Neuroimmunomodulation最新文献

{"title":"Contents Vol. 29, 2022","authors":"","doi":"10.1159/000528166","DOIUrl":"https://doi.org/10.1159/000528166","url":null,"abstract":"<br />Neuroimmunomodulation 2022;29:I–VI","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"16 1-12","pages":""},"PeriodicalIF":2.4,"publicationDate":"2022-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138514060","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}

{"title":"Acknowledgement to Reviewers","authors":"","doi":"10.1159/000527679","DOIUrl":"https://doi.org/10.1159/000527679","url":null,"abstract":"<br />Neuroimmunomodulation 2022;29:523","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"24 8","pages":""},"PeriodicalIF":2.4,"publicationDate":"2022-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138514062","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}

{"title":"Retraction Statement","authors":"","doi":"10.1159/000525130","DOIUrl":"https://doi.org/10.1159/000525130","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 1","pages":"250 - 250"},"PeriodicalIF":2.4,"publicationDate":"2022-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48170514","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}

{"title":"Front & Back Matter","authors":"F. Dhabhar, S. Fetissov, Dan Frenkel, Vincent Geenen","doi":"10.1159/000524409","DOIUrl":"https://doi.org/10.1159/000524409","url":null,"abstract":"submission deadline: Tuesday 19 April 2022 Submit your abstract today! #ESPE2022 Join the conversation! @EuroSPE Find out more about the event, how to register, abstracts submissions and more by visiting www.espe2022.org EA 22 04 2","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43943305","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}

{"title":"14th Conference of the German Endocrine-Brain-Immune-Network (GEBIN).","authors":"","doi":"10.1159/000524082","DOIUrl":"10.1159/000524082","url":null,"abstract":"<p><p>None.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 1","pages":"1-50"},"PeriodicalIF":2.4,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47216929","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}

{"title":"Retraction Statement.","authors":"","doi":"10.1159/000523681","DOIUrl":"10.1159/000523681","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 1","pages":"1"},"PeriodicalIF":2.4,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46185948","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}

{"title":"Could SARS-CoV-2 Infection Be a Novel Risk Factor for Multiple Sclerosis?","authors":"Rehab Magdy,&nbsp;Mona Hussein","doi":"10.1159/000521891","DOIUrl":"https://doi.org/10.1159/000521891","url":null,"abstract":"<p><p>The outbreak of the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has challenged the healthcare community worldwide. The SARS-CoV-2 primarily affects the respiratory system; however, strong evidence suggests that SARS-CoV-2 can be neuroinvasive, resulting in several neurological complications. It was previously assumed that some coronaviruses are involved in multiple sclerosis (MS) pathology via various mechanisms. The mechanisms involved in coronavirus-induced central demyelination are complex and largely redundant. Molecular mimicry was proposed to be one of the possible mechanisms. Disruption of the blood-brain barrier, dysregulation in several inflammatory cytokines, and upregulation of matrix metalloproteinases were also thought to induce central demyelinating pathology. This raises a question about the possible role of SARS-CoV-2 as a novel risk factor for MS.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 4","pages":"251-254"},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9059011/pdf/nim-0001.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10742103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Immune and Inflammatory Mechanisms in Stroke: A Review of Current Advances.","authors":"Hui Zhao,&nbsp;Yan Li,&nbsp;Ying Zhang,&nbsp;Wen-Yan He,&nbsp;Wei-Na Jin","doi":"10.1159/000524951","DOIUrl":"https://doi.org/10.1159/000524951","url":null,"abstract":"<p><p>Stroke accounts for a large proportion of morbidity and mortality burden in China. Moreover, there is a high prevalence of the leading risk factors for stroke, including hypertension and smoking. Understanding the underlying mechanisms and developing effective therapeutic interventions for patients with stroke is a key imperative. The pathophysiology of stroke involves a complex interplay between the immune and inflammatory mechanisms. Focal brain inflammation triggered by neuronal cell death and the release of factors such as damage-associated molecular patterns can further exacerbate neuronal injury; in addition, impairment of the blood-brain barrier, oxidative stress, microvascular dysfunction, and brain edema cause secondary brain injury. Immune cells, including microglia and other infiltrating inflammatory cells, play a key role in triggering focal and global brain inflammation. Anti-inflammatory therapies targeting the aforementioned mechanisms can alleviate primary and secondary brain injury in the aftermath of a stroke. Further experimental and clinical studies are required to explore the beneficial effects of anti-inflammatory drugs in stroke.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 4","pages":"255-268"},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10743211","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}

