Journal of Inflammation Research最新文献

{"title":"Identification of Cardiometabolic Protein Biomarkers for Acute Myocardial Infarction Using Olink Proteomics.","authors":"Xin Tan, Xiangyu Wang, Shuai Xu, Yiyao Zeng, Ge Zhang, Anchen Xu, Yufeng Jiang, Hezi Jiang, Yahui Song, Jili Fan, Yangjun Fu, Xiaohong Bo, Huimin Fan, Yafeng Zhou","doi":"10.2147/JIR.S495784","DOIUrl":"10.2147/JIR.S495784","url":null,"abstract":"<p><strong>Background: </strong>Acute myocardial infarction (AMI) is a critical cardiovascular event characterized by sudden coronary blood flow interruption, leading to myocardial ischemia and necrosis. Despite advances in acute therapeutic measures, understanding the metabolic damage related to AMI, particularly through specific protein expressions, remains limited. This study utilized Olink cardiovascular metabolomics technology to explore cardiovascular metabolism-related protein biomarkers associated with AMI, aiming to address the clinical need for early diagnosis and targeted therapy.</p><p><strong>Methods: </strong>This study utilized Olink cardiovascular metabolomics technology to analyze 92 cardiovascular metabolism-related proteins in coronary blood samples from 20 AMI patients and 10 healthy controls. Differentially expressed proteins were identified using statistical t-tests, followed by functional enrichment analysis (GO and KEGG) and protein-protein interaction network construction. Five core proteins were validated in plasma samples from an additional 125 AMI patients and 120 healthy controls via enzyme-linked immunosorbent assay. To evaluate diagnostic performance, receiver operating characteristic curves were generated using GEO-related datasets, and Mendelian randomization analysis was employed to investigate the causal relationship between core proteins and AMI risk.</p><p><strong>Results: </strong>The study identified 32 proteins with significantly altered expression levels between AMI patients and healthy controls. Among these, five core proteins-PCOLCE, FCN2, REG1A, DEFA1, and CRTAC1-were significantly associated with key biological processes such as metabolism, collagen formation, and the PI3K/AKT signaling pathway. These proteins showed strong correlations with clinical indicators, including BMI, LVEF, NT-proBNP, CK-MB, and cTnT. FCN2 and DEFA1 were further validated as having a causal relationship with AMI risk, indicating their potential as diagnostic biomarkers.</p><p><strong>Conclusion: </strong>The identified core proteins PCOLCE, FCN2, REG1A, DEFA1, and CRTAC1 are potential biomarkers for the early diagnosis and risk assessment of AMI. These findings suggest that these proteins could serve as targets for future therapeutic interventions aimed at mitigating cardiovascular metabolic damage in AMI.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2629-2646"},"PeriodicalIF":4.2,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11863793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515721","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":"RND1 Induces Ferroptosis to Alleviate Inflammatory Response, Proliferation, Invasion, and Migration of Rheumatoid Synoviocytes.","authors":"Qiuhua Chen, Donglan Chen, Sijie Wang, Xiaomei Huang, Liang Liang, Tong Xie, Jie Lu","doi":"10.2147/JIR.S500630","DOIUrl":"10.2147/JIR.S500630","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis is involved in the occurrence and development of inflammatory arthritis. RND1 has been reported to possess pro-ferroptosis activity.</p><p><strong>Objective: </strong>This study was designed to explore the role and the molecular mechanism of RND1 in rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>DBA/1 mice were exposed to type II collagen immunization. The pathological damage of the knee joints of mice was observed with H&E staining and RND1 expression in synovial tissues was detected using Western blot. In vitro, Western blot was used to measure RND1, ferroptosis-, migration- and inflammation-related proteins. The cell proliferation, migration and invasion were detected using CCK-8 method, EdU staining, wound healing and transwell assays. The levels of inflammatory factors were detected with ELISA and RT-qPCR. Relative iron level, GSH and MDA concentrations were detected with corresponding assay kits. BODIPY 581/591 C11 kit measured lipid ROS. 4-HNE and GPX4 expression were detected using immunofluorescence assay.