Journal of neuroimmunology最新文献

{"title":"MOGAD presenting as fulminant intracranial hypertension","authors":"Sai Nagaratnam ,&nbsp;Amardeep Gill ,&nbsp;Niroshan Jeyakumar ,&nbsp;Shuo Xi ,&nbsp;Ming-Wei Lin ,&nbsp;Andrew Martin ,&nbsp;Winny Varikatt ,&nbsp;Michael W.K. Fong ,&nbsp;Hugo Morales-Briceno","doi":"10.1016/j.jneuroim.2024.578487","DOIUrl":"10.1016/j.jneuroim.2024.578487","url":null,"abstract":"<div><h3>Objectives</h3><div>Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) has an expanding phenotype. We describe two cases of MOGAD with associated severe intracranial hypertension.</div><div>Case 1: A 21-year-old male presented with diffuse cortical encephalitis and intracranial hypertension with both serum and CSF MOG antibody positivity. Initial brain CT scan was normal but subsequent demyelination was evident on MRI. Case 2: A 44-year-old female presented with a progressive brainstem encephalitis and intracranial hypertension and normal MRI, with later development of subcortical demyelination which was confirmed on brain biopsy. CSF-restricted MOG antibody was detected following the biopsy results.</div></div><div><h3>Results</h3><div>Both patients presented with clinical features of severe intracranial hypertension requiring surgical management followed by immunosuppressive therapy (methylprednisone and plasma exchange; and intravenous immunoglobulin and plasma exchange) leading to clinical improvement.</div></div><div><h3>Discussion</h3><div>MOGAD should be in the differential diagnosis of acute severe intracranial hypertension even in the absence of demyelination on initial neuroimaging. Clinicians should be alert of this syndrome that requires combined management of intracranial pressure in addition to early and intensive immunotherapy.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578487"},"PeriodicalIF":2.9,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639222","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":"Minocycline inhibits microglial activation in the CA1 hippocampal region and prevents long-term cognitive sequel after experimental cerebral malaria","authors":"E.T. Moreira ,&nbsp;M.P. Lourenço ,&nbsp;T. Cunha-Fernandes ,&nbsp;T.I. Silva ,&nbsp;L.D. Siqueira ,&nbsp;H.C. Castro-Faria-Neto ,&nbsp;P.A. Reis","doi":"10.1016/j.jneuroim.2024.578480","DOIUrl":"10.1016/j.jneuroim.2024.578480","url":null,"abstract":"<div><div>Cerebral malaria is the worst complication of malaria infection, has a high mortality rate, and may cause different neurodysfunctions, including cognitive decline. Neuroinflammation is an important cause of cognitive damage in neurodegenerative diseases, and microglial cells can be activated in a disease-associated profile leading to tissue damage and neuronal death. Here, we demonstrated that treatment with minocycline reduced blood-brain barrier breakdown and modulated ICAM1 mRNA expression; reduced proinflammatory cytokines, such as TNF-α, IL-1β, IFN-γ, and IL-6; and prevented long-term cognitive decline in contextual and aversive memory tasks. Taken together, our data suggest that microglial cells are activated during experimental cerebral malaria, leading to neuroinflammatory events that end up in cognitive damage. In addition, pharmacological modulation of microglial activation, by drugs such as minocycline may be an important therapeutic strategy in the prevention of long-term memory impairment.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578480"},"PeriodicalIF":2.9,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142586463","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":"Influence of cocaine use reduction on markers of immune function","authors":"William W. Stoops ,&nbsp;Thomas P. Shellenberg ,&nbsp;Sean D. Regnier ,&nbsp;David H. Cox ,&nbsp;Reuben Adatorwovor ,&nbsp;Lon R. Hays ,&nbsp;Danielle M. Anderson ,&nbsp;Joshua A. Lile ,&nbsp;Joy M. Schmitz ,&nbsp;Jennifer R. Havens ,&nbsp;Suzanne C. Segerstrom","doi":"10.1016/j.jneuroim.2024.578470","DOIUrl":"10.1016/j.jneuroim.2024.578470","url":null,"abstract":"<div><div>This study determined the effects of reduced cocaine use on immune function. Treatment seeking participants with Cocaine Use Disorder enrolled in a 12-week contingency management trial to reduce cocaine use. Participants were randomly assigned 1:1:1 to High Value Reinforcers (i.e., $55/negative urine sample) for cocaine abstinence (<em>n</em> = 41), Low Value Reinforcers (i.e., $13/negative urine sample) for cocaine abstinence (<em>n</em> = 33) or Non-Contingent Control (n = 33). Immune measures were collected at 6-week intervals. The High Value group had greatest use reductions, increased erythema and IL-6 and decreased IL-10 and CCL5, suggesting an activated immune response. Cocaine use reduction may promote changes in immune health.