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Omega-3 polyunsaturated fatty acids attenuates cognitive impairment via the gut-brain axis in diabetes-associated cognitive dysfunction rats Omega-3多不饱和脂肪酸通过肠-脑轴减轻糖尿病相关认知功能障碍大鼠的认知损伤。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-09 DOI: 10.1016/j.bbi.2025.03.015
Hongying Huang , Tong Zhao , Weiwei Ma
{"title":"Omega-3 polyunsaturated fatty acids attenuates cognitive impairment via the gut-brain axis in diabetes-associated cognitive dysfunction rats","authors":"Hongying Huang ,&nbsp;Tong Zhao ,&nbsp;Weiwei Ma","doi":"10.1016/j.bbi.2025.03.015","DOIUrl":"10.1016/j.bbi.2025.03.015","url":null,"abstract":"<div><div>Diabetes-related cognitive dysfunction (DACD) is a comorbidity of type 2 diabetes that has a negative effect on patients’ quality of life. Research has indicated that disruption of the gut microbiota (GM) may be linked to dementia with altered cognitive performance. Conversely, omega-3 polyunsaturated fatty acids (n-3 PUFAs) may reverse DACD. The present study aimed to assess the effects of an n-3 PUFA intervention and fecal microbiota transplantation (FMT) on high-fat and streptozotocin-induced DACD model rats. In DACD rats, n-3 PUFA treatment restored fasting blood glucose (FBG) levels and cognitive function, increased the expression of anti-inflammatory cytokines and downregulated the expression of proinflammatory cytokines in the cortex and colon. Additionally, the expression of the postsynaptic density protein-95 mRNA and protein varied with n-3 PUFA treatment. Treatment with n-3 PUFAs also increased the expression of tight junction proteins. Beneficial and short-chain fatty acid-producing bacteria were more abundant when rats were exposed to n-3 PUFAs. After FMT from the rats with DACD symptoms that were improved by the n-3 PUFA dietary intervention into another batch of DACD rats, we observed recovery in recipient DACD rats. These results indicated that the alleviation of DACD symptoms by n-3 PUFAs was attributed to gut microbiota remodeling.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 147-169"},"PeriodicalIF":8.8,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prefrontal cortical microglial transcriptome relates to mouse offspring executive function deficits after perinatal opioid exposure in a sex-dependent manner 围产期阿片类药物暴露后,前额叶皮质小胶质细胞转录组与小鼠后代执行功能缺陷有关。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-09 DOI: 10.1016/j.bbi.2025.03.016
Brittany L. Smith , Brandon Brooks-Patton , Justin L. Bollinger , Tess A. Guzman , Alexander H. Brendle , Samuel C. Woodburn , Anna G. Makela , Eric S. Wohleb , Teresa M. Reyes
{"title":"Prefrontal cortical microglial transcriptome relates to mouse offspring executive function deficits after perinatal opioid exposure in a sex-dependent manner","authors":"Brittany L. Smith ,&nbsp;Brandon Brooks-Patton ,&nbsp;Justin L. Bollinger ,&nbsp;Tess A. Guzman ,&nbsp;Alexander H. Brendle ,&nbsp;Samuel C. Woodburn ,&nbsp;Anna G. Makela ,&nbsp;Eric S. Wohleb ,&nbsp;Teresa M. Reyes","doi":"10.1016/j.bbi.2025.03.016","DOIUrl":"10.1016/j.bbi.2025.03.016","url":null,"abstract":"<div><div>Opioid use during pregnancy affects over 7% of pregnancies in the United States. While efforts have been directed at mitigating effects of prenatal opioid exposure acutely in the neonatal period, long-term neurodevelopmental studies in humans remain challenging. Using a preclinical model, we previously found that perinatal morphine (MO) exposure induces sex-dependent executive function deficits in adult offspring, and sexually divergent shifts in microglia phenotype. Therefore, this study used transcriptional profiling to test whether perinatal MO exposure would cause sex-specific transcriptional changes in microglia that would relate to offspring executive function outcomes in BXD F1 mice. Female C57BL/6 mice were given MO via the drinking water or saccharin only (SCH) one