Journal of Inflammation Research最新文献

{"title":"Association Between Preoperative Lymphocyte-to-Monocyte Ratio and Occurrence of Postoperative Cognitive Dysfunction: A Prospective Cohort Study.","authors":"Xudong Hu, Sihui Zhu, Xiao Yang, Menglei Shan, Jiawei Wang, Xin Da, Yongkang Gui, Yang Liu, Rui Yang, Guanghong Xu","doi":"10.2147/JIR.S481106","DOIUrl":"10.2147/JIR.S481106","url":null,"abstract":"<p><strong>Purpose: </strong>Postoperative cognitive dysfunction (POCD) is a common postoperative complication. Studies have reported that lymphocyte-to-monocyte ratio (LMR) was a predictor of many diseases associated with inflammation. However, further examination of the relationship between preoperative LMR and POCD is needed. We aimed to investigate the association between POCD and preoperative LMR levels to examine the potential of LMR to predict POCD.</p><p><strong>Patients and methods: </strong>This was a prospective cohort study that included patients who underwent elective major abdominal surgery at our hospital between January 2019 and January 2022. Multivariate logistic regression analysis was used to analyze the effects of preoperative LMR on POCD development. The optimal threshold of preoperative LMR for predicting POCD was determined by receiver operating characteristic (ROC) approach. A subgroup analysis was performed according to age, sex, type of surgery and hypertension.</p><p><strong>Results: </strong>Of 964 patients, 362 (37.6%) developed POCD. The preoperative LMR level in the Non-POCD group was higher than that in the POCD group. According to the ROC curve, a cutoff value of 3.758 of the preoperative LMR level could be used to predict POCD occurrence and the area under the curve (AUC) was 0.747 (95% CI: 0.715-0.779, P < 0.001). The results of the subgroup analyses were consistent with the primary ones, and no heterogeneity was observed in the subgroup analyses (P for interaction > 0.05).</p><p><strong>Conclusion: </strong>LMR was significantly associated with the occurrence of POCD after major abdominal surgery. Preoperative low LMR levels can be used to identify patients who may be at high risk of POCD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9527-9537"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729621","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":"CITED2 Mediates Metabolic Reprogramming in Renal Tubular Epithelial Cells via the AKT Signaling Pathway to Induce Sepsis-Associated Acute Kidney Injury.","authors":"Ruiming Deng, Hang Yang, Weibo Zhong, Juan Zhou, Guiming Huang, Kai Zeng","doi":"10.2147/JIR.S486596","DOIUrl":"10.2147/JIR.S486596","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-associated acute kidney injury (S-AKI) is a prevalent and severe clinical complication in intensive care units (ICUs) and is associated with high mortality and poor prognosis. The dysfunction of renal tubular epithelial cells (TECs), particularly through their metabolic reprogramming, plays a critical role in the onset and progression of S-AKI. CITED2 is shown to regulate a variety of cellular processes, but its specific impact on TECs metabolism and S-AKI pathogenesis remains unclear. The aim of this study was to investigate the role of CITED2 in the metabolic reprogramming of TECs and its effects on inflammation and kidney injury in S-AKI.</p><p><strong>Material and methods: </strong>The C57BL/6 mouse model of S-AKI was established using cecal ligation and puncture (CLP). We assessed the inflammatory responses, glucose metabolism and CITED2 expression in the kidneys of septic mice. Additionally, the effect of CITED2 on TECs metabolism and inflammation was evaluated using in vivo and in vitro models. CITED2 silencing and overexpression were employed to elucidate its regulatory role, focusing on the AKT signaling pathway.</p><p><strong>Results: </strong>S-AKI causes structural and functional kidney damage, aggravated inflammatory responses, and dysregulated glucose metabolism, accompanied by increased expression of CITED2. CITED2 silencing attenuated TECs metabolic dysfunction and reduced inflammation, thereby protecting the kidney from injury. Conversely, CITED2 overexpression exacerbated TECs metabolic dysfunction, promoted inflammatory responses, and worsened kidney injury. Mechanistically, CITED2 regulates TEC metabolism through the AKT signaling pathway, promoting S-AKI-related inflammation and contributing to kidney injury.