Journal of Inflammation Research最新文献

{"title":"MiR-133a-5p Facilitates Cuproptosis in Hepatocellular Carcinoma Through Targeting of ATP7B.","authors":"Qiaohui Ren, Xinyue Zhu, Nannan Wang, Kang Yu, Wei Lv, Lianzi Wang, Yan Zang, Dongyue Ma, Xinyi Zhou, Junxiao Yao, Mengjiao Shen, Li Yu, Tao Li","doi":"10.2147/JIR.S515647","DOIUrl":"https://doi.org/10.2147/JIR.S515647","url":null,"abstract":"<p><strong>Purpose: </strong>We explored the effects of miR-133a-5p and ATP7B on cuproptosis in hepatocellular carcinoma.</p><p><strong>Methods: </strong>Initially, we assessed the impact of miR-133a-5p on hepatocellular carcinoma (HCC) using CCK-8 assays, cell scratch assays, and flow cytometry. Subsequently, we utilized elesclomol in combination with copper ions to induce cuproptosis in the HCC cell lines PLC/PRF/5 and Huh-7. We evaluated the influence of miR-133a-5p on cuproptosis using CCK-8 assays, cell scratch assays, flow cytometry, and Western blotting. To elucidate the underlying mechanisms, we employed bioinformatics to identify potential downstream target genes of miR-133a-5p and conducted dual-luciferase reporter assays to confirm the binding sites. Finally, we validated the regulatory effect of miR-133a-5p on ATP7B by modulating miR-133a-5p expression through cell transfection experiments.</p><p><strong>Results: </strong>The results from the CCK-8 assay, cell scratch assay, and flow cytometry demonstrated that miR-133a-5p significantly inhibits the proliferation and migration of HCC cells while promoting their apoptosis. Furthermore, Elesclomol in combination with copper ions induces cuproptosis in HCC cells. Compared to the cuproptosis observed in HCC as a control, miR-133a-5p further suppresses the proliferation and migration of HCC cells, enhances their death, and increases the expression of cuproptosis-related proteins more prominently. Bioinformatics analysis suggested that ATP7B might be a downstream target gene of miR-133a-5p. This was confirmed by dual luciferase assays, which identified a binding site between miR-133a-5p and ATP7B. Additionally, the expression levels of ATP7B were found to decrease or increase in response to the regulation by miR-133a-5p.</p><p><strong>Conclusion: </strong>MiR-133a-5p facilitates cuproptosis in hepatocellular carcinoma through targeting of ATP7B.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6607-6622"},"PeriodicalIF":4.2,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144159647","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}

{"title":"Guillain-Barré Syndrome During the Outbreak of Omicron in Southern China: A Multicenter Case-Control Study.","authors":"Mengcui Gui, Peicai Fu, Lijun Luo, Qunhui Liu, Jun Chen, Zhongmou Han, Liying Chang, Hui Chen, Daokai Gong, Juan Chen, Yafang Liu, Rong Zhang, Ming Zhang, Mingqing Xiang, Xiaohua Yang, Jing Lin, Bitao Bu, Zhijun Li","doi":"10.2147/JIR.S503263","DOIUrl":"https://doi.org/10.2147/JIR.S503263","url":null,"abstract":"<p><strong>Purpose: </strong>The largest nationwide outbreak of Omicron, a severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) variant, occurred between December 2022 and February 2023 in China. This multicenter case-control study investigated the clinical features of GBS during this period.</p><p><strong>Methods: </strong>The clinical characteristics of patients diagnosed with GBS associated with SARS-CoV-2 were assessed during an Omicron outbreak at 14 referral hospitals in Hubei Province, Southern China. In the case-control study, patients with GBS were identified and diagnosed between 2021 and 2022 at Tongji Hospital in Wuhan, Hubei province.</p><p><strong>Results: </strong>Forty-one patients were diagnosed with GBS during the Omicron outbreak. The median patient age was 57.5 years, and 51.2% were male. The median period between the preceding infection and onset of neurological symptoms was 10 days. The majority of the patients (38 cases [92.7%]) presented with classic sensorimotor neuropathy, with the lower limbs involved more often; 17 cases (41.5%) were accompanied by cranial neuropathies, which was most observed with the bilateral or unilateral facial paralysis (13 cases [31.7%]). Albuminocytologic dissociation was observed in 27 patients (71.1%), and mild pleocytosis was found in five patients (12.2%), with a maximum of 22 cells/mm³. Thirty-two patients finished the electrophysiological studies, and axonal variants were confirmed in 21 cases predominantly as acute motor-sensory axonal neuropathy (40.6%) or acute motor axonal neuropathy (25.0%). Anti-ganglioside antibodies were detected in 19 patients (46.3%). Intravenous immunoglobulin administration improved the patients' symptoms.</p><p><strong>Conclusion: </strong>The characteristics of SARS-CoV-2-associated GBS during the Omicron outbreak appear clinically as sensorimotor neuropathy, with a predominant electrophysiological axonal form. A mainly classic post-infectious immune-mediated mechanism may be involved in this process, such as a temporal profile of clinical symptoms, axon-associated autoantibodies, and improvement by immunotherapy.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6543-6555"},"PeriodicalIF":4.2,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150754","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}

