Stress Biology study (NCHAT-BIO). The current analyses focus on data from 289 participants in NCHAT-BIO who identified as a non-heterosexual identity. Participants self-reported demographic, mental health, and LGBTQ+ identity items. Finger stick dried blood spot (DBS) sampling was self-administered by participants and assayed for C-reactive protein (CRP), interleukin-6 (IL-6), and antibodies against Epstein-Barr virus (EBV). Multivariable regression analyses were used to assess the relationship between each of the biomarkers and: 1) individual LGBTQ+ identity items and 2) latent profiles of LGBTQ+ identity items. Models were adjusted for demographic factors and other confounders. Among those assigned female at birth, a greater sense of pride in one’s LGBTQ+ identity was associated with lower EBV antibody levels. Among those assigned male at birth, greater desire to keep one’s identity private was associated with elevated CRP while those who would choose to be straight or wish they were heterosexual had elevated levels of IL-6. Meanwhile, being proud of one’s LGBTQ+ identity predicted lower IL-6. These results provide novel evidence from a large sample that internalized stigma related to one’s LGBTQ+ identity is associated with elevated inflammation and poorer cellular immune function while identity affirmation is associated with reduced inflammation. Future research should aim to develop and target both behavioral and biomedical interventions aimed at reducing health disparities among sexual minority populations.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages 333-341"},"PeriodicalIF":8.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514685","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":"From smooth brains to rocky mountains: Quentin Pittman in a Quintessentially Canadian career","authors":"K. Crosby ,&nbsp;A.C. Kentner ,&nbsp;J.B. Kuzmiski ,&nbsp;A. Mouihate ,&nbsp;A. Reid ,&nbsp;S.J. Spencer","doi":"10.1016/j.bbi.2025.02.024","DOIUrl":"10.1016/j.bbi.2025.02.024","url":null,"abstract":"<div><div>This commentary is to honour Dr Quentin Pittman as he steps back from an active role in academia. Pittman’s work leaves a legacy of ground-breaking discoveries, impeccable research, and generous mentorship. His work on thermoregulation, vasopressin, perinatal programming, and hypothalamic function laid a good part of the foundation of the psychoneuroimmunology research we do today. His interest in neuroinflammation led to important findings in animal models of chronic peripheral inflammation including colitis and central inflammatory states observed in epilepsy and multiple sclerosis. His integrative approach, ranging from electrophysiological recordings to whole animal behaviour helped answer physiological questions involving the orchestrated functions and interactions of multiple organs. He is one of a few neuroscientists who raised the question of the contribution of peripheral organs to brain function and plasticity at a time when the field was largely neurocentric. Pittman has enhanced our collective understanding of the effects of neonatal inflammation (and other models of perinatal programming) on the adult brain, and has even revealed key ways in which neurons in the brain communicate with each other, through his work on vasopressin, endocannabinoids, and other transmitters. Altogether, Quentin Pittman’s interdisciplinary work has laid a solid foundation for psychoneuroimmunology research and groundbreaking insight into brain-body integration.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages 330-332"},"PeriodicalIF":8.8,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499211","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":"Neuroimmunity at the edge: The skull as a brain – periphery immunological hub in autism spectrum disorder","authors":"Daniel Martins","doi":"10.1016/j.bbi.2025.02.023","DOIUrl":"10.1016/j.bbi.2025.02.023","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages 327-329"},"PeriodicalIF":8.