</p><p><strong>Results: </strong>This study found that RND1 expression was reduced in the synovial tissues of RA mice and human fibroblast-like MH7A synoviocytes. It was also found that the upregulation of RND1 inhibited the proliferation, migration, invasion and inflammatory response in rheumatoid synovial cells via ferroptosis.</p><p><strong>Conclusion: </strong>Collectively, RND1 exerted protective impacts on RA, which might be mediated by ferroptosis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2647-2659"},"PeriodicalIF":4.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11853921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501948","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":"IL-6 and CD4⁺/CD8⁺ are Important Indicators for Predicting Prognosis in Elderly AECOPD Patients: A Retrospective Study.","authors":"Qingqing Liu, Yanhui Wang, Xueshuai Cao, Shan Zhang, Juan Xie","doi":"10.2147/JIR.S496735","DOIUrl":"10.2147/JIR.S496735","url":null,"abstract":"<p><strong>Purpose: </strong>Evaluating the role of IL-6 and CD4⁺/CD8⁺ in predicting the prognosis of elderly patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD).</p><p><strong>Patients and methods: </strong>This study retrospectively enrolled 413 elderly patients who were hospitalized for AECOPD between January 2019 and December 2021. Patients were divided into event and non-event groups based on whether they were readmitted or died due to AECOPD during 18 months of follow-up. The associations between IL-6 and CD4⁺/CD8⁺ with adverse events were assessed using Cox proportional hazards regression models, Kaplan-Meier survival analysis, and restricted cubic spline (RCS) models. Additionally, subgroup analyses were conducted to evaluate the stability of these associations, and ROC curves were used to assess the predictive ability of IL-6 combined with CD4⁺/CD8⁺ for adverse events.</p><p><strong>Results: </strong>A total of 413 patients were included in the study, with 218 experiencing adverse events. Patients with high levels of IL-6 and low levels of CD4⁺/CD8⁺ had a higher risk of adverse events. There was a non-linear relationship between IL-6 and CD4⁺/CD8⁺ with adverse events (p<0.05). Subgroup analyses further confirmed the robustness of this association. ROC curve analysis indicated that combining IL-6 with CD4⁺/CD8⁺ significantly improved the predictive value for adverse events.</p><p><strong>Conclusion: </strong>There is a non-linear relationship between IL-6 and CD4⁺/CD8⁺ and adverse events in elderly patients with AECOPD. Combining IL-6 with CD4⁺/CD8⁺ ratios significantly enhances the predictive value for adverse events.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2601-2611"},"PeriodicalIF":4.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11853116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501855","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":"Role and Mechanism of Mitochondrial Ribosomal Proteins in Septic Myocardial Injury.","authors":"Liuli Wu, Junchao Huang, Xiongfei Jia, Xiaoqin Mao","doi":"10.2147/JIR.S495987","DOIUrl":"10.2147/JIR.S495987","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of mitochondrial ribosomal proteins (MRPs) in the pathogenesis and progression of septic myocardial injury. Additionally, we aim to propose new technical strategies and experimental foundations for the prevention and treatment of septic myocardial injury.</p><p><strong>Methods: </strong>Animal and cell models of septic myocardial injury were established. Aberrantly expressed MRPs were screened using transcriptome sequencing, and their expression was verified by RT-qPCR and Western blot. Subsequently, overexpressed and knockdown cell models of myocardial injury were constructed. The effects on CO I, PGC-1α, ATP content, ROS fluorescence intensity, mitochondrial membrane potential, and GSDMD were assessed, along with changes in caspase-4 and IL-1β expression levels.