</p><p><strong>Conclusion: </strong>CITED2 drives the metabolic reprogramming of TECs through the AKT signaling pathway, thereby aggravating the inflammatory response and leading to kidney injury, highlighting its critical role in S-AKI. Targeting CITED2 inhibition may represent a novel therapeutic approach for managing S-AKI.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9485-9505"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729630","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":"Expression and Clinical Significance of Lymphocyte Subpopulations and Peripheral Inflammatory Markers in Glioma.","authors":"Chunxiao Zhou, Lei Xu, Mo Geng, Shaoshan Hu","doi":"10.2147/JIR.S474577","DOIUrl":"10.2147/JIR.S474577","url":null,"abstract":"<p><strong>Purpose: </strong>Patients with glioma often fail to achieve satisfactory outcomes despite receiving surgery, radiotherapy, and chemotherapy. Photodynamic therapy (PDT) shows promise in addressing the limitations of traditional treatments. However, the immunological effects of PDT in glioma patients remain underexplored. This study aims to fill this gap by analyzing lymphocyte subpopulations and inflammatory markers in glioma patients undergoing PDT-assisted surgery.</p><p><strong>Patients and methods: </strong>To enhance our comprehension of the immunobiology of glioma within a clinical framework, we conducted a retrospective analysis of glioma patients from September 2019 to December 2023. Peripheral blood lymphocyte subpopulations (CD3+, CD19+, CD4+, CD8+, CD4+/CD8+) and hematological inflammatory factors were compared among 18 patients who underwent surgery with PDT, 10 patients treated with surgery alone, and healthy controls. Additionally, lymphocyte subpopulations from 48 healthy individuals and hematology inflammatory factors from 38 healthy controls were regarded as controls.</p><p><strong>Results: </strong>PDT-assisted surgery resulted in significant alterations in lymphocyte subpopulations and inflammatory markers before and after treatment, particularly in CD4+ and CD8+ T cells. PDT-treated patients demonstrated a superior therapeutic response compared to surgery alone (P=0.035). Notably, primary glioma patients had more prolonged overall survival than recurrent glioma patients (P=0.039).</p><p><strong>Conclusion: </strong>PDT-assisted surgery significantly affects lymphocyte subpopulations and inflammatory markers, enhancing immune response in glioma patients. These findings support the use of PDT as an effective adjuvant therapy. Monitoring lymphocyte subpopulations and inflammatory markers may be valuable for glioma prognosis and treatment optimization.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9423-9451"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729632","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":"Association between Stress Hyperglycemia Ratio and In-Hospital Mortality in Patients with Sepsis [Letter].","authors":"Yu Hao","doi":"10.2147/JIR.S507089","DOIUrl":"10.2147/JIR.S507089","url":null,"abstract":"","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9509-9510"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729623","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":"Higher Expression of Ku80 and Ku70 Indicates Hotter Tumor Immune Microenvironment in Hepatocellular Carcinoma and Better CTL-Centered Immunotherapy.","authors":"Lukun Yang, Ling Li, Peiping Li, Jiafan Chen, Chaonong Cai, Yingbin Jia, Jian Li, Baojia Zou","doi":"10.2147/JIR.S496123","DOIUrl":"10.2147/JIR.S496123","url":null,"abstract":"<p><strong>Purpose: </strong>Both Ku80 and Ku70 are promising drug targets for hepatocellular carcinoma (HCC) and crucial for immune regulation. However, their correlation with HCC immune signatures has not yet been investigated. Therefore, we aimed to investigate the relationship between Ku80, Ku70, and immune signatures in HCC and validate their significance in cytotoxic lymphocyte (CTL) immunotherapy.</p><p><strong>Patients and methods: </strong>Analyses of Ku70, Ku80, and immune signatures in public datasets was performed using R software, an online Kaplan-Meier plotter, g:Profiler, GeneTrail, and Metascape. Uniform manifold approximation and projection, correlation chord diagrams, Pearson's correlation tests, and Spearman correlation tests were used to describe various correlation levels. HCC mRNA sequencing data (n=373 tumor samples and n=50 para-tumor samples) were drawn from The Cancer Genome Atlas (TCGA) public database. Immunofluorescent staining was used to validate Ku70/Ku80 and CD8⁺CTL expression in 120 HCC patients from our center. Survival analysis was performed using the Kaplan-Meier survival analysis with the Log rank test and was adopted to analyze immunotherapy outcomes correlated with Ku70/Ku80 expression in various solid tumors. Multivariate analysis of HCC patient data from our center was performed using a Cox proportional hazards model.