week prior to mating with DBA males, throughout gestation, and lactation until offspring were weaned. Offspring executive function was assessed in adulthood using the 5-choice serial reaction time task (5CSRTT), and microglia from the PFC were isolated and characterized via RNA-seq. In the 5CSRTT, male MO-exposed offspring had reduced accuracy and female MO-exposed offspring had increased inattentive behavior. There were a similar number of genes altered in female vs. male microglia, but only 3 differentially expressed genes were evident in both sexes. Further, hierarchical clustering analysis and WGCNA identified genes that related to behavioral deficits. Together, our data identify individual genes and pathways in microglia within each sex that may relate to executive function deficits observed after perinatal opioid exposure, even though the transcriptional profiles are highly divergent between the sexes.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 112-125"},"PeriodicalIF":8.8,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Age and Inflammation: Insights on “Age Three Ways” from Midlife in the United States Study 年龄与炎症:美国中年研究对“年龄三种方式”的洞察
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-09 DOI: 10.1016/j.bbi.2025.03.018
Dakota D. Witzel , Aarti C. Bhat , Jennifer E. Graham-Engeland , David M. Almeida
{"title":"Age and Inflammation: Insights on “Age Three Ways” from Midlife in the United States Study","authors":"Dakota D. Witzel ,&nbsp;Aarti C. Bhat ,&nbsp;Jennifer E. Graham-Engeland ,&nbsp;David M. Almeida","doi":"10.1016/j.bbi.2025.03.018","DOIUrl":"10.1016/j.bbi.2025.03.018","url":null,"abstract":"<div><h3>Introduction</h3><div>Chronological age is a particularly well-known indicator of variability in systemic inflammation. Other pertinent aspects of age (or “age proxies”) – subjective or epigenetic age – may offer nuanced information about age and inflammation associations. Using the Midlife in the United States Study, we explored how chronological, subjective, and epigenetic age were associated with inflammation. Further, we tested whether chronological age remained a unique predictor of inflammation after accounting for the variance of subjective and epigenetic age. Using an intersectionality framework, we also tested whether associations differed by race and gender. <strong>Method:</strong> 1,307 (85.39% White, 52.99% men) participants reported on their chronological and subjective age and provided blood from which epigenetic DNA and inflammatory biomarkers (IL-6, IL-8, fibrinogen, TNF-α, and E-selectin) were determined. <strong>Results:</strong> Linear regressions showed that being chronologically older was related to higher levels of inflammation. Being biologically older (higher epigenetic age or pace of aging) was also related to higher levels of all but IL-8. Subjective age was related to inflammatory biomarkers but only for people who identified their racial identity as White. Gender differences emerged, primarily with biological and chronological age. With all age indicators in one model, chronological age remained a unique indicator of inflammation in the sample, as similar to or a better predictor than biological age. <strong>Conclusion:</strong> The current study provides a better scientific understanding of the relative association of chronological age versus subjective and epigenetic age on inflammation with evidence suggesting that chronological age provides novel information above and beyond other proxies of age.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 72-80"},"PeriodicalIF":8.8,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143601848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of the kynurenine pathway in cognitive function in brain Disorders: Insights and challenges 犬尿氨酸通路在脑疾病认知功能中的作用:见解和挑战。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-09 DOI: 10.1016/j.bbi.2025.03.017
Manuel Morrens