{"title":"Erratum: Quantitative Assessment of Baseline Serum HDL-C to Predict Gout Flares During Urate-Lowering Therapy Initiation: A Prospective Cohort Study [Corrigendum].","authors":"","doi":"10.2147/JIR.S540816","DOIUrl":"https://doi.org/10.2147/JIR.S540816","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.2147/JIR.S493376.].</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6489-6490"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150753","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}

{"title":"Comparative Imaging Analysis of Kimura's Disease Using ¹⁸F-FDG PET/CT and [¹⁸F]AlF-NOTA-FAPI-04 PET/CT.","authors":"Chuanyin Sun, Haopeng Ni, Mengdi Jiang, Guolin Wang, Xinhui Su, Zhenfeng Liu","doi":"10.2147/JIR.S513892","DOIUrl":"10.2147/JIR.S513892","url":null,"abstract":"<p><p>Kimura's disease is a rare, chronic inflammatory disorder characterized by subcutaneous nodules, eosinophilia, and elevated serum IgE levels. It commonly affects young Asian males and typically presents in the head and neck region. Diagnosis is confirmed via histopathological examination, while treatment options include corticosteroids, surgery, and radiotherapy. [¹⁸F]AlF-NOTA-FAPI-04 PET/CT demonstrated superior imaging, with clearer background and higher target-to-background ratio, highlighting lesions with higher SUV values and greater specificity for fibroblast activity. Compared to ¹⁸F-FDG PET/CT, which is limited by nonspecific uptake in inflammatory tissues, [¹⁸F]AlF-NOTA-FAPI-04 PET/CT offers superior sensitivity and specificity in visualizing fibroblast activation. These advantages not only improve diagnostic accuracy in Kimura's disease but may also have broader implications for other eosinophilic or inflammatory disorders sharing similar clinical features. This technique improves diagnostic accuracy, facilitates treatment planning, and may guide the development of future treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6483-6488"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142637","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}

{"title":"Ferroptosis: New Strategies for Clinical Treatment of Rheumatoid Arthritis.","authors":"Yanqiu Sun, Jian Liu, Mingyu He, Dan Huang, Yuan Wang","doi":"10.2147/JIR.S523410","DOIUrl":"10.2147/JIR.S523410","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that can lead to joint deformities, functional loss, and a significant reduction in patients' quality of life. It also imposes a considerable medical and socio-economic burden. Iron-induced cell death, or ferroptosis, is a unique form of programmed cell death characterized by dysregulated iron metabolism and the accumulation of lipid peroxides resulting from increased reactive oxygen species (ROS) and reduced activity of glutathione peroxidase 4 (GPX4). The accumulation of lipid peroxides can cause cellular damage, promotes inflammatory responses and joint destruction. This process not only plays a crucial role in the pathogenesis of RA, but also provides new therapeutic targets for its treatment. In this review, we summarize the regulatory mechanisms of ferroptosis in the pathogenesis of RA. These include its roles in regulating oxidative stress and lipid peroxidation, inhibiting the abnormal proliferation of synovial fibroblasts (FLSs), preventing cartilage erosion, restoring immune homeostasis and inflammatory responses, and other aspects. Finally, we also discuss the potential clinical applications, and future prospects of ferroptosis-based therapies for RA treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6529-6541"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142576","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}