</p><p><strong>Results: </strong>Increased Ku70/Ku80 expression positively correlated with more enriched immune microenvironment signatures, indicating increased immune infiltration in HCC. Upregulation of Ku70/Ku80 indicated better anti-PD1 and anti-PDL1 treatment outcomes in various solid tumors. Higher Ku70/Ku80 expression with lower CD8⁺CTL signatures indicated worse survival outcomes, whereas lower Ku70/Ku80 expression with higher CD8⁺CTL signatures indicated the best prognosis.</p><p><strong>Conclusion: </strong>Higher Ku70/Ku80 expression indicated an immune-hot infiltration signature in HCC. Patients with increased Ku70/Ku80 expression and high CD8⁺CTL signatures may potentially benefit from CTL-centered immunotherapies.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9511-9525"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729567","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":"Network Pharmacology and Machine Learning Reveal Salidroside's Mechanisms in Idiopathic Pulmonary Fibrosis Treatment.","authors":"Chenchun Ding, Zhenzhen Guo, Quan Liao, Renjie Zuo, Junjie He, Ziwei Ye, Weibin Chen","doi":"10.2147/JIR.S493171","DOIUrl":"10.2147/JIR.S493171","url":null,"abstract":"<p><strong>Purpose: </strong>Idiopathic pulmonary fibrosis (IPF) is an irreversible respiratory disease. In this study, we evaluated the efficacy of salidroside (SAL), the main component of Rhodiola rosea, in treating IPF.</p><p><strong>Methods: </strong>The pharmacological effects of SAL against epithelial-mesenchymal transition (EMT) and IPF were assessed through in vivo and in vitro experiments. Targets for SAL in treating IPF were identified from various databases and a PPI network was constructed. Functional analyses of target genes were performed using GO, KEGG, DO, and GSEA. Core target genes were identified using LASSO logistic regression and support vector machine (SVM) analysis, followed by molecular docking simulations. Predicted targets and pathways were validated through Western blotting, qRT-PCR, and IHC.</p><p><strong>Results: </strong>Our results demonstrated that SAL ameliorated alveolar epithelial cells (AECs) EMT and mitigated bleomycin -induced pulmonary fibrosis. Through network pharmacology, we identified 74 targets for SAL in the treatment of IPF (P_FDR<0.05) and analyzed their biological functions. Based on these findings, we further applied machine learning techniques to narrow down 9 core targets (P_FDR<0.05). Integrating the results from molecular docking, KEGG, and GSEA analyses, we selected three key targets-IGF1, hypoxia-inducible factor 1-alpha (HIF-1α), and MAPK (P_FDR<0.05)-for further investigation. Our study revealed that SAL inhibits the IGF1 signaling pathway, thereby improving AECs senescence and cell cycle arrest. By inhibiting the HIF-1α pathway, SAL alleviates endoplasmic reticulum stress and reduces intracellular ROS accumulation. Moreover, SAL suppresses the activation of the MAPK signaling pathway, leading to a decrease in inflammation markers in AECs and lung tissue.</p><p><strong>Conclusion: </strong>Experimental results suggest that SAL effectively ameliorates BLM-induced EMT and IPF, likely through the inhibition of IGF1, HIF-1α, and MAPK signaling pathways. This study holds potential translational prospects and may provide new perspectives and insights for the use of traditional Chinese medicine in the treatment of IPF.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9453-9467"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729652","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":"Inflammation-Associated Coagulation Reactions are Associated with the Prognosis in Critically Ill Very Old Patients (VOPs) with Infection.","authors":"Hui Lian, Huacong Cai, Xiaoting Wang, Hongmin Zhang, Yuan Gao, Shuyang Zhang, Yan Zhang","doi":"10.2147/JIR.S474990","DOIUrl":"10.2147/JIR.S474990","url":null,"abstract":"<p><strong>Background: </strong>Dysregulated host response is an important cause of critical illness. Coagulation reaction is the most primitive response and can be used to assess patient status. Coagulation reactions may be amplified in very old patients (VOPs). This study aimed to demonstrate coagulation reactions in critically ill VOPs by linking cytokines, coagulation, and fibrinolytic processes.