Journal of neuroimmunology最新文献_第7页

Co-localization and co-expression of Olfml3 with Iba1 in brain of mice Olfml3 与 Iba1 在小鼠大脑中的共定位和共表达

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-25 DOI: 10.1016/j.jneuroim.2024.578411

Himanshi Yadav , Amrita Bakshi , Anamika , Vishal Singh , Prateek Paul , N. Arul Murugan , Shashank Kumar Maurya

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Characterization of Japanese multiple sclerosis patients with progression independent of relapse activity: A 2-year multicenter cohort study 日本多发性硬化症患者病情进展与复发活动无关的特征：一项为期两年的多中心队列研究。

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-24 DOI: 10.1016/j.jneuroim.2024.578407

Hiroaki Yokote , Yusei Miyazaki , Juichi Fujimori , Yoichiro Nishida , Shuta Toru , Masaaki Niino , Ichiro Nakashima , Yoshiharu Miura , Takanori Yokota

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Severe cerebral amyloid angiopathy related inflammation (CAA-ri) associated with vaccination: Case report and literature review 与疫苗接种有关的严重脑淀粉样血管病相关炎症（CAA-ri）：病例报告和文献综述

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-23 DOI: 10.1016/j.jneuroim.2024.578406

Michael Tang , Jane Kim , Kui Kai Lau , Koon Ho Chan

{"title":"Severe cerebral amyloid angiopathy related inflammation (CAA-ri) associated with vaccination: Case report and literature review","authors":"Michael Tang , Jane Kim , Kui Kai Lau , Koon Ho Chan","doi":"10.1016/j.jneuroim.2024.578406","DOIUrl":"10.1016/j.jneuroim.2024.578406","url":null,"abstract":"<div><p>Cerebral amyloid angiopathy-related inflammation (CAA-ri) is a rapid but reversible autoimmune encephalopathy where spontaneous autoantibody reaction against amyloid beta deposited in cerebral blood vessels produces characteristic neuroinflammatory changes such as vasogenic edema and microhemorrhages on MRI. The term amyloid-related imaging abnormalities (ARIA) is sometimes used to describe these changes but are more often reserved for similar MRI signal abnormalities seen after administration of anti-amyloid immunotherapy, using treatment exposure as an antecedent. It is unclear if there is any biological basis for this dichotomized distinction. We report a case of severe CAA-ri after exposure to SARS-CoV-2 vaccine and performed a literature review of CAA-ri related to vaccination. CAA-ri precipitated by immunogenic triggers other than anti-amyloid therapy would lend support to the hypothesis that ARIA seen on MRI may represent the same disease underpinned by a shared anti-Aβ autoantibody response irrespective of etiology. A thorough history should be taken before labelling CAA-ri as spontaneous.</p></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"394 ","pages":"Article 578406"},"PeriodicalIF":2.9,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141780971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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A case report of lymphoproliferative disease in brain following therapies with mycophenolate Mofetil and Fingolimod and literature review 使用霉酚酸莫非替酯和芬戈莫德治疗后出现脑部淋巴组织增生症的病例报告和文献综述

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-23 DOI: 10.1016/j.jneuroim.2024.578410

Ge Bai , Ying Bai , Hongzhi Guan , Haitao Ren , Haifeng Li , Yan Wang

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Macrophage-derived exosomes exacerbate postoperative cognitive dysfunction in mice through inflammation 巨噬细胞源性外泌体通过炎症加剧小鼠术后认知功能障碍

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-18 DOI: 10.1016/j.jneuroim.2024.578403