</p><p><strong>Results: </strong>Transcriptome sequencing revealed a reduction in MRPs expression in mice with septic myocardial injury. Both RT-qPCR and Western blot analysis confirmed the decreased expression of MRPs in animal and cell models of septic myocardial injury. Furthermore, overexpression of both MRPS16 and MRPL47 mitigated the decrease in CO I and PGC-1α levels induced by septic myocardial injury. Additionally, overexpression of MRPS16 and MRPL47 alleviated the elevated levels of IL-1β, caspase-4, and GSDMD caused by septic myocardial injury.</p><p><strong>Conclusion: </strong>The findings suggest that both MRPS16 and MRPL47 can mitigate mitochondrial injury by attenuating mitochondrial biosynthesis dysfunction, energy metabolism disorders, and Ca²⁺ disturbances caused by septic myocardial injury. This ultimately reduces cellular damage and alleviates septic myocardial injury.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2677-2698"},"PeriodicalIF":4.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11853951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501952","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":"Screening and Validation of Potential Biomarkers of Immune Cells in Childhood Asthma Patients via Mendelian Randomization and Machine Learning.","authors":"Yang Zhang, Yang Hai, Bangguo Song, Jing Xu, Liangjia Cao, Rukeye Yasen, Wenjuan Xu, Jiaxuan Zhang, Jihong Hu","doi":"10.2147/JIR.S498017","DOIUrl":"10.2147/JIR.S498017","url":null,"abstract":"<p><strong>Purpose: </strong>Asthma is one of the most common chronic respiratory diseases affecting children, and there is currently no clear remedy. Immune cells play a key role in childhood asthma. Therefore, a deeper investigation of the correlation between immune cells and childhood asthma could lead to a better understanding of asthma's origin, the identification of potential treatment targets, and the development of personalized treatment strategies.</p><p><strong>Patients and methods: </strong>We used a two-sample Mendelian randomization (MR) analysis to investigate the possible causal relationship between childhood asthma and a total of 731 immune cells, including B cell (190), Maturation stages of T cell (79), Monocyte (43), Myeloid cell (64), TBNK (124), Treg (167), and CDC (64). LASSO logistic regression and SVM algorithms were used to identify key genes associated with childhood asthma. Specific signaling pathways associated with these key genes were further explored through gene set variation analysis (GSVA) and gene set enrichment analysis (GSEA). Subsequently, the four key genes FCGR3A, TCTN3, ALOX5, and IL4R were verified in an established asthma mouse model using quantitative real-time PCR and Western blotting.</p><p><strong>Results: </strong>MR analysis showed that 60 immune cells were associated with childhood asthma, of which 32 were associated with high risk and 28 were associated with low risk. LASSO logistic regression and SVM algorithm identified six key genes that affect childhood asthma as ATF4, FCGR3A, GAS5, MGAT3, TAB1, and TCTN3. In addition, four genes, FCGR3A, TCTN3, ALOX5, and IL4R, were verified through animal experiments.</p><p><strong>Conclusion: </strong>Our findings confirmed that immune cells contribute to childhood asthma, highlighting the importance of key genes in the role of the immune microenvironment in this disease. These insights provide a new path for the exploration of the biological underpinnings of childhood asthma and the development of early intervention therapies.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2583-2600"},"PeriodicalIF":4.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11853831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501960","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":"Role of the Gut-Lung Microbiome Axis in Airway Inflammation in OVA-Challenged Mice and the Effect of Azithromycin.","authors":"Jun Zheng, Yuying Huang, Liang Zhang, Tiantian Liu, Ya Zou, Li He, Sheng Guo","doi":"10.2147/JIR.S506688","DOIUrl":"10.2147/JIR.S506688","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the role of the gut-lung microbiome axis in airway inflammation in asthma and to evaluate the effect of azithromycin on this axis, with a focus on the potential mechanism by which azithromycin reduces allergic airway inflammation.