</p><p><strong>Methods: </strong>We analyzed 33 critically ill VOPs admitted to our hospital, with an average age of 91.97. Laboratory test results were collected and double checked. In-hospital mortality, Intensive Care Unit (ICU) stay, and length of in-hospital stay (LOS)-associated variables were assessed using a generalized additive mix model. Smooth curves and interaction tests were used to quantify statistical interactions.</p><p><strong>Results: </strong>The in-hospital mortality rate was 45.5% in this study. The D-dimer level was correlated with ICU stay [risk ratio (RR), 1.39; 95% confidential interval (CI), 1.16-1.67] and LOS (RR, 1.75; 95% CI, 1.19-2.57). Other function or quantity indices, such as platelet (PLT), prothrombin time (PT), activated partial prothrombin time (APTT), and thrombomodulin (TM), were all correlated with clinical outcomes. After the link between coagulation reaction and the outcomes was constructed, it was revealed that, compared to lower level of IL-6, under high level of IL-6, elevated TM was likely to be associated with tissue plasminogen activator inhibitor complex (t-PAIC) elevation, which probably promoted the production of D-dimer (RR, 3.216; 95% CI, 1.840-4.592).</p><p><strong>Conclusion: </strong>D-dimer levels are associated with outcomes in VOPs with critical illness. There is a certain link between inflammatory cytokines and the coagulation process. Under high IL-6 levels, the elevated TM may contribute to the increased t-PAIC, which contributes to the higher D-dimer level. Conversely, under low IL-6 levels, elevated TM levels are associated with reduced t-PAIC levels.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9335-9346"},"PeriodicalIF":4.2,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11586478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715939","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 Role of the TRPV4 Channel in Intestinal Physiology and Pathology.","authors":"Dandan Liu, Mingli Mao, Wenjia Liu, Lihua Xie, Xiaolin Zhong, Wenyu Cao, Ling Chen","doi":"10.2147/JIR.S483350","DOIUrl":"10.2147/JIR.S483350","url":null,"abstract":"<p><p>The transient receptor potential vanilloid 4 channel (TRPV4) is an important member of the TRP superfamily of cation channels. The channel can be activated by different physical and chemical stimuli, such as heat, osmotic, and mechanical stress. It regulates the release of nociceptive peptides (substance P and calcitonin gene-related peptide), and mediates neurogenic inflammation, which indicates the involvement of TRPV4 as a nociceptor. Previous studies show that TRPV4 regulates the contraction of intestinal smooth muscle, mucosal barrier permeability, intestinal ion transport, activation of submucosal enteric neurons, and generation of immune cells. TRPV4 is involved in various pathophysiological activities, and altered TRPV4 expression has been detected in some intestinal diseases (IBD, IBS, intestinal tumors, etc). Evidence indicates that TRPV4 plays a noxious role in intestinal barrier function when the intestine is damaged. This review focuses on the role of the TRPV4 channel in the physiological and pathological functions of the intestine, and evaluates the potential clinical significance to target TRPV4 channel in the treatment of intestinal diseases.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9307-9317"},"PeriodicalIF":4.2,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716119","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":"Bioinformatics Identification and Validation of Ferroptosis-Related Key Genes and Therapeutic Compounds in Septic Lung Injury.","authors":"Zhile Li, Han Gan, Siyuan Li, Yuchen Xue, Kai Luo, Kai Huang, Yunqian Zhang, Yan Wang, Lai Jiang, Hui Zhang","doi":"10.2147/JIR.S476522","DOIUrl":"10.2147/JIR.S476522","url":null,"abstract":"<p><strong>Background: </strong>Septic lung injury (SLI) is a severe condition with high mortality, and ferroptosis, a form of programmed cell death, is implicated in its pathogenesis. However, the explicit mechanisms underlying this condition remain unclear. This study aimed to elucidate and validate key ferroptosis-related genes involved in the pathogenesis of SLI through bioinformatics analysis and experimental validation.