{"title":"Exportin-T Promotes Breast Cancer Progression via PI3K/AKT/mTOR Signaling Pathway.","authors":"Zhichao Hou, Wenxia Ma, Dongliang Ren, Ningning Shen, Weilin Bi, Meiqin Guo, Xinzheng Li, Yanhong Wang, Hongyan Jia","doi":"10.2147/JIR.S512905","DOIUrl":"10.2147/JIR.S512905","url":null,"abstract":"<p><strong>Purpose: </strong>Breast cancer (BC) is the most common malignant tumor in women. Exportin-T (XPOT) which is a member of the karyopherin -β family has been identified as a prognostic biomarker in various cancers, but its role in BC remains inadequately understood. This study aims to investigate the clinical characterization and molecular mechanism of XPOT in BC.</p><p><strong>Material and methods: </strong>A retrospective RNA-seq data analysis based on a cohort of 966 BC patients from The Cancer Genome Atlas database (TCGA) and 1904 patients from the Molecular Taxonomy of Breast Cancer International Consortium database was conducted for analyzing the correlation between XPOT expression and BC clinical pathological features. In addition, small interfering RNA transfection was used to downregulate XPOT expression in MDA-MB-468/231 cell lines followed by cell proliferation assessed via Cell Counting Kit-8 assays, meanwhile, BC cell migration and invasion capabilities were measured using Transwell test. Expression levels of CDK4/6 and key proteins in the PI3K/Akt/mTOR signaling pathway were assessed using Western blotting.</p><p><strong>Results: </strong>We found that XPOT was enriched in estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, larger tumor size, and cases with increased lymph node metastasis BC. XPOT was identified as a potential biomarker for the basal subtype of BC and a prognostic factor for the overall survival of patients with BC. Furthermore, XPOT promoted the proliferation and invasion of BC cells, likely through activation of the PI3K/AKT/mTOR signaling pathway, which in turn to upregulate cyclin D and CDK4/6 to drive tumor progression.</p><p><strong>Conclusion: </strong>Our findings indicate that XPOT overexpression is associated with poor clinical characteristics and poor prognosis in BC, promoting disease progression by activating PI3K/AKT/mTOR pathway. These findings highlight XPOT as a potential therapeutic target in BC.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6467-6481"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142648","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}

{"title":"The Association Between Neonatal Respiratory Distress Syndrome and Plasma IgG N-Glycosylation: A Case-Control Study.","authors":"Yingjie Wang, Qingqing Shen, Ruxu Yan, Meng Wang, Min Xu, Hanxiang Chen, Dong Li","doi":"10.2147/JIR.S524188","DOIUrl":"10.2147/JIR.S524188","url":null,"abstract":"<p><strong>Background: </strong>Neonatal respiratory distress syndrome (NRDS) is the leading cause of neonatal death. Changes in plasma immunoglobulin G (IgG) N-glycosylation have been demonstrated in a variety of diseases. However, its implications and clinical significance in NRDS remain to be clarified.</p><p><strong>Methods: </strong>To determine the effect of IgG N-glycosylation on NRDS, we recruited 88 NRDS participants and 120 control participants from December 2021 to September 2022. Plasma was collected, IgG was isolated and purified, and the glycogram was analyzed by ultra performance liquid chromatography (UPLC) with fluorescence detector.</p><p><strong>Results: </strong>The occurrence of premature rupture of membranes (PROM) [OR=9.043(1.036-78.966), P=0.046] and the elevation of γ-glutamyltransferase (GGT) [OR=1.015(1.001-1.029), P=0.032] were independent risk factors for the occurrence of NRDS. Furthermore, the area percentages of GP1, GP3, GP4, GP11, GP13, and GP24 were significantly higher in NRDS patients compared with control group. Conversely, GP14 was observed to be significantly lower. Furthermore, an increase in plasma IgG sialylation and core fucosylation was observed in NRDS, whereas the modification with galactosylation was decreased. The model constructed using GP1, GP13, GP14, PROM, and GGT as composite indices demonstrated robust predictive performance (AUC=0.902, 95% CI: 0.851-0.953).</p><p><strong>Conclusion: </strong>Patients with NRDS frequently exhibit alterations in the glycosylation of plasma IgG. These findings provide new insights into the diagnosis of NRDS and clinical treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6439-6451"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142612","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}