</p><p><strong>Methods: </strong>Haematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining were used to assess pathological changes in the lung tissues of asthmatic mice. Leukocyte cell types in bronchoalveolar lavage fluid (BALF) samples were quantified following Wright-Giemsa staining. Total IgE, OVA-specific IgE, IL-4, IL-6, and IL-17A levels in BALF and total IgE in serum were measured by ELISA. The respiratory and gut microbiota were analysed using 16S rRNA gene sequencing and subsequent taxonomic analysis.</p><p><strong>Results: </strong>OVA-challenged asthmatic mice with gut microbiota dysbiosis exhibited alterations in the respiratory microbiota, resulting in further aggravation of airway inflammation. Following faecal microbiota transplantation (FMT) to restore gut microbiota, respiratory microbiota dysbiosis was partially improved, and airway inflammation was significantly alleviated. Furthermore, azithromycin reduced airway inflammation in asthmatic mice, particularly non-eosinophilic inflammation, for which low-dose azithromycin combined with budesonide proved more effective. Azithromycin significantly enhanced the diversity and microbial composition of the gut microbiota and also affected the respiratory microbiota. At the phylum level, azithromycin decreased the abundance of Proteobacteria in the gut microbiota. At the genus level, azithromycin reduced the abundance of Pseudomonas in the respiratory microbiota.</p><p><strong>Conclusion: </strong>The gut-lung microbiome axis plays a crucial role in airway inflammation in asthma. Azithromycin may reduce airway inflammation in asthma through modulation of the gut-lung microbiome axis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2661-2676"},"PeriodicalIF":4.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11853874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501956","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":"A Novel Inflammation-Marker-Based Prognostic Model for Advanced Pulmonary Lymphoepithelioma-Like Carcinoma.","authors":"Xueyuan Chen, Tingting Liu, Silang Mo, Yuwen Yang, Xiang Chen, Shaodong Hong, Ting Zhou, Gang Chen, Yaxiong Zhang, Yuxiang Ma, Yuanzheng Ma, Li Zhang, Yuanyuan Zhao","doi":"10.2147/JIR.S502286","DOIUrl":"10.2147/JIR.S502286","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the prognostic value of inflammation markers for advanced pulmonary lymphoepithelioma-like carcinoma (PLELC) and develop an effective prognostic model based on inflammation markers to predict the overall survival (OS) of this population.</p><p><strong>Methods: </strong>Cox regression analysis was performed on 18 clinical and inflammation features, and a nomogram was created to predict overall survival (OS). The nomogram was evaluated by the concordance index (C-index), the time-dependent area under the receiver operating (ROC) curves (AUCs), calibration curves, and Decision Curve Analysis (DCA).</p><p><strong>Results: </strong>This study included a training cohort (n = 177) and a validation cohort (n = 77). The following variables were found to be independent prognostic factors for OS and used in the nomogram: Hepatitis B virus surface antigen status, gender, neutrophil-to-lymphocyte ratio (NLR), and C-reactive protein-to-albumin ratio (CAR). The C-indexes of the nomogram in the training and validation cohort were 0.740 (95% CI: 0.706-0.747) and 0.733 (95% CI: 0.678-0.788), respectively. Furthermore, time-dependent AUCs and well-fitted calibration curves showed good discriminative ability in both cohorts. Additionally, among the subset of EBV DNA data (n = 111), both ROC curve and DCA curve analysis demonstrated that the nomogram plus EBV DNA provided superior predictive performance compared to EBV DNA or the nomogram alone. Patients who received chemoimmunotherapy as the first-line treatment had better OS (not reached vs 44.4 months, P = 0.015) than those with chemotherapy alone and those who received immunotherapy at any line had better OS than those who never received it (not reached vs 31.0 months, P < 0.001).</p><p><strong>Conclusion: </strong>This study established and validated a prognostic nomogram model for patients with advanced PLELC. Combining the nomogram with EBV DNA more effectively predicted the prognosis of patients than the nomogram alone. Immunotherapy was found to be a critical treatment option for PLELC.