</p><p><strong>Methods: </strong>Microarray data related to SLI from the GSE130936 dataset were downloaded from the Gene Expression Omnibus (GEO) database. These data were then intersected with the FerrDb database to obtain ferroptosis-related differentially expressed genes (DEGs). Protein-protein interaction (PPI) networks and functional enrichment analysis were employed to identify key ferroptosis-related DEGs. The Connectivity Map (c-MAP) tool was used to search for potential compounds or drugs that may inhibit ferroptosis-related DEGs. The transcriptional levels of the key genes and potential therapeutic compounds were verified in an LPS-induced mouse model of lung injury. The expression of these key genes was further verified using the GSE60088 and GSE137342 datasets.</p><p><strong>Results: </strong>38 ferroptosis-related DEGs were identified between the septic and control mice. PPI network analysis revealed four modules, the most significant of which included eight ferroptosis-related DEGs. Functional enrichment analysis showed that these genes were enriched in the HIF-1 signaling pathway, including IL-6 (Interleukin-6), TIMP1 (Tissue Inhibitor of Metalloproteinase 1), HIF-1α (Hypoxia-Inducible Factor-1α), and HMOX1 (Heme Oxygenase-1). Phloretin, a natural compound, was identified as a potential inhibitor of these genes. Treatment with phloretin significantly reduced the expression of these genes (<i>p</i> < 0.05), mitigated lung injury, improved inflammatory profiles by approximately 50%, and ferroptosis profiles by nearly 30% in the SLI models.</p><p><strong>Conclusion: </strong>This study elucidates the significant role of ferroptosis in SLI and identifies phloretin as a potential therapeutic agent. However, further research, particularly involving human clinical trials, is necessary to validate these findings for clinical use.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9215-9230"},"PeriodicalIF":4.2,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11589777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142729628","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":"High Translocation of High Mobility Group Box 1 in the Brain Tissue of Patients with Sturge-Weber Syndrome.","authors":"Zizhang Cheng, Xiaoli Li, Shu Wang, Weijin Sun, Junhong Pan, Xiongfei Wang, Jian Zhou, Tianfu Li, Guoming Luan, Yuguang Guan","doi":"10.2147/JIR.S473377","DOIUrl":"10.2147/JIR.S473377","url":null,"abstract":"<p><strong>Purpose: </strong>Sturge-Weber syndrome (SWS), a rare congenital neurological and skin disorder, is frequently associated with drug-resistant epilepsy. Translocation of high mobility group box 1 (HMGB1) protein from the nucleus to the cytoplasm or extracellular milieu has been implicated in neuroinflammatory processes contributing to the development of epileptogenesis. This study aimed to explore the expression and distribution of HMGB1 in brain tissue from SWS patients with drug-resistant epilepsy, with the goal of elucidating its potential involvement in the pathogenesis of epilepsy.</p><p><strong>Patients and methods: </strong>The study enrolled eight patients with drug-resistant epilepsy who underwent hemispherectomy. Brain tissue specimens were obtained and analyzed using immunofluorescence staining to detect HMGB1 distribution in microglia, astrocytes, or different neuronal subtypes. Correlation analyses were performed to investigate the potential relationship between HMGB1 translocation within cells and the clinical characteristics of SWS patients.</p><p><strong>Results: </strong>In lesional tissues of SWS patients, we observed significantly higher cytoplasmic HMGB1 levels. Meanwhile, HMGB1 was widely distributed in the cytoplasm of microglia and neurons, while in astrocytes, it was primarily localized in the nucleus. This translocation occurred across many neuronal subtypes, including excitatory glutamatergic, inhibitory GABAergic, and cholinergic neurons. The lower proportion of HMGB1-translocated cholinergic neurons was seen compared to the other two neuronal subtypes. Furthermore, no correlation was found between cytoplasmic HMGB1 levels and clinical characteristics of SWS patients.</p><p><strong>Conclusion: </strong>The results suggest the involvement of HMGB1 in the pathogenesis of drug-resistant epilepsy in SWS patients. Additional research is required to elucidate the precise mechanisms and potential therapeutic targets associated with HMGB1 that underlie the epilepsy linked to SWS.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"17 ","pages":"9347-9358"},"PeriodicalIF":4.2,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715936","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}