Journal of neuroimmunology最新文献

{"title":"Are corneal nerve and dendritic cell parameters assessed via corneal confocal microscopy good markers for multiple sclerosis? – A systematic review and meta-analysis","authors":"Prince K. Akowuah ,&nbsp;Esther Botchway ,&nbsp;Ebenezer Owusu ,&nbsp;Dominic A. Ohene ,&nbsp;Teresa Abonambugre ,&nbsp;Yusif Saeed Adam ,&nbsp;Phoebe Ahimah Asherow ,&nbsp;Berlinda E. Deletsu ,&nbsp;Jesse Doe ,&nbsp;Felicia Akyaa Akomeah ,&nbsp;David Totoe","doi":"10.1016/j.jneuroim.2025.578697","DOIUrl":"10.1016/j.jneuroim.2025.578697","url":null,"abstract":"<div><h3>Objective</h3><div>The current study evaluated corneal nerve and dendritic cell changes in multiple sclerosis (MS) compared to healthy controls.</div></div><div><h3>Methods</h3><div>The study was registered with PROSPERO (ID: CRD42024606762) and adhered to the PRISMA guidelines. PubMed, Scopus, and Web of Science databases were searched. Mean difference (MD), with a 95 % confidence interval, was used to assess outcomes. The quality of evidence was assessed using the GRADE system.</div></div><div><h3>Results</h3><div>12 cross-sectional comparative studies (<em>n</em> = 485 MS patients, <em>n</em> = 319 controls) met the inclusion criteria. Corneal nerve fiber density (MD = −8.35 fibers/mm², 95 % CI: −11.90 to −4.79; number of studies = 6), corneal nerve fiber length (MD = −4.05 mm/mm², 95 % CI: −5.74 to −2.36; number of studies = 9) and corneal nerve branch density (MD = −18.76 branches/mm², 95 % CI: −21.51 to −16.02; number of studies = 6) were significantly lower in MS compared to healthy controls. Heterogeneity was significant for corneal nerve fiber density and corneal nerve fiber length, but insignificant for corneal nerve branch density. No significant difference was found in corneal dendritic cell density; however, in the subgroup with disease duration ≤8 years, multiple sclerosis patients had significantly higher dendritic cell density (MD = 17.36 cells/mm², 95 % CI: 4.17 to 30.56; number of studies = 3).</div></div><div><h3>Conclusion</h3><div>Corneal nerve degeneration and dendritic cell changes assessment with corneal confocal microscopy may be an emerging tool with potential for disease monitoring. Further longitudinal studies are needed to validate these findings and clarify their correlation with MS progression and severity.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578697"},"PeriodicalIF":2.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720922","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":"Celia Fildes Brosnan (Jan. 5, 1938 – Feb. 10, 2025) Neuroimmunologist and Friend Extraordinaire","authors":"Cedric S. Raine","doi":"10.1016/j.jneuroim.2025.578702","DOIUrl":"10.1016/j.jneuroim.2025.578702","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578702"},"PeriodicalIF":2.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765013","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":"Maresin1 improves postoperative delirium-like behavior in mice with tibial fractures by inhibiting the TLR4/MyD88/NF-kB pathway","authors":"Wenyi Liu,&nbsp;Maoji Zhao,&nbsp;Longmin He,&nbsp;Daiyu Chen,&nbsp;Jun Cao","doi":"10.1016/j.jneuroim.2025.578703","DOIUrl":"10.1016/j.jneuroim.2025.578703","url":null,"abstract":"<div><h3>Background</h3><div>Postoperative delirium (POD) is a common complication in elderly patients following surgery, contributing to increased morbidity and healthcare costs. Although the pathophysiological mechanisms of POD are not fully understood, it is believed to involve significant inflammatory responses, particularly the activation of astrocytes. This study investigates the neuroprotective potential of Maresin1 (MaR1), alone and in combination with the TLR4 inhibitor TAK-242, in a mouse model of POD. Our findings indicate that MaR1 reduces astrocyte activation by inhibiting the TLR4/MyD88/NF-κB signaling pathway, which mitigates inflammatory responses associated with POD. These results suggest that targeting astrocytic TLR4/MyD88/NF-κB activation could be a promising therapeutic strategy for POD prevention and treatment.</div></div><div><h3>Purpose</h3><div>This study aims to evaluate the effects of Maresin1 (MaR1), a bioactive molecule derived from the omega-3 fatty acid DHA, alone or in combination with TAK-242, a synthetic TLR4 inhibitor, on cognitive outcomes and inflammatory responses in a mouse model of POD induced by tibial fracture internal fixation.