{"title":"Expression of Zinc-Finger Antiviral Protein in hCMEC/D3 Human Cerebral Microvascular Endothelial Cells: Effect of a Toll-Like Receptor 3 Agonist.","authors":"Mako Okudera,&nbsp;Minami Odawara,&nbsp;Masashi Arakawa,&nbsp;Shogo Kawaguchi,&nbsp;Kazuhiko Seya,&nbsp;Tomoh Matsumiya,&nbsp;Riko Sato,&nbsp;Jiangli Ding,&nbsp;Eiji Morita,&nbsp;Tadaatsu Imaizumi","doi":"10.1159/000521012","DOIUrl":"https://doi.org/10.1159/000521012","url":null,"abstract":"<p><strong>Introduction: </strong>Invasion of viruses into the brain causes viral encephalitis, which can be fatal and causes permanent brain damage. The blood-brain barrier (BBB) protects the brain by excluding harmful substances and microbes. Brain microvascular endothelial cells are important components of the BBB; however, the mechanisms of antiviral reactions in these cells have not been fully elucidated. Zinc-finger antiviral protein (ZAP) is a molecule that restricts the infection of various viruses, and there are 2 major isoforms: ZAPL and ZAPS. Toll-like receptor 3 (TLR3), a pattern-recognition receptor against viral double-stranded RNA, is implicated in antiviral innate immune reactions. The aim of this study was to investigate the expression of ZAP in cultured hCMEC/D3 human brain microvascular endothelial cells treated with an authentic TLR3 agonist polyinosinic-polycytidylic acid (poly IC).</p><p><strong>Methods: </strong>hCMEC/D3 cells were cultured and treated with poly IC. Expression of ZAPL and ZAPS mRNA was investigated using quantitative reverse transcription-polymerase chain reaction, and protein expression of these molecules was examined using western blotting. The role of nuclear factor-κB (NF-κB) was examined using the NF-κB inhibitor, SN50. The roles of interferon (IFN)-β, IFN regulatory factor 3 (IRF3), tripartite motif protein 25 (TRIM25), and retinoic acid-inducible gene-I (RIG-I) in poly IC-induced ZAPS expression were examined using RNA interference. Propagation of Japanese encephalitis virus (JEV) was examined using a focus-forming assay.</p><p><strong>Results: </strong>ZAPS mRNA and protein expression was upregulated by poly IC, whereas the change of ZAPL mRNA and protein levels was minimal. Knockdown of IRF3 or TRIM25 decreased the poly IC-induced upregulation of ZAPS, whereas knockdown of IFN-β or RIG-I did not affect ZAPS upregulation. SN50 did not affect ZAPS expression. Knockdown of ZAP enhanced JEV propagation.</p><p><strong>Conclusion: </strong>ZAPL and ZAPS were expressed in hCMEC/D3 cells, and ZAPS expression was upregulated by poly IC. IRF3 and TRIM25 are involved in poly IC-induced upregulation of ZAPS. ZAP may contribute to antiviral reactions in brain microvascular endothelial cells and protect the brain from invading viruses such as JEV.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 4","pages":"349-358"},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10476833","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}

{"title":"Catalpol Alleviates Isoflurane-Induced Hippocampal Learning and Memory Dysfunction and Neuropathological Changes in Aged Mice.","authors":"Weiqing Shi,&nbsp;Wenbing Zhang,&nbsp;Jinping Wang","doi":"10.1159/000524236","DOIUrl":"https://doi.org/10.1159/000524236","url":null,"abstract":"<p><strong>Introduction: </strong>Isoflurane-associated perioperative neurocognitive disorders (PNDs) is a common complication that occurs commonly in elderly patients characterized by deterioration of hippocampus-dependent cognitive function. Mounting evidence has shown that hippocampal impairment and inflammatory processes are implicated in the pathogenesis of PNDs. Catalpol has been suggested to play a role in the modulation of neuroprotection and neurotransmission. Therefore, we surmised that catalpol may play a similar role during isoflurane-induced PNDs.</p><p><strong>Methods: </strong>In our current study, aged mice were exposed to isoflurane to develop a mouse model of PNDs and preconditioned with catalpol for 2 weeks before modeling. Three weeks after isoflurane exposure, behavioral, histological, biochemical, electrophysiological, and immunofluorescent assays were performed.</p><p><strong>Results: </strong>Our results showed that catalpol preadministration significantly alleviated cognitive impairment in the Morris water maze, novel object recognition, and Y-maze behavioral tests. Neuropathological analyses showed that catalpol preadministration reduced the loss of neurons and synapses; in line with this, it is revealed that hippocampal synaptic plasticity was restored. Mechanistically, catalpol preadministration suppressed the activation of microglia and decreased the expression of NLRP3 inflammasome.</p><p><strong>Conclusion: </strong>Our results indicate that catalpol preadministration could effectively alleviate cognitive impairment and neuropathological damage in isoflurane-exposed aged mice with its neuroprotective effects via modulation of the NLRP3 inflammatory pathway. Furthermore, the NLRP3 inflammatory pathway was revealed to be involved in these effects.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"29 4","pages":"414-424"},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10386291","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}