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578470"},"PeriodicalIF":2.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590665","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":"Kidney injury: An overlooked manifestation in autoimmune encephalitis","authors":"Zhirong Fan ,&nbsp;Jing Li ,&nbsp;Yingchi Zhang ,&nbsp;Juan Kang ,&nbsp;Di Wang ,&nbsp;Lijuan Liu ,&nbsp;Min Li ,&nbsp;Xiaodan Shi ,&nbsp;Na Yuan ,&nbsp;Yuanli Zhang ,&nbsp;Fang Du ,&nbsp;Wen Jiang","doi":"10.1016/j.jneuroim.2024.578472","DOIUrl":"10.1016/j.jneuroim.2024.578472","url":null,"abstract":"<div><h3>Aim</h3><div>To investigate the prevalence and clinical features of kidney injury in patients with autoimmune encephalitis (AE).</div></div><div><h3>Methods</h3><div>Kidney injury was suspected in kidney-involving group due to persistent abnormal in urinary protein and serum albumin. Data on demographics and clinical features were compared between kidney-involving group and kidney-sparing group (patients without kidney injury) using Wilcoxon rank-sum test or chi-square test. Renal biopsy was conducted to identify the type of kidney injury.</div></div><div><h3>Results</h3><div>Approximate 30 % (32 of 108) patients with AE were suspicious of kidney injury. Nine patients further tested 24 h urine total protein, and seven of them had an elevated urine protein higher than 150 mg. The predominantly patterns of kidney injury were elevated urine protein, decreased serum albumin and normal kidney function. Compared to kidney-sparing group, the spectrum of AE antibodies in kidney-involving group was different, manifested as less anti-<em>N</em>-methyl-<span>d</span>-aspartate receptor antibodies (50 % vs. 72.4 %, <em>p</em> = 0.025) and more anti-contactin-associated protein like 2 antibodies (18.8 % vs. 1.3 %, <em>p</em> = 0.003). Definite pathological changes indicative of IgA nephropathy and membranous nephropathy in renal biopsy of two cases provided evidence of autoimmune attacks.</div></div><div><h3>Discussion</h3><div>Kidney injury occurred in considerable proportion of patients with AE. An in-depth screening for nephropathy could be essential for AE.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578472"},"PeriodicalIF":2.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142561070","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":"Corrigendum to “Clinical features and outcomes of patients with muscle-specific kinase antibody-positive myasthenia gravis in Japan” [Journal of Neuroimmunology 385 (2023) 578241].","authors":"Manato Yasuda ,&nbsp;Akiyuki Uzawa ,&nbsp;Satoshi Kuwabara ,&nbsp;Shigeaki Suzuki ,&nbsp;Hiroyuki Akamine ,&nbsp;Yosuke Onishi ,&nbsp;Yukiko Ozawa ,&nbsp;Naoki Kawaguchi ,&nbsp;Tomoya Kubota ,&nbsp;Masanori P. Takahashi ,&nbsp;Yasushi Suzuki ,&nbsp;Genya Watanabe ,&nbsp;Takashi Kimura ,&nbsp;Takamichi Sugimoto ,&nbsp;Makoto Samukawa ,&nbsp;Naoya Minami ,&nbsp;Masayuki Masuda ,&nbsp;Shingo Konno ,&nbsp;Yuriko Nagane ,&nbsp;Kimiaki Utsugisawa","doi":"10.1016/j.jneuroim.2024.578465","DOIUrl":"10.1016/j.jneuroim.2024.578465","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578465"},"PeriodicalIF":2.9,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142502427","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":"Modulating sonic hedgehog (SHH) pathway to create a rapid CNS-TB model: Facilitating drug discovery","authors":"Mohamad Mosa Mubarak ,&nbsp;Shahnawaz Majeed ,&nbsp;Zubair Ahmad Wani ,&nbsp;Hadiya Amin Kantroo ,&nbsp;Abbass Malik ,&nbsp;Ishfaq Ahmad Baba ,&nbsp;Radhika Mhatre ,&nbsp;Zahoor Ahmad","doi":"10.1016/j.jneuroim.2024.578471","DOIUrl":"10.1016/j.jneuroim.2024.578471","url":null,"abstract":"<div><div>Tuberculous meningitis, a severe complication of <em>Mycobacterium tuberculosis</em> (<em>M. tb</em>) infection, involves the dissemination of bacilli in the brain. This study explored the role of the sonic hedgehog (SHH) signaling pathway in regulating blood-brain barrier (BBB) integrity, <em>M. tb</em> invasion into the central nervous system (CNS), and disease progression of Central Nervous System Tuberculosis (CNS-TB) in a Balb/c mouse model. The modulation of the SHH pathway using agonist Purmorphamine (PUR) and antagonist Cyclopamine (CYC) revealed that CYC treatment led to a rapid and extensive invasion of <em>M. tb</em> in the brain, with bacterial loads increasing by 99 % compared to the untreated-infected group. In contrast, PUR reduced <em>M. tb</em> loads by 50 % and delayed disease progression. Histopathological analysis showed that CYC exacerbated inflammation and immune cell infiltration, while PUR mitigated these responses. Immunohistochemistry demonstrated that CYC caused severe BBB breakdown and reactive gliosis, while PUR partially attenuated this response. Further analysis revealed that CYC upregulated Matrix Metalloproteinase-9 (MMP-9) secretion, a key contributor to BBB disruption. These findings highlight the critical role of the SHH pathway in maintaining BBB integrity and regulating the immunopathological response during CNS-TB, opening up future scope for drug discovery. This Cyclopamine-induced model of rapid <em>M. tb</em> invasion and chronic inflammation provides a new tool for studying CNS-TB pathogenesis and evaluating potential therapeutic interventions targeting the SHH signaling axis.