</div></div><div><h3>Methods</h3><div>Ninety C57BL/6 mice were subjected to tibial fracture surgery and divided into six groups to receive different treatments: sham, surgery only, surgery with normal saline, surgery with MaR1, surgery with TAK-242, and surgery with both MaR1 and TAK-242. Cognitive functions were assessed using the Buried Food Test, Y Maze Test and Open Field Test. Western blotting, qRT-PCR, immunofluorescence, and transmission electron microscopy were utilized to examine astrocytic activation and the integrity of the TLR4/MyD88/NF-κB pathway.</div></div><div><h3>Results</h3><div>Compared to the sham-operated group, mice pretreated with MaR1 exhibited significant improvements in postoperative delirium-like behavior. Furthermore, in contrast to the positive control group treated with TAK-242 alone, Combination treatment with MaR1 and TAK-242 improved the delirium-like behavior in mice, and effectively reduced the activation of astrocytes as well as the expression of associated markers (GFAP and S100β) in the mouse brain. Additionally, these treatments modulated the TLR4/MyD88/NF-κB signaling pathway, which serves as a potential neuroprotective mechanism to mitigate the impact of surgical trauma and prevent postoperative delirium.</div><div>Conclusion: MaR1, whether used alone or in combination with TAK-242, demonstrates significant anti-inflammatory and neuroprotective effects in a POD mouse model, achieved likely through the inhibition of TLR4/MyD88/NF-kB activation. These findings suggest that targeting TLR4/MyD88/NF-kB inflammatory pathway may help prevent or mitigate POD in surgical patients.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578703"},"PeriodicalIF":2.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144711091","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":"When gut and nerves collide: A case of Neuromyelitis Optica Spectrum disorder after golimumab for ulcerative colitis","authors":"Bernardo de Faria Moraes ,&nbsp;Josemary Cavalcante Lemos Sucupira ,&nbsp;Marcus Gualberto de Oliveira Junior ,&nbsp;Gabriel André Pedral Diniz Leite ,&nbsp;Gustavo André Pedral Diniz Leite ,&nbsp;Guilherme Grossi Lopes Cançado","doi":"10.1016/j.jneuroim.2025.578700","DOIUrl":"10.1016/j.jneuroim.2025.578700","url":null,"abstract":"<div><div>Anti-TNF alpha agents, such as golimumab, are effective treatment options for moderate to severe inflammatory bowel disease. However, demyelinating syndromes have been reported as rare adverse events. We present the first documented case of Neuromyelitis Optica Spectrum Disorder with positive aquaporin-4 antibodies following golimumab therapy for ulcerative colitis, manifesting as intractable hiccups secondary to Area Postrema Syndrome. The patient was treated with plasmapheresis and rituximab, with partial improvement.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578700"},"PeriodicalIF":2.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144703118","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":"OPA1 modulates NLRP3 inflammasome activation and microglial-mediated neuroinflammation in neonatal hypoxic-ischemic brain injury","authors":"Qingchen Lv ,&nbsp;Fei Hong ,&nbsp;Zhanyuan Sun ,&nbsp;Haiyan Shen ,&nbsp;Hongyi Lu ,&nbsp;Ye Jin ,&nbsp;Liming Mao ,&nbsp;Lei Song","doi":"10.1016/j.jneuroim.2025.578701","DOIUrl":"10.1016/j.jneuroim.2025.578701","url":null,"abstract":"<div><h3>Background</h3><div>Hypoxic-ischemic brain injury (HIBD) represents a primary cause of neurological impairment in neonates and is frequently associated with persistent cognitive and motor deficits. This study explores the regulatory function of optic atrophy 1 (OPA1) in modulating NLRP3 inflammasome-mediated neuroinflammation in a neonatal rat model of hypoxic-ischemic encephalopathy (HIE), and evaluates the impact of the OPA1 inhibitor MYLS22 on neuroinflammatory responses and cerebral injury.</div></div><div><h3>Methods</h3><div>Neonatal rats were subjected to HIBD. Temporal expression patterns of OPA1 and inflammasome-associated proteins were assessed using Western blotting, immunofluorescence, and histopathological analyses. The influence of MYLS22 treatment on neuroinflammatory markers, brain pathology, and cognitive outcomes was also investigated.