{"title":"Identifying KL-6-Associated Immune Cell Signatures and Key Genes in Emphysematous COPD.","authors":"Xinru Xiao, Wenwen Guo, Na Li, Nuo Chen, Qian Zhang","doi":"10.2147/JIR.S515653","DOIUrl":"10.2147/JIR.S515653","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate the potential of Krebs von den lungen-6 (KL-6) as a biomarker for distinguishing emphysematous chronic obstructive pulmonary disease (COPD-E) from non-emphysematous COPD (COPD-NE), and to explore the underlying mechanisms associated with KL-6 expression.</p><p><strong>Methods: </strong>We enrolled 154 patients with COPD and 170 healthy controls to assess serum KL-6 levels. Receiver operating characteristic curve was used to determine the diagnostic sensitivity and specificity. Pearson's correlation analysis was used to evaluate the correlation. Univariate and multivariate linear regression analyses were performed to explore the factors influencing KL-6 levels in COPD. Transcriptomic sequencing was performed on peripheral blood mononuclear cells from COPD patients with varying KL-6 levels to explore underlying biological mechanisms. A Mendelian randomization analysis was employed to ascertain the association between the expression quantitative trait loci of key genes and emphysema risk.</p><p><strong>Results: </strong>Serum KL-6 levels were significantly elevated in COPD patients, particularly in COPD-E. Pearson analyses revealed that the serum KL-6 concentration was positively correlated with eosinophil count. Transcriptomic analysis revealed 237 differentially expressed genes (DEGs) between patients with high and low levels of KL-6. Gene set enrichment analysis revealed that these DEGs were associated with immune responses. No significant difference in immune cell proportions were observed between high and low KL-6 groups, but KL-6 showed a negative correlation with T cell gamma delta. By intersecting the DEGs with those from the GSE248493 dataset, we identified seven key genes and further validated their association with the risk of emphysema using Mendelian randomization, with amidohydrolase domain containing 2 (AMDHD2) potentially reducing the risk of the disease.</p><p><strong>Conclusion: </strong>KL-6 is a promising biomarker for distinguishing COPD-E from COPD-NE and AMDHD2 may be involved in the regulation of increased KL-6 levels in COPD-E.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6453-6466"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142627","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}

{"title":"The Inhibitory Effect of the Active Ingredients in the Bushen Huoxue Formula on the IL-17A Signaling Pathway and Its Alleviating Effect on Osteoarthritis.","authors":"Xuan Wang, Yunheng Zhang, Xin Chang, Xiaodong Wen, Feng Tian, Hanjie Yu, Yi Li","doi":"10.2147/JIR.S506716","DOIUrl":"https://doi.org/10.2147/JIR.S506716","url":null,"abstract":"<p><strong>Objective: </strong>Osteoarthritis (OA) stands as a prevalent degenerative disease worldwide. Despite the demonstrated therapeutic efficacy of the Bushen Huoxue formula (BSHXF) in treating OA, its underlying mechanism remains elusive. Network pharmacology is commonly employed for investigating drug-disease associations and processes. In this study, we employed network pharmacology alongside in vitro and in vivo experiments to elucidate the molecular mechanism by which BSHXF treats OA.</p><p><strong>Methods: </strong>Based on the TCMSP database, active components of BSHXF were screened, and OA-related targets were retrieved from GeneCard and DisGeNET to construct a \"component-target-pathway\" network using Cytoscape. Core target functions and pathways (KEGG/GO) were analyzed through STRING and Metascape, while component-target binding affinity was validated via Autodock. For in vitro experiments, an IL-1β-induced chondrocyte inflammation model was established, and key protein expression was detected by Western blot and immunofluorescence. For in vivo experiments, an OA model was created by medial meniscectomy of the knee joint in rats, and therapeutic efficacy was assessed using histological staining and micro-CT.</p><p><strong>Results: </strong>This study screened 89 active ingredients of BSHXF and identified 189 common targets. Network pharmacological analysis revealed luteolin and tanshinone IIA as the most crucial active ingredients in treating OA with BSHXF. The potential mechanisms of action for BSHXF in OA treatment involve inflammation inhibition, immune function regulation, and resistance to oxidative stress, with a significant regulatory role played by the IL-17 signaling pathway. Molecular docking results demonstrated luteolin's strong binding affinity to key targets such as B-cell lymphoma 2 (Bcl-2), Matrix metalloproteinase-9 (Mmp-9), and IL-6.In vitro experiments demonstrated that BSHXF significantly suppressed IL-1β-induced inflammatory responses in chondrocytes, downregulating IL-17A expression (<i>p</i> < 0.05), reducing the expression of MMP-9 (<i>p</i> < 0.05) and IL-6 (<i>p</i> < 0.05), and inhibiting apoptosis. Additionally, in vivo experiments revealed that the high-dose BSHXF group (150 mg/kg) markedly alleviated cartilage damage in OA rats, with OARSI scores significantly decreased compared to the model group (<i>p</i> < 0.05). Micro-CT analysis showed that BSHXF inhibited osteophyte formation and ameliorated OA pathological conditions.</p><p><strong>Conclusion: </strong>BSHXF has the potential to alleviate OA by suppressing inflammation, inhibiting cartilage apoptosis and hindering extracellular matrix degradation via the IL-17 signaling pathway. Our study elucidated the molecular mechanisms underlying the therapeutic effects of BSHXF on OA, thus highlighting its further research implications as a novel drug candidate.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6505-6527"},"PeriodicalIF":4.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150758","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}

