Journal of Inflammation Research最新文献

{"title":"Comprehensive Analysis of Differences in N6-Methyladenosine RNA Methylation Groups in CVB3-Induced Viral Myocarditis and Identification of the Anti-Apoptotic Role of RBM15B.","authors":"Yanan Hu, Jiahui Lin, Lu Yi, Sha Cheng, Gao You, Huan Chang, Hanmin Liu, Zuocheng Yang, Shuyue Chen","doi":"10.2147/JIR.S503823","DOIUrl":"10.2147/JIR.S503823","url":null,"abstract":"<p><strong>Background: </strong>Viral myocarditis (VMC) is a leading cause of sudden cardiac death in children and young adults, with Coxsackievirus B3 (CVB3) identified as the primary viral pathogen responsible. N⁶-methyladenosine (m⁶A), the most abundant and reversible RNA methylation modification in mammals, plays a pivotal role in regulating numerous biological processes. However, the potential effects of CVB3 infection on m⁶A methylation within the myocardium remain unexplored. In this study, we investigated alterations in global RNA m⁶A methylation levels during CVB3 infection using both in vitro and in vivo models, and further examined the regulatory role of the m⁶A methyltransferase RBM15B in vitro.</p><p><strong>Methods: </strong>First, the total quantity of m6A was quantified in Balb/c mice and HL-1 cells with CVB3 infection via m⁶A dot blot analysis. Subsequently, m⁶A methylation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) were performed on cell model, while RNA-seq was conducted on animal tissues. We further analyzed the expression of m⁶A regulatory genes and their involvement in key pathways linked to VMC pathogenesis to elucidate underlying mechanisms. Given the pronounced expression of RBM15B in vitro, we knocked down RBM15B and assessed its regulatory effects on CVB3-infected HL-1 cells using Western blotting, viral plaque assays, and Calcein AM/PI double staining.</p><p><strong>Results: </strong>Quantitative m⁶A analysis revealed elevated m⁶A modification levels in CVB3 infection group. MeRIP-seq identified 327 significantly altered m⁶A peaks (116 upregulated, 211 downregulated). RNA-seq detected 1,597 upregulated and 2,942 downregulated mRNAs. Integrated analysis of MeRIP-seq and RNA-seq identified 38 hypermethylated-upregulated, 23 hypermethylated-downregulated, 65 hypomethylated-downregulated, and 13 hypomethylated-upregulated genes. GO and KEGG pathway analyses of these differentially methylated genes highlighted their roles in broad biological functions. Furthermore, qRT-PCR validation of mice RNA-seq data confirmed significant differences in four key genes (<i>Igtp, ApoI9b, Ddit3</i>, and <i>Irgm3</i>), along with altered expression of m⁶A regulators (<i>IGF2BP2, EIF3H, RBM15B</i>, and <i>YTHDC2</i>), with <i>RBM15B</i> showing the most pronounced changes. RBM15B knockdown in HL-1 cells reduced CVB3 replication (viral plaque assay) and attenuated apoptosis induced by CVB3 infection (Calcein AM/PI staining and Western blotting).</p><p><strong>Conclusion: </strong>These findings establish a foundation for exploring the role of m⁶A methylation in CVB3-associated VMC and may provide novel therapeutic insights for managing CVB3-induced viral myocarditis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7933-7949"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368961","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":"Integrated Multi-Omics Analyses Reveal Innovative Diagnostic and Therapeutic Targets Associated with Atopic Dermatitis.","authors":"Xiangjie Chen, Bochun Cao, Zhiren Tan, Xiaoping Li, Wenrong Xu, Ying Liu, Fang Gong","doi":"10.2147/JIR.S526983","DOIUrl":"10.2147/JIR.S526983","url":null,"abstract":"<p><strong>Background: </strong>Atopic dermatitis (AD) is a chronic skin disorder that impacts patients' physical and mental health. Diagnosing AD mainly depends on evaluating medical history and symptoms, as there are no universally accepted biomarkers for it. Identifying novel, reliable biomarkers is crucial to enhance diagnostic accuracy, reduce healthcare costs, and aid in developing new treatments.</p><p><strong>Methods: </strong>Data from the Gene Expression Omnibus database were used to identify potential AD biomarkers through Weighted Gene Co-expression Network Analysis and machine-learning. External datasets confirmed these biomarkers' diagnostic utility and their effectiveness in assessing clinical treatment. We also gathered peripheral blood mononuclear cells from healthy individuals and AD patients to validate these biomarkers' diagnostic capability for AD. Correlation analyses linked these biomarkers to AD severity indicators. Euclidean distance clustering was employed to assess the ability of these biomarkers to distinguish between healthy individuals and AD patients. The study also examined their relationships with major inflammatory pathways in AD to understand their mechanisms.</p><p><strong>Results: </strong>The study identified Ribonucleotide Reductase Regulatory Subunit M2 (RRM2), Late Cornified Envelope 3D (LCE3D), Cornifelin (CNFN), and Small Proline Rich Protein 2G (SPRR2G) as biomarkers with greater diagnostic value for AD than traditional biomarkers like eosinophil count and IgE levels. Treatment led to decreased expression of RRM2, LCE3D, and CNFN in AD patients' skin, indicating their potential as markers for evaluating treatment efficacy. LCE3D, CNFN, and SPRR2G correlated with AD severity indicators such as the SCORAD score and serum IgE levels. Additionally, the overexpression of these biomarkers was linked to the activation of inflammatory pathways, suggesting their role in AD pathogenesis and progression.</p><p><strong>Conclusion