</div></div><div><h3>Result</h3><div>HIBD led to a marked reduction in long-form OPA1 (L-OPA1) expression and a concomitant increase in short-form OPA1 (S-OPA1). Activation of the NLRP3 inflammasome peaked between 24 and 48 h post-injury. Treatment with MYLS22 suppressed OPA1 expression in a dose-dependent manner, further enhancing inflammasome activation and aggravating brain injury, characterized by enlarged infarct volumes, increased edema, and impaired cognitive performance. Conversely, in vitro overexpression of L-OPA1 attenuated inflammasome activation and reduced microglial inflammation following ischemia/reperfusion insult, indicating a neuroprotective effect.</div></div><div><h3>Conclusion</h3><div>These findings demonstrate a pivotal role for OPA1 in controlling neuroinflammation and mitochondrial integrity in the context of HIE. Modulation of OPA1 expression or targeting inflammasome signaling may represent promising therapeutic strategies to alleviate neuroinflammatory injury and improve neurological outcomes in neonates.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578701"},"PeriodicalIF":2.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738909","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":"Fisetin alleviates Aβ-induced neuronal cell ferroptosis by regulating Sirt6-mediated deacetylation modification","authors":"Yuqin Xie ,&nbsp;Changlan Li ,&nbsp;Yangbo Zhang ,&nbsp;Xu Liu ,&nbsp;Wei Wang ,&nbsp;Lili Zheng ,&nbsp;Xunhu Gu","doi":"10.1016/j.jneuroim.2025.578699","DOIUrl":"10.1016/j.jneuroim.2025.578699","url":null,"abstract":"<div><h3>Background</h3><div>Ferroptosis contributes to Alzheimer's disease (AD) pathology. Fisetin, a flavonoid with neuroprotective properties, has shown potential in reducing oxidative stress and inflammation. This study investigates the protective effects and underlying molecular pathways of fisetin against amyloid-β (Aβ)-induced ferroptosis in neuronal cells.</div></div><div><h3>Methods</h3><div>HT22 mouse hippocampal neuronal cells were pre-incubated with fisetin before exposure to amyloid-β (Aβ). Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay, and lipid peroxidation was measured with the C11-BODIPY probe. Protein expression patterns were determined via Western blot analysis. Co-immunoprecipitation (CoIP) and ubiquitination assays were used to explore the interactions between Sirtuin 6 (Sirt6), nuclear factor erythroid 2-related factor 2 (Nrf2), and kelch-like ECH-associated protein 1 (Keap1).</div></div><div><h3>Results</h3><div>Fisetin pre-treatment significantly alleviated Aβ-induced ferroptosis in HT22 cells. Sirt6 upregulation was observed following fisetin treatment, and silencing Sirt6 reversed its protective effects on Aβ-induced neuronal cell ferroptosis. Mechanistically, Sirt6 deacetylated Nrf2 and enhanced its stability by preventing its degradation through Keap1-mediated ubiquitination. As expected, fisetin alleviated Aβ-induced ferroptosis in neuronal cells through activation of the Sirt6/Nrf2 axis.</div></div><div><h3>Conclusion</h3><div>Fisetin alleviated Aβ-induced neuronal cell ferroptosis by activating the Sirt6/Nrf2 axis. These results underscore fisetin's therapeutic potential for AD by targeting ferroptosis, providing a new strategy for disease intervention.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578699"},"PeriodicalIF":2.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764136","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":"Therapeutic effects of estrogens on inflammatory demyelination in a mouse model of multiple sclerosis","authors":"Francisco P. Gomez ,&nbsp;Shameena Bake ,&nbsp;Colin R. Young ,&nbsp;Farida Sohrabji ,&nbsp;Candice L. Brinkmeyer-Langford ,&nbsp;C. Jane R. Welsh","doi":"10.1016/j.jneuroim.2025.578698","DOIUrl":"10.1016/j.jneuroim.2025.578698","url":null,"abstract":"<div><div>Multiple Sclerosis (MS) is a neurodegenerative autoimmune disease in which the immune system targets the myelin sheath of nerve axons, leading to a variety of neurological signs. Sex hormones are thought to be important factors in MS since pregnancy and oral contraceptives reduce both symptoms and relapses. During pregnancy, remissions occur primarily in the third trimester when estradiol and estriol are elevated. We have investigated the role of these two hormones in an experimental model of virus-induced MS.