</div></div><div><h3>Significance statement</h3><div>Understanding how tuberculosis (TB) infection can spread to the brain is crucial, as this “central nervous system TB” (CNS-TB) is a serious and potentially life-threatening health complication. However, studying CNS-TB in humans is very difficult. Animal models are needed to better understand how TB gets into the brain and the resulting damage. This study in mice showed that blocking a signaling pathway called Sonic Hedgehog (SHH) allowed TB to rapidly spread to the brain, damaging the blood-brain barrier and causing severe inflammation. In contrast, activating the SHH pathway helped protect the brain from TB. These findings provide important insights that could lead to new ways to prevent or treat this dangerous form of TB.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578471"},"PeriodicalIF":2.9,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622542","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":"NAD+ supplement relieved chronic sleep restriction (CSR)-induced microglial proinflammation in vivo and in vitro","authors":"Qiqiang Chen ,&nbsp;Jinrong Xiao ,&nbsp;Zhenya Lin ,&nbsp;Xin Xu ,&nbsp;Jinlan Chen","doi":"10.1016/j.jneuroim.2024.578469","DOIUrl":"10.1016/j.jneuroim.2024.578469","url":null,"abstract":"<div><div>Sleep insufficiency is a significant health problem worldwide and can induce multiple neurodevelopmental disorders in the central nervous system (CNS). Sleep deprivation (SD), especially chronic SD, leads to cognition and memory loss and worsens neurodegenerative disease liability. Microglia are the main inflammation-dominant glia and play a crucial role in SD-induced neurological impairments. Nicotinamide adenine dinucleotide (NAD+) is a redox reaction coenzyme that exerts anti-inflammatory and mitochondria-protective effects in microglia. Whether NAD+ mitigated SD-induced neurological disorders by regulating microglial functions is still unknown. In the current study, we designed an <em>in vivo</em> and <em>in vitro</em> model to evaluate the neuroprotective effect of NAD+ on chronic sleep restriction (CSR) and further investigate the underlying mechanisms. Behavioral tests and immunofluorescence staining were applied to investigate the cognition impairments and microglial activation. Biochemical experiments were tested to analyze the oxidative status and possible mechanism. <em>In vitro</em> data were used to verify the <em>in vivo</em> data. Our results displayed that NAD+ supplement mitigated CSR-induced cognitive decline and microglial activation response by suppressing the expression of pro-inflammatory cytokines <em>in vivo</em>. NAD+ administration also decreased oxidative stress and mitochondrial impairments in microglia. <em>In vitro</em> results showed that NAD+ treatment inhibited ROS production and prompted M1 conversion to M2 phenotype. cGAS-STING/NF-κB pathways were significantly activated but down-regulated by NAD+ administration. H151, a STING antagonist, was applied to validate that NAD+ treatment alleviates neuroinflammation partially by regulating cGAS-STING pathways in microglia. Our findings suggest that NAD+ supplement is a promising therapy for sleep disorders-induced neurological problems, and cGAS-STING pathway may act as a critical regulator in microglial proinflammation.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578469"},"PeriodicalIF":2.9,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622544","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":"Nicotine is an Immunosuppressant: Implications for Women's Health and Disease","authors":"Ashley M. White ,&nbsp;Ashley J. Craig ,&nbsp;Daryl L. Richie ,&nbsp;Christa Corley ,&nbsp;Safiyah M. Sadek ,&nbsp;Heather N. Barton ,&nbsp;Cassandra D. Gipson","doi":"10.1016/j.jneuroim.2024.578468","DOIUrl":"10.1016/j.jneuroim.2024.578468","url":null,"abstract":"<div><div>A plethora of evidence supports that nicotine, the primary alkaloid in tobacco products that is generally accepted for maintaining use, is immunoregulatory and may function as an immunosuppressant. Women have unique experiences with use of nicotine-containing products and also undergo significant reproductive transitions throughout their lifespan which may be impacted by