Jinling Qin , Hui Yuan , Xiujun An, Rongjun Liu, Bo Meng

{"title":"Macrophage-derived exosomes exacerbate postoperative cognitive dysfunction in mice through inflammation","authors":"Jinling Qin , Hui Yuan , Xiujun An, Rongjun Liu, Bo Meng","doi":"10.1016/j.jneuroim.2024.578403","DOIUrl":"10.1016/j.jneuroim.2024.578403","url":null,"abstract":"<div><p>This study investigated the impact of two-hit inflammation on postoperative cognitive dysfunction (POCD) in mice and the role of macrophage-derived exosomes in regulating this process. Mice models were used to mimic the state of two-hit inflammation, and cognitive function was assessed through behavioral experiments. Proinflammatory cytokine expression levels and blood-brain barrier (BBB)-associated functional proteins were measured using ELISA and Western blot, respectively. An in vitro macrophage inflammation two-hit model was created, and the role of exosomes was examined using the previously mentioned assays. Additionally, exosomes were injected into mice to further understand their impact in the two-hit inflammation model. Mice exposed to two-hit inflammation experienced impaired cognitive function, increased BBB permeability, and elevated levels of proinflammatory cytokines. Macrophages subjected to two-hit inflammation released higher levels of proinflammatory cytokines compared to the control group and other treatment groups. Treatment with an exosome inhibitor GW4869 effectively reduced the expression levels of proinflammatory cytokines in macrophages exposed to two-hit inflammation. Moreover, injection of macrophage-released exosomes into healthy mice induced inflammation, hippocampal damage, and cognitive disorders, which were mitigated by treatment with GW4869. In mice with two-hit inflammation, macrophage-released exosomes worsened cognitive disorders by promoting inflammation in the peripheral blood and central nervous system. However, treatment with GW4869 protected cognitive function by suppressing exosome release. These findings highlight the importance of two-hit inflammation in POCD and emphasize the critical role of exosomes as regulatory factors. This research provides valuable insights into the pathogenesis of POCD and potential intervention strategies.</p></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"394 ","pages":"Article 578403"},"PeriodicalIF":2.9,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Authors' response to letter to the editor: Electroconvulsive therapy in N-methyl-d-aspartate receptor encephalitis 作者对致编辑信的回复：N-甲基-d-天冬氨酸受体脑炎的电休克疗法

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-18 DOI: 10.1016/j.jneuroim.2024.578405

Melissa A. Wright , Mar Guasp , Christian Lachner , Gregory S. Day , Grace Gombolay , Maarten J. Titulaer , Stacey L. Clardy

引用次数: 0

Toxoplasma gondii infection supports the infiltration of T cells into brain tumors 弓形虫感染有助于 T 细胞浸润脑肿瘤。

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-08 DOI: 10.1016/j.jneuroim.2024.578402

Yen T.M. Nguyen , Lydia Sibley , Piotr Przanowski , Xiao-Yu Zhao , Michael Kovacs , Shengyuan Wang , Marieke K. Jones , Maureen Cowan , Wenjie Liu , Andrea R. Merchak , Alban Gaultier , Kevin Janes , Chongzhi Zang , Tajie Harris , Sarah E. Ewald , Hui Zong

引用次数: 0

HMGB1/TLR4 axis promotes pyroptosis after ICH by activating the NLRP3 inflammasome HMGB1/TLR4 轴通过激活 NLRP3 炎症小体促进 ICH 后的脓毒症

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-07-08 DOI: 10.1016/j.jneuroim.2024.578401

Chunyan Lei , Keyang Chen , Yu Gu, Yongyu Li, Lu Wang, Xiaoyan Zhu, Qionghua Deng

{"title":"HMGB1/TLR4 axis promotes pyroptosis after ICH by activating the NLRP3 inflammasome","authors":"Chunyan Lei , Keyang Chen , Yu Gu, Yongyu Li, Lu Wang, Xiaoyan Zhu, Qionghua Deng","doi":"10.1016/j.jneuroim.2024.578401","DOIUrl":"https://doi.org/10.1016/j.jneuroim.2024.578401","url":null,"abstract":"<div><h3>Background</h3><p>We previously reported that the HMGB1/TLR4 axis promoted inflammation during the acute phase of intracerebral hemorrhage. Given that this phase is known to involve neuronal pyroptosis and neuroinflammation, here we explore whether HMGB1/TLR signaling activate inflammasome and pyroptosis after intracerebral hemorrhage.</p></div><div><h3>Methods</h3><p>Autologous blood was injected into Sprague–Dawley rats to induce intracerebral hemorrhage. Neurological deficits were assessed using a modified neurological severity score. These expression and localization of NLRP1 and NLRP3 inflammasomes, as well as the levels of pyroptosis and pyroptosis-associated proteins were assessed using Western blot or immunocytochemistry. These experiments were repeated in animals that received treatment with short interfering RNAs against NLRP1 or NLRP3, with HMGB1 inhibitor ethyl pyruvate or TLR4 inhibitor TAK-242.</p></div><div><h3>Results</h3><p>Intracerebral hemorrhage upregulated NLRP1 and NLRP3 in the ipsilateral striatum and increased the proportions of these cells that were pyroptosis-positive. Additionally, the levels of caspase protein family (e.g., pro-caspase-1 and caspase-1), apoptosis-associated speck-like protein (ASC), pro-interleukin-1β (IL-1β), and IL-1β were also elevated. These effects on pyroptosis and associated neurological deficit, were partially reversed by knockdown of NLRP1 or NLRP3, or by inhibition of HMGB1 or TLR4. Inhibition of HMGB1 or TLR4 resulted in the downregulation NLRP3 but not NLRP1.</p></div><div><h3>Conclusions</h3><p>The HMGB1/TLR4 signaling may activate the NLRP3 inflammasome during the acute phase of intracerebral hemorrhage, resulting in the inflammatory process known as pyroptosis. These insights suggest potential therapeutic targets for the mitigation tissue injury and associated neurological deficits following hemorrhagic stroke.</p></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"393 ","pages":"Article 578401"},"PeriodicalIF":2.9,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141596196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Geraniol (GER) attenuated chronic sleep restriction (CSR)-induced neuroinflammation in adolescent mice 香叶醇（GER）可减轻慢性睡眠限制（CSR）诱导的青少年小鼠神经炎症