{"title":"The role of the kynurenine pathway in cognitive function in brain Disorders: Insights and challenges","authors":"Manuel Morrens","doi":"10.1016/j.bbi.2025.03.017","DOIUrl":"10.1016/j.bbi.2025.03.017","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 110-111"},"PeriodicalIF":8.8,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Pawsitive impact: How pet contact ameliorates adult inflammatory stress responses in individuals raised in an urban environment 积极影响:宠物接触如何改善在城市环境中长大的个体的成人炎症应激反应。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-08 DOI: 10.1016/j.bbi.2025.03.013
Dominik Langgartner , Katja Weimer , Jonas Brunner-Weisser , Raphael Winkler , Marco Mannes , Markus Huber-Lang , John D. Sterrett , Christopher A. Lowry , Nicolas Rohleder , Besnik Bajrami , Andreas H. Luippold , Alexander Groß , Hans A. Kestler , Heike Tost , Andreas Meyer-Lindenberg , Harald Gündel , Marc N. Jarczok , Stefan O. Reber
{"title":"Pawsitive impact: How pet contact ameliorates adult inflammatory stress responses in individuals raised in an urban environment","authors":"Dominik Langgartner ,&nbsp;Katja Weimer ,&nbsp;Jonas Brunner-Weisser ,&nbsp;Raphael Winkler ,&nbsp;Marco Mannes ,&nbsp;Markus Huber-Lang ,&nbsp;John D. Sterrett ,&nbsp;Christopher A. Lowry ,&nbsp;Nicolas Rohleder ,&nbsp;Besnik Bajrami ,&nbsp;Andreas H. Luippold ,&nbsp;Alexander Groß ,&nbsp;Hans A. Kestler ,&nbsp;Heike Tost ,&nbsp;Andreas Meyer-Lindenberg ,&nbsp;Harald Gündel ,&nbsp;Marc N. Jarczok ,&nbsp;Stefan O. Reber","doi":"10.1016/j.bbi.2025.03.013","DOIUrl":"10.1016/j.bbi.2025.03.013","url":null,"abstract":"<div><h3>Background</h3><div>Individuals raised in an urban environment (URBANs) show an exaggerated inflammatory response to the Trier Social Stress Test (TSST) compared with individuals raised in a rural environment (RURALs). The underlying mechanisms are unclear but may relate to childhood animal contact. As an exaggerated immune (re)activity plays a causal role in the pathogenesis of stress-associated disorders, these findings might explain the higher prevalence of stress-associated disorders in urban vs. rural areas.</div></div><div><h3>Methods</h3><div>We recruited physically and emotionally healthy male URBANs, raised in a city with more than 40,000 residents either in the absence (noPETs) or presence (PETs) of household pets. Participants were individually exposed to the TSST, and before and after the TSST, blood and saliva were collected for assessment of different stress-related parameters. An additional saliva sample before the TSST was collected for salivary microbiome analysis. Heart rate (HR) and HR variability (HRV) were recorded continuously. Mental and physical health status, early-life and perceived life stress, current animal contact, and subjective strain induced by TSST exposure were assessed using validated questionnaires.</div></div><div><h3>Results</h3><div>Here we show that adult healthy male noPETs vs. PETs still reported less animal contact during adulthood and were characterized by deficits in their immunoregulatory and intestinal barrier function, which under basal conditions did not translate into a chronic low-grade inflammatory state. This was different under acute psychosocial stress conditions. Exposure to the TSST resulted in a facilitated mobilization of particularly neutrophil granulocytes in noPETs vs. PETs, accompanied by an enhanced pro- and compromised anti-inflammatory systemic stress response.</div></div><div><h3>Conclusion</h3><div>Together, the presence of pets seems to reduce the risk for URBANs to develop stress-associated disorders later in life (i.e., primary prevention) by facilitating immunoregulatory and barrier functions, in turn preventing an overshooting immune activation in response to acute stressors and chronic low-grade inflammation in response to repeated/chronic stressors.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 217-228"},"PeriodicalIF":8.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584632","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}