nicotine use. Within the extant literature, there is conflicting evidence that nicotine may confer beneficial health effects in specific disease states (e.g., in ulcerative colitis). Use prevalence of nicotine-containing products is exceptionally high in individuals presenting with some comorbid disease states that impact immune system health and can be a risk factor for the development of diseases which disproportionately impact women; however, the mechanisms underlying these relationships are largely unclear. Further, little is known regarding the impacts of nicotine's immunosuppressive effects on women's health during the menopausal transition, which is arguably an inflammatory event characterized by a pro-inflammatory peri-menopause period. Given that post-menopausal women are at a higher risk than men for the development of neurodegenerative diseases such as Alzheimer's disease and are also more vulnerable to negative health effects associated with diseases such as HIV-1 infection, it is important to understand how use of nicotine-containing products may impact the immune milieu in women. In this review, we define instances in which nicotine use confers immunosuppressive, anti-inflammatory, or pro-inflammatory effects in the context of comorbid disease states, and focus on how nicotine impacts neuroimmune signaling to maintain use. We posit that regardless of potential health benefits, nicotine use cessation should be a priority in the clinical care of women. The synthesis of this review demonstrates the importance of systematically defining the relationships between volitional nicotine use, immune system function, and comorbid disease states in women to better understand how nicotine impacts women's health and disease.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"397 ","pages":"Article 578468"},"PeriodicalIF":2.9,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142502428","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":"Myelin oligodendrocyte glycoprotein antibody–associated disease with histopathologic features of primary CNS angiitis without demyelination: Case report and literature review","authors":"Seongmi Kim ,&nbsp;Suin Lee ,&nbsp;Yeon Hak Chung ,&nbsp;Hyunjin Ju ,&nbsp;Yeon-Lim Suh ,&nbsp;Ju-Hong Min","doi":"10.1016/j.jneuroim.2024.578467","DOIUrl":"10.1016/j.jneuroim.2024.578467","url":null,"abstract":"<div><div>Primary angiitis of the central nervous system (PACNS) is a rare inflammatory disease that affects both small- and medium-sized vessels of the CNS, while myelin oligodendrocyte glycoprotein (MOG) antibody–associated disease (MOGAD) is a novel antibody-mediated inflammatory demyelinating disorder that causes damage to the myelin in CNS. We report a case diagnosed as MOGAD due to a history of recurrent myelitis, brain lesions, and positive anti-MOG, but the brain biopsy showed vasculitis without demyelination.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"396 ","pages":"Article 578467"},"PeriodicalIF":2.9,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142502426","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":"May high mobility group box protein-1 be a biomarker for major depressive disorder?","authors":"Ali Emre Köse ,&nbsp;Tayfun Turan ,&nbsp;Eser Kilic","doi":"10.1016/j.jneuroim.2024.578466","DOIUrl":"10.1016/j.jneuroim.2024.578466","url":null,"abstract":"<div><div>High Mobility Group Box Protein-1 (HMGB1), which has proinflammatory properties, is known to be involved in psychiatric disorders as far as we know, there are only one clinical studies investigating the role of HMGB1 in major depressive disorder (MDD). In this study, we aimed to investigate the role of HMGB1 in the etiopathogenesis of MDD and whether HMGB1 can be used as a biomarker in MDD by measuring the serum HMGB1 levels of depressed patients in the episode and remission periods. This study included 30 patients diagnosed with MDD in episode, 30 patients in remission and 30 healthy controls. Each group comprised 20 female and 10 male participants. In this study, serum HMGB1 levels were found to be lower in the patient group in the episode compared to the patient group in the remission period and the healthy control group. There was no significant difference between the patient group in remission and the healthy control group in terms of serum HMGB1 levels. The fact that serum HMGB1 levels were lower in the patient group in the episode compared to the patient group in the remission period and the control group may be related to the neuroprotective effects of HMGB1. HMGB1 may be used as a biomarker for MDD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"396 ","pages":"Article 578466"},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468198","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}