</div><div>Theiler's murine encephalomyelitis virus (TMEV) causes an inflammatory demyelinating disease in mice that resembles chronic progressive MS. To investigate the efficacy of estrogen therapy in the TMEV model, we used 6 experimental groups of 5-week-old female SJL/J mice. Mice were either infected with TMEV or were sham infected with PBS. At 15 weeks pi, during the chronic inflammatory disease, all mice were ovariectomized and implanted with slow-release pellets of either 1) vehicle 2) estradiol or 3) estriol. Weekly evaluation of clinical signs of disease revealed that estradiol treatment was associated with better clinical scores throughout the disease, and both treatment groups had significantly better scores than placebo (vehicle). At termination (24 weeks) we examined the percent demyelination and inflammation in spinal cords, and measured serum levels of TMEV antibodies, for all mice. Estradiol and estriol significantly decreased inflammation in the spinal cord, but only estradiol significantly decreased demyelination. Virus infection and hormone treatment each significantly affected levels of TMEV antibodies. Antibody levels also differed significantly between estradiol and placebo groups, and between estriol and placebo groups, for all mice regardless of infection status. These results suggest that estrogens may be effective therapies for progressive multiple sclerosis induced by viral infections.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578698"},"PeriodicalIF":2.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144703117","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":"Gut dysbiosis influences the pathophysiology of multiple sclerosis: A case-control study from North India","authors":"Gurkeerat Kaur ,&nbsp;Pallawi Kumari ,&nbsp;Priti Devi ,&nbsp;Aparna Swaminathan ,&nbsp;Ashok Kumar ,&nbsp;Usha Dutta ,&nbsp;Poonam Khanna ,&nbsp;Deepak Sharma ,&nbsp;Pallab Ray ,&nbsp;Aarti Darra ,&nbsp;Rajesh Pandey ,&nbsp;Dheeraj Khurana","doi":"10.1016/j.jneuroim.2025.578696","DOIUrl":"10.1016/j.jneuroim.2025.578696","url":null,"abstract":"<div><h3>Background and objectives</h3><div>Alterations in gut microbiota have been linked to pathophysiology of immune-mediated diseases like multiple sclerosis (MS). This study was undertaken to characterise the gut microbiome profile in North Indian MS patients and to evaluate gut health using biomarkers like zonulin (intestinal permeability) and calprotectin (intestinal inflammation).</div></div><div><h3>Methods</h3><div>84 Patients with relapsing-remitting MS patients (RRMS) of 18–75 years of age with an expanded disability status scale (EDSS) score less than or equal to 5.5 and 106 healthy controls (HC) were recruited for the study. Gut microbiota was sequenced using Illumina MiSeq. Clinical, demographic, anthropometric, and dietary details were recorded. Sandwich ELISA was used to quantify serum zonulin and fecal calprotectin levels.</div></div><div><h3>Results</h3><div>MS patients had lower alpha microbial diversity, while distinct beta diversity metrics were observed in MS and HC. Firmicutes was found to be the most abundant phylum in both groups with significant enrichment in MS than HC. In MS, significant depletion of commensal bacterial species like <em>Faecalibacterium prausnitzii</em>, <em>Monoglobus pectinilyticus</em>, and <em>Bacillus</em> species indicated gut dysbiosis. These alterations influenced the prevalence and functioning of metabolic pathways. Therefore, pathways involved in biosynthesis of long-chain fatty acids (LCFA) were significantly enriched in MS than HC, while generation of short-chain fatty acids were predominant in HC. In addition, high zonulin, without an increase in calprotectin levels was observed in MS patients.