引用次数: 0
Assessment of complement cascade components in patients with major depressive disorder 重度抑郁症患者补体级联成分的评估。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-08 DOI: 10.1016/j.bbi.2025.03.009
Brandi Quintanilla , Dede Greenstein , Ashutosh Tripathi , Alona Bartosh , Peixiong Yuan , Carlos A. Zarate , Anilkumar Pillai
{"title":"Assessment of complement cascade components in patients with major depressive disorder","authors":"Brandi Quintanilla ,&nbsp;Dede Greenstein ,&nbsp;Ashutosh Tripathi ,&nbsp;Alona Bartosh ,&nbsp;Peixiong Yuan ,&nbsp;Carlos A. Zarate ,&nbsp;Anilkumar Pillai","doi":"10.1016/j.bbi.2025.03.009","DOIUrl":"10.1016/j.bbi.2025.03.009","url":null,"abstract":"<div><div>Recent evidence suggests that the rapid-acting antidepressant ketamine has immune regulatory functions. The complement system is an important component of the innate immune response and plays a key role in synaptic plasticity. An increase in complement component 3 (C3) expression was previously found in the prefrontal cortex of individuals with depression. Given the complement system’s role in depression and ketamine’s potential anti-inflammatory properties, there is reason to suspect overlap between the complement system and ketamine’s mechanism of action. This post-hoc study analyzed data from 39 individuals with major depressive disorder (MDD) and 25 healthy volunteers who previously participated in a randomized, double-blind trial comparing intravenous ketamine (0.5 mg/kg) to placebo. Blood was obtained at baseline, 230 min, Day 1, and Day 3. Plasma levels of C3a and C4a, two key complement proteins implicated in synaptic plasticity, were determined by ELISA. Linear mixed models were used to test baseline sex differences, whether differences varied by diagnosis, and ketamine’s effects (versus placebo) on C3a and C4a levels in the MDD group only. A significant diagnosis-by-sex interaction was observed for C3a but not C4a levels. Drug effects on C3a and C4a levels did not vary over time. These results suggest that treatment strategies targeting the complement pathway may yield fruitful insights and/or advances in treatment options for MDD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 229-237"},"PeriodicalIF":8.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Differential immune profiles in the context of chronic stress among childhood adversity-exposed adolescents 儿童逆境暴露青少年慢性应激背景下的差异免疫特征
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-08 DOI: 10.1016/j.bbi.2025.03.004
Kate Ryan Kuhlman , Ece N. Tan , Steve W. Cole , Uma Rao
{"title":"Differential immune profiles in the context of chronic stress among childhood adversity-exposed adolescents","authors":"Kate Ryan Kuhlman ,&nbsp;Ece N. Tan ,&nbsp;Steve W. Cole ,&nbsp;Uma Rao","doi":"10.1016/j.bbi.2025.03.004","DOIUrl":"10.1016/j.bbi.2025.03.004","url":null,"abstract":"<div><div>Psychosocial stress has been linked to myriad mental and physical health conditions. Stress-induced changes to functioning of the immune system is a plausible mechanism in this association. Psychosocial stress is a well-established contributor to immune dysregulation, though the extant literature to date falls short of addressing the role of distal relative to contemporary stress in immune function, particularly as they relate to distinctions between innate and adaptive immunity. The present study directly addressed this knowledge gap by characterizing vertically-integrated markers of immune functioning as a function of both recent chronic stress during adolescence and childhood adversity. In the present study, childhood adversity (before age 10) and recent psychosocial stressors (past 6 months) were characterized via semi-structured clinical interviews among 127 adolescent girls (aged 13–17; 31 % Black, 