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2433-2445"},"PeriodicalIF":4.2,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11859127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501906","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":"Coix Seed Oil Alleviates DSS-Induced Ulcerative Colitis via Intestinal Barrier Repair and Ferroptosis Regulation.","authors":"Yi-Xuan Zeng, Ni-Ren Li, Bing-Ying Deng, Yu-Feng Gu, Si-Fan Lu, Yi Liu","doi":"10.2147/JIR.S501745","DOIUrl":"10.2147/JIR.S501745","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis is a chronic intestinal disease linked to intestinal barrier damage, ferroptosis and dysbiosis. <i>Coix lacryma-jobi</i> is a natural food with food-medicine homology, whose seed-derived oil (Coix seed oil, CSO) has been shown anti-inflammatory activity in vitro. Here, the effects and mechanisms of CSO on ulcerative colitis (UC) in vivo are systematically investigated.</p><p><strong>Methods: </strong>Firstly, the UC mice was replicated by 3% DSS, and assessed the efficacy of CSO by observing the fecal occult blood, colon length, DAI score and pathological histomorphological changes of colon tissues. The anti-inflammatory and barrier-protective effects of CSO were observed by AB staining and qRT-PCR. Secondly, the biological targets of CSO were obtained from TCMSP database and Swiss Target Prediction database, ferroptosis targets were downloaded from FerrDb platform, and UC-related disease targets were obtained from GEO database, and the intersection of the above three was taken to obtain \"CSO-UC-Ferroptosis\" intersection targets, which were analysed by GO and KEGG enrichment, GSEA analysis, and immune cell infiltration and validation. Finally, the core genes of \"CSO-UC-Ferroptosis\" were molecular docking with the potential active components of CSO. In order to further verify the effect of CSO on ferroptosis, the GPX4 agonist RSL-3 was used to stimulate mice in vivo, and the levels of Iron, MDA and SOD were measured, and immunohistochemistry was used to detect the effects of tight junction proteins and the \"CSO-UC-Ferroptosis\" core protein in mice. Besides, the effect of CSO was further evaluated by observing the intercellular junctions of the colon tissues of each group under electron microscope. In addition, 16sRNA sequencing was performed on the intestinal contents of the mice to observe the effects of CSO on the intestinal flora of UC mice.</p><p><strong>Results: </strong>CSO improved physiological parameters, reduced inflammation response and intestinal barrier damage, regulated ferroptosis, and restored gut microbiota balance in UC mice. Bioinformatics results showed that <i>G6PD, ABCC1</i> were core targets at the intersection of CSO, UC and ferroptosis, which also demonstrated the similar expression of the core genes in DSS-induced UC mice models in vivo.</p><p><strong>Conclusion: </strong>Our findings demonstrate for the first time that CSO ameliorated UC by regulating intestinal barrier damage, ferroptosis and the gut microbiota in DSS-induced mice, suggesting that CSO as a promising candidate for UC treatment and warranting further investigation.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2557-2581"},"PeriodicalIF":4.2,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492367","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":"Efficacy Assessment and Prognostic Value of Inflammatory Markers in Patients with Stage IV Acral and Cutaneous Melanoma Receiving PD-1 Inhibitors.","authors":"Yan Zhang, Ziting Qu, Han Xuan, Lili Lu, Cuicui Ding, Ziran He, Kangsheng Gu, Yiyin Zhang","doi":"10.2147/JIR.S509928","DOIUrl":"10.2147/JIR.S509928","url":null,"abstract":"<p><strong>Background: </strong>Malignant melanoma (MM) is a highly aggressive cancer. Different subtypes have different sensitivities to immunotherapy and lack peripheral blood markers. Few studies have examined the role of inflammatory markers in predicting the overall survival (OS) in stage IV acral melanoma (AM) and cutaneous melanoma (CM) patients receiving immunotherapy.</p><p><strong>Purpose: </strong>This study aimed to investigate the value of inflammatory markers in efficacy and prognosis for stage IV melanoma patients who underwent immunotherapy.