</div></div><div><h3>Conclusions</h3><div>RRMS patients in North India have a decreased microbial diversity in terms of depletion of commensals. The dominance of LCFA generating pathways in MS patients might have triggered the proinflammatory reactions, that are possibly linked to the development of a highly permeable/leaky gut in MS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578696"},"PeriodicalIF":2.9,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144713390","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":"miR-92a-3p regulates neuropathic pain and neuroinflammation by regulating the expression of WNT5A","authors":"Xia Geng ,&nbsp;Xiaona Guo ,&nbsp;Tingting Wang,&nbsp;Jingjing Xu,&nbsp;Linkai Jiang","doi":"10.1016/j.jneuroim.2025.578695","DOIUrl":"10.1016/j.jneuroim.2025.578695","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the mechanism of miR-92a-3p involved in neuropathic pain (NP) and neuroinflammation through <em>Wnt5a</em>.</div></div><div><h3>Methods</h3><div>Cellular model was established using LPS stimulation of rat highly aggressive proliferating immortalized (HAPI) microglia cell. CCI surgery was performed to establish the NP model in rats. Pain responses were assessed by paw withdrawal threshold (PWT) and withdrawal latency (PWL) in rats. miR-92a-3p and <em>Wnt5a</em> expression levels were detected by RT-qPCR; inflammatory factor changes were monitored by ELISA; and the targeting relationship between miR-92a-3p and <em>Wnt5a</em> was verified by dual fluorescein reporter assay.</div></div><div><h3>Results</h3><div>The expression of miR-92a-3p and anti-inflammatory cytokines (IL-4, IL-10) was decreased, and the levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ) were increased in LPS-stimulated HAPIs. <em>Wnt5a</em>, as a miR-92a-3p target gene, was involved in NP regulation, and LPS transfected with miR-92a-3p glial cells showed decreased <em>Wnt5a</em> expression and markedly reduced inflammation levels. Animal experiments demonstrated that CCI rats with low miR-92a-3p and high <em>Wnt5a</em> expression had reduced PWT and PWL pain thresholds and increased levels of inflammatory factors compared with the sham group. Intrathecal injection of miR-92a-3p agomir +oe-<em>Wnt5a</em> noticeably decreased pain threshold and elevated <em>Wnt5a</em> and inflammatory factor expression in CCI rats.</div></div><div><h3>Conclusion</h3><div>Low levels of miR-92a-3p continuously lower the pain response threshold in rats by promoting <em>Wnt5a</em>-induced inflammatory factor expression, participating in NP.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578695"},"PeriodicalIF":2.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757729","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":"Rapid one-step protocol for exploring immune cells in cerebrospinal fluid","authors":"Ewa Wallisky Millet ,&nbsp;Fabrice Malergue ,&nbsp;Gregorio Petrirena Hernandez ,&nbsp;José Boucraut","doi":"10.1016/j.jneuroim.2025.578687","DOIUrl":"10.1016/j.jneuroim.2025.578687","url":null,"abstract":"<div><div>Flow cytometry analysis of the cerebrospinal fluid's immune cell subset profiles can be used to help in the diagnosis and prognosis of nervous system pathologies. However, the cells need to be analyzed rapidly after collection. Furthermore, immune cells are quite rare in CSF, samples are limited in volume and immune staining protocols, sometime including washing steps, are not fully standardized among laboratories. It is therefore useful and necessary to improve the pre-analytical and analytical processes.</div><div>We have thus developed the one-step protocol for the analysis of CSF cells, without washing step, using a panel of labeled antibodies for both enumeration of red and white blood cells and the analysis of main immune cell subsets. We first investigated repeatability of this protocol for the main immune cell subsets count and staining and its stability over a 3-day period using a mild fixation protocol. Then, using this protocol, we evaluated the impact of delays in treatment after lumbar puncture.</div><div>We demonstrate that cell count and staining are stable over 3 days in both CSF and whole blood samples. Direct labeling with no washing step combined with the cytometer's analytical performance enable precise and reproducible cell counting. Using this simple and robust protocol, we showed that monocytes are lost if the biological samples are not processed rapidly following the lumbar puncture.</div><div>This one-step method allows for rapid, standardized, and reproducible multiparametric CSF immune cell analysis.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578687"},"PeriodicalIF":2.9,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144662817","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}