{"title":"Clinical Characteristics and Mechanism Discussion of Peripheral Nerve Injury in 2 Cases of Severe Viral Meningoencephalitis.","authors":"Xiaosu Guo, Mengyi Zheng, Zibin Wei, Jianghua Song, Xue Wang, Zhiyuan Shen, Xin Guo, Nan Zhang, Yuan Xing, Yaxin Zhang, Wei Zhang, Runxuan Du, Bo Qiu, Shujuan Tian, Zhiwei Wang","doi":"10.2147/JIR.S505159","DOIUrl":"10.2147/JIR.S505159","url":null,"abstract":"<p><strong>Purpose: </strong>Peripheral neuropathy(PN) secondary to central nervous system(CNS) infections is rare in clinical practice. This study analyze the prognosis, clinical characteristics, and outcomes of patients with PN secondary to CNS infections to aid early diagnosis and improve prognosis.</p><p><strong>Methods: </strong>Clinical data from two patients admitted to our Neurology Department with PN secondary to severe viral meningoencephalitis were collected, summarized, and analyzed. Using diagnostic tools like body fluid tests, imaging, EEG, and EMG, and based on the criteria of the International Encephalitis Consortium, encephalitis was diagnosed in Case 1 and Case 2. The European Academy of Neurology/Peripheral Nerve Society recommendations were applied to confirm patients' PN diagnosis.</p><p><strong>Results: </strong>Patient 1 was diagnosed with encephalitis, presenting with elevated serum IL-6 levels, and received IVIG treatment upon admission. One week later, the infection remitted and IL-6 levels decreased. Physical and EMG examinations revealed peripheral nerve demyelination damage. After treatment, the nerve damage improved, and the patient had a good prognosis post-discharge. Upon admission, Patient 2 exhibited viral meningoencephalitis symptoms, with elevated serum IL-8 and normal IL-6 levels; limb muscle strength and tone were normal. Five days later, the infection deteriorated, accompanied by reduced lower limb strength, and elevated IL-6 and IL-8 in serum and CSF, with a striking peak of CSF IL-6. EMG confirmed peripheral nerve demyelination and axonal damage. Following 5-day IVIG treatment, IL-6 and IL-8 levels in serum and CSF declined. Peripheral nerve injury recovery was modest despite treatment, and the patient's prognosis remained moderate.</p><p><strong>Conclusion: </strong>This study reported two rare cases of PN following CNS infection. Comparative analysis of symptoms, cytokine in body fluids, treatments, disease courses, and prognosis indicates that elevated peripheral and/or central cytokines, particularly IL-6 and IL-8, correlate with the severity and prognosis of this complication. IVIG modulates inflammation, and its administration timing likely determines differential outcomes.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6397-6410"},"PeriodicalIF":4.2,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142601","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}