38 % Hispanic, 32 % NHW) who have all measures included in this report. Vertically-integrated markers of immune activity were also collected: an <em>a priori</em> subset of immune-related genes using genome-wide transcriptional profiling, an 11-plex of circulating cytokines (IL-6, TNF-α, IL-10, IL-8, IFN-γ, IL-1β, IL-1α, IL-27, MCP-1, IL-12p70, IP-10), and systemic inflammation (C-reactive protein; CRP). The association between recent chronic stress and intracellular immune outcomes differed based on childhood adversity. Genome-wide transcriptional profiling implicated myeloid lineage cells, specifically monocytes and dendritic cells, in differential patterns of gene expression among childhood adversity-exposed youth in the context of chronic stress. These differential patterns were also reflected in expression of proinflammatory genes and CRP such that among adolescents without exposure to childhood adversity, more recent chronic stress was associated with less proinflammatory gene expression, <em>b</em> = -0.45 (<em>SE</em> = 0.22), <em>p</em> = 0.04, <em>95 %CI</em> [-0.87, −0.02], and somewhat higher CRP, <em>b</em> = 0.62 (<em>SE</em> = 0.35), <em>p</em> = 0.08, <em>95 %CI</em> [-0.07, 1.31], while among adolescents with exposure to childhood adversity, more recent chronic stress was not associated with any immune activity markers. However, these patterns among circulating markers did not survive corrections for multiple comparisons. Immune adaptation in the context of chronic stress may indicate plasticity to environmental demands that conserves biological resources, which may be a source of resilience that is negatively impacted by childhood adversity.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 183-192"},"PeriodicalIF":8.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Voluntary wheel exercise improves learning and memory impairment caused by hippocampal Hb-α deficiency by reducing microglial activation and reversing synaptic damage 通过减少小胶质细胞激活和逆转突触损伤,自主车轮运动可改善海马Hb-α缺乏引起的学习和记忆障碍。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-07 DOI: 10.1016/j.bbi.2025.03.010
Yi-ying Wang , Yu-ning Zhou , Shun Wang , Li Liu , Lin Jiang , Yi Zhang , Lei Zhang , Chun-ni Zhou , Yan-min Luo , Jing Tang , Xin Liang , Qian Xiao , Xiao-yun Dou , Jian-rong Zhou , Feng-lei Chao , Yong Tang
{"title":"Voluntary wheel exercise improves learning and memory impairment caused by hippocampal Hb-α deficiency by reducing microglial activation and reversing synaptic damage","authors":"Yi-ying Wang ,&nbsp;Yu-ning Zhou ,&nbsp;Shun Wang ,&nbsp;Li Liu ,&nbsp;Lin Jiang ,&nbsp;Yi Zhang ,&nbsp;Lei Zhang ,&nbsp;Chun-ni Zhou ,&nbsp;Yan-min Luo ,&nbsp;Jing Tang ,&nbsp;Xin Liang ,&nbsp;Qian Xiao ,&nbsp;Xiao-yun Dou ,&nbsp;Jian-rong Zhou ,&nbsp;Feng-lei Chao ,&nbsp;Yong Tang","doi":"10.1016/j.bbi.2025.03.010","DOIUrl":"10.1016/j.bbi.2025.03.010","url":null,"abstract":"<div><div>Decreased hemoglobin (Hb) levels in peripheral blood may be a risk factor for Alzheimer’s disease (AD). Hb-α is a monomeric form of Hb that exists in the central nervous system. Our previous RNA sequencing results revealed a decrease in the expression of the Hb-α gene in the hippocampus of AD model mice. However, the effects of Hb-α deficiency in the hippocampus on cognitive function and the underlying mechanism are unclear. Running exercise has been shown to improve cognition, but whether it can reverse the damage caused by Hb-α deficiency in the hippocampus needs to be further researched. In the present study, Mendelian randomization (MR) analyses revealed that lower levels of mean corpuscular Hb and Hemoglobin alpha 1 (HBA1) increased the risk of developing AD. When an adeno-associated virus (AAV) was used to knock down hippocampal Hb-α, the learning and memory ability of the resulting model mice decreased, similar to that of AD model mice. Moreover, the expression levels of advanced glycation end products (AGE) and their receptor (RAGE) were upregulated, microglia were activated, and the number of engulfed synapses increased, which damaged the number and structure of hippocampal synapses in the model mice. However, four weeks of voluntary wheel exercise effectively improved these conditions. In addition, we found that voluntary wheel exercise may compensate for Hb-α protein deficiency in the hippocampus by increasing the expression levels of Hb-α protein in plasma, cerebrospinal fluid, and other brain regions without altering Hb-α mRNA in the hippocampus of model mice. These results highlight the key role of Hb-α in hippocampal synaptic damage, elucidate the mechanism by which running exercise improves cognition by connecting the peripheral circulation and central nervous system through Hb-α, and provide new ideas for the diagnosis and treatment of AD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 81-95"},"PeriodicalIF":8.8,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Maternal peptidoglycan overexposure during late pregnancy alters neurodevelopment and behavior in juvenile offspring 妊娠后期母体多肽聚糖过度暴露会改变幼仔的神经发育和行为。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-07 DOI: 10.1016/j.bbi.2025.03.014
Inés Martínez Sánchez, Julia Spielbauer, Rochellys Diaz Heijtz
{"title":"Maternal peptidoglycan overexposure during late pregnancy alters neurodevelopment and behavior in juvenile offspring","authors":"Inés Martínez Sánchez,&nbsp;Julia Spielbauer,&nbsp;Rochellys Diaz Heijtz","doi":"10.1016/j.bbi.2025.03.014","DOIUrl":"10.1016/j.bbi.2025.03.014","url":null,"abstract":"<div><div>Emerging evidence suggests that maternal gut microbiota-derived metabolites and components influence fetal brain development and subsequent neurodevelopment. This study investigates the effects of maternal overexposure to muramyl dipeptide (MDP)—a bacterial peptidoglycan (PGN) motif recognized by Nod2 receptors—on offspring neurodevelopment and behavior. Time-mated C57BL/6J female mice received MDP via drinking water from gestational days 16–19. Nod2 activation in amniotic fluid was assessed using a Nod2 cell-based reporter assay, showing a significant increase in males 24 h after MDP exposure. Gene expression analysis revealed upregulation of PGN transporters in fetal brains, with males showing higher levels of <em>Slc15a1</em>/<em>PepT1</em>, <em>Slc15a2</em>/<em>PepT2</em>, and <em>Slc46a2</em>. No changes in inflammatory or microglia-related markers were found. Behavioral assessments during the juvenile period revealed sex-specific effects: prenatally exposed males showed reduced social interaction, while females exhibited reduced novelty-induced locomotion and impaired social recognition. These behavioral changes were linked to altered expression of synaptic (<em>Dlg4</em>, <em>Ppp1r9b</em>, <em>Darpp-32</em>) and microglial (<em>Trem-2</em>, <em>Cx3cr1</em>) genes in the prefrontal cortex. Our findings underscore the sex-specific effects of maternal PGN overexposure on offspring neurodevelopment, highlighting the potential role of the maternal microbiome in the neurobiology of neurodevelopmental disorders, even in the absence of infection or robust inflammation.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"127 ","pages":"Pages 96-102"},"PeriodicalIF":8.8,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Corrigendum to “The antidepressant effect of whole-body hyperthermia is associated with the classical interleukin-6 signaling pathway” [Brain Behav. Immunity 119 (2024) 801–806] “全身热疗的抗抑郁作用与经典的白细胞介素-6信号通路有关”[脑行为]的更正。豁免119(2024)801-806]。
IF 8.8 2区 医学
Brain, Behavior, and Immunity Pub Date : 2025-03-01 DOI: 10.1016/j.bbi.2025.01.005
Naoise Mac Giollabhui , Christopher A. Lowry , Maren Nyer , Simmie L. Foster , Richard T. Liu , David G. Smith , Steven P. Cole , Ashley E. Mason , David Mischoulon , Charles L. Raison
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