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482179","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":"Oleoylethanolamide-producing Lactobacillus paracasei F19 improves metabolic and behavioral disorders by restoring intestinal permeability and microbiota-gut-brain axis in high-fat diet-induced obese male mice","authors":"Luisa Seguella ,&nbsp;Chiara Corpetti ,&nbsp;Jie Lu ,&nbsp;Marcella Pesce ,&nbsp;Silvia Basili Franzin ,&nbsp;Irene Palenca ,&nbsp;Aurora Zilli ,&nbsp;Martina Vincenzi ,&nbsp;Daniele Caprioli ,&nbsp;Andreu Paytuví-Gallart ,&nbsp;Walter Sanseverino ,&nbsp;Sara Rurgo ,&nbsp;Giovanni Sarnelli ,&nbsp;Giuseppe Esposito","doi":"10.1016/j.bbi.2025.02.014","DOIUrl":"10.1016/j.bbi.2025.02.014","url":null,"abstract":"<div><div>Metabolic and mood disorders elicited by chronic exposure of high-fat diet (HFD) are often associated with intestinal dysbiosis and persistent low-grade inflammation in the small intestine. This leads to remodeling of the epithelial barrier with disruption of the neuroepithelial circuits that control energy homeostasis by the gut-brain axis. Therefore, therapies that restoreintestinal microbial niche and barrier function are promising candidates to counter peripheral metabolic challenges that affect behaviors controlled by the brain. The endogenous oleoylethanolamine (OEA) was found to shape the intestinal microbiota profile towards a “lean-like phenotype”, ameliorating pathological profiles of metabolic diseases. Further, OEA displays beneficial effects in several cognitive paradigms and preserves the epithelial barrier integrity, acting as an intestinal “gate-keeper”. Here, we developed an “intestinal OEA factory” for the <em>in-situ</em> and controlled release of OEA by using a probiotic-based delivery system. We engineered the <em>Lactobacillus paracasei F19</em> (LP) to express the human N-acylphosphatidylethanolamine-preferring phospholipase D (NAPE<em>pld</em>) gene and to produce OEA in response to dietary ultra-low oleate supply. We treated 12-week HFD male mice with oleate-probiotic formulations and assessed their impact on metabolic and behavioral dysfunctions, and microbiota-gut-brain signaling after 8 weeks of treatment. NAPE-expressing LP (pNAPE-LP) led to significant reduced weight loss and improved metabolic dysfunction in HFD-treated mice. Further, a parallel improvement in depressive- and anxiety-like phenotypes was associated with the duodenal barrier function retrieval, the restoration of the <em>Firmicutes/Bacteroidetes</em> ratio, and an increase in beneficial bacteria, such as <em>Lactobacillus</em>, <em>Prevotella</em>, and <em>Parabacteroides</em>. The HFD-driven changes both in the enteric and central nervous system were prevented by pNAPE-LP/oleate treatment. Collectively, our data suggest that these effects were mediated by the oleate-dependent release of OEA by pNAPE-LP since no significant effects were observed in HFD mice treated with the native probiotic alone (pLP). This oleate-regulated delivery system of OEA is a safe and efficient probiotic-based strategy for the treatment of metabolic syndrome and related behavioral disorders.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 25-44"},"PeriodicalIF":8.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482197","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":"Mutation S139N on Zika virus prM protein shifts immune response from Asian to contemporary strain","authors":"Jingzhe Shang ,&nbsp;Chao Zhou ,&nbsp;Mengjiao He ,&nbsp;Xing-Yao Huang ,&nbsp;Cheng-feng Qin ,&nbsp;Aiping Wu","doi":"10.1016/j.bbi.2025.02.012","DOIUrl":"10.1016/j.bbi.2025.02.012","url":null,"abstract":"<div><div>Zika virus (ZIKV) has been associated with neurological diseases like microcephaly and Guillain-Barré syndrome. The S139N single mutation on the prM protein of the FSS13025 Asian strain increases the mortality rate in mice. Therefore, it is a valuable tool for studying the impact of immune responses on neural damage. Here, we used single-cell sequencing technology to systematically assess the immune response induced by three ZIKV strains: Asian ancestral strain FSS13025/2010, FSS13025 strain with S139N mutation (FSS13025-S139N), and contemporary strain GZ01/2016. By infecting 1-day-old mice, we observed that the immune spectrum elicited by FSS13025-S139N mutant resembled that induced by the contemporary strain. The FSS13025-S139N strain induces the proliferation of inflammatory microglial cells earlier than the FSS13025 strain, similar to GZ01. A specific cell cluster, Microglia_Ccr7, was induced by the S139N mutant strain and GZ01 strain, which suppresses T cell activation through the PDCD1LG2-PDCD1 signaling pathway. Furthermore, the proliferation of CD8⁺ T cells was weakened and prolonged in S139N strain-infected samples. Finally, we found that the S139N mutant strain causes more apoptosis of neurons compared to the FSS13025 strain. These results indicate that the S139N mutation plays an important role in the immune response pattern of ZIKV and prolongs the duration of neuroinflammation.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages 247-259"},"PeriodicalIF":8.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143464492","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}