</p><p><strong>Patients and methods: </strong>This multicenter study reviewed the clinicopathological characteristics and inflammatory markers of 94 stage IV AM and CM patients receiving PD-1 inhibitors therapy. Pearson's chi-squared test or Fisher's exact test was used to compare baseline characteristics. The optimal cut-off values for these markers were stratified using time-dependent receiver operating characteristic curves (t-ROC). Kaplan-Meier (KM) curves and Log rank test were used to explore the relationship between inflammatory markers and survival outcomes. Cox regression analysis was performed to screen for independent prognostic factors and a nomogram was constructed. The model ability was tested by the C-index, t-ROC, calibration curves, and decision curve analysis curves.</p><p><strong>Results: </strong>High NLR level was significantly correlated with lymph node metastasis and 3 or above metastatic sites (P=0.009, P=0.012). High PNI level favored a better ECOG PS (P=0.023). According to the KM curves, patients with baseline NLR>2.37, PNI<=42.65, and RLR>11.08 had worse OS (P<0.001, P<0.001, P<0.001). Cox regression analysis based on P<0.05 showed that M1c/M1d (P<0.001), NLR (P=0.003), and PNI (P<0.001) were significantly correlated with OS, and were visualized in a nomogram. C-index, t-ROC, area under the curve (AUC), and calibration curves revealed promising discrimination and accuracy of the nomogram. Decision curve analysis curves showed good clinical utility.</p><p><strong>Conclusion: </strong>We established a prognostic predictive model based on distant metastatic sites, NLR, and PNI, and verified its superior performance and potential for clinical application.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2531-2544"},"PeriodicalIF":4.2,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492368","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":"Exploration of Hub Genes and Immune Cell Infiltration Characteristics Associated With Spinal Cord Injury in Mice.","authors":"Wentao Chen, Qian Zhang, Zhiwei Zhang, Yaping Ding, Feng Zhang, Guo Chen","doi":"10.2147/JIR.S499402","DOIUrl":"10.2147/JIR.S499402","url":null,"abstract":"<p><strong>Background: </strong>Spinal cord injury (SCI) is a major disabling disease. However, the complex secondary injury mechanisms make the results of treatment unsatisfactory. This study aimed to screen for key biomarkers of SCI and explore immune cell infiltration to identify novel therapeutic targets for improving neurological recovery after the injury.</p><p><strong>Methods: </strong>The SCI-associated gene microarray dataset was downloaded from GEO. The differential genes (DEGs) were first screened and analyzed according to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment for DEGs biological functions and pathways, while the protein-protein interaction (PPI) network was established using STRING. Then, the Hub genes of SCI were mined by WGCNA and LASSO regression analysis. Finally, the level of infiltration of 24 immune cells was analyzed using the CIBERSORT method.</p><p><strong>Results: </strong>A total of 522 DEGs were filtered. Enrichment analysis of their biological functions and pathways yielded the most closely related results for inflammatory response, regulation of cytokine production, neutrophil chemotaxis and degranulation, angiogenesis, cell death, TNF signaling pathway, and osteoclast differentiation. Four co-expression modules were obtained using WGCNA. Four Hub genes (2010004M13Rik, Cdkn1c, Nox4, and Gpr101) were obtained by analysis using the LASSO algorithm and validated by qRT-PCR. Finally, the infiltration of M0 and M2 macrophages, T Cells CD4 Follicular, and DC activated was assessed by immune infiltration analysis and was found to be associated with SCI.</p><p><strong>Conclusion: </strong>2010004M13Rik, Cdkn1c, Nox4, and Gpr101 are Hub genes in SCI. Infiltration of M0, M2 macrophages, T Cells CD4 Follicular, and DC activated may also be associated with inflammation and neurological recovery after SCI.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"2613-2628"},"PeriodicalIF":4.2,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492370","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}