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-06-29 DOI: 10.1016/j.jneuroim.2024.578400

Hengdao Chen , Jinrong Xiao , Bin Huang, Jun Que, Minsheng Liu

{"title":"Geraniol (GER) attenuated chronic sleep restriction (CSR)-induced neuroinflammation in adolescent mice","authors":"Hengdao Chen , Jinrong Xiao , Bin Huang, Jun Que, Minsheng Liu","doi":"10.1016/j.jneuroim.2024.578400","DOIUrl":"10.1016/j.jneuroim.2024.578400","url":null,"abstract":"<div><p>Sleep insufficiency is a significant health problem worldwide, and adolescent sleep restriction (SR) could induce multiple neurodevelopmental disorders in the central nervous system (CNS). Microglial-mediated neuroinflammation plays a vital role in multiple neurological diseases, and recent research showed the regulation effect of immunoproteasome on microglia functions. Geraniol (GER), an important ingredient in many essential oils, possesses diverse pharmacological properties like anti-inflammatory and antioxidant. The present study was designed to evaluate the neuroprotective effect of GER on SR in adolescent mice and further investigate the underlying mechanisms. Our results displayed that 14 days of chronic sleep restriction (CSR) induced cognitive decline, and anxiety-like and attention-deficit behaviors, which were mitigated by GER pretreatment. GER administration also reversed microglial pro-inflammatory response under CSR stimulation in the anterior cingulate cortex (ACC) regions by reducing the expression and secretion of cytokines like IL-1β and TNF-α. Mechanism research showed that LMP7 mRNA was selectively up-regulated under CSR treatment but down-regulated by GER administration. Proteasome activity and protein expression of LMP7 were consistent with mRNA data. ONX-0914 was applied to inhibit LMP7 selectively, and data validated that GER might alleviate CSR-induced neuroinflammation by regulating LMP7. Our study provides evidence that LMP7 is a critical regulator of CSR-induced proinflammation, and geraniol might be a promising therapy against CSR-induced neurodevelopmental disorders.</p></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"393 ","pages":"Article 578400"},"PeriodicalIF":2.9,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141587067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Corrigendum to “Germinal center B cells are dispensable in prion transport and neuroinvasion”. [2007 Dec;192(1–2):113–23. doi: 10.1016/j.jneuroim.2007.09.022. Epub 2007 Oct 26. PMID: 17964667] 对《生殖中心B细胞在朊病毒转运和神经入侵中可有可无》的更正》。[doi: 10.1016/j.jneuroim.2007.09.022.Epub 2007 Oct 26.PMID: 17964667].

IF 2.9 4区医学

Journal of neuroimmunology Pub Date : 2024-06-28 DOI: 10.1016/j.jneuroim.2024.578399

Mathias Heikenwalder, Christian Federau, Lotta von Boehmer, Petra Schwarz, Mareike Wagner, Nicolas Zeller, Johannes Haybaeck, Marco Prinz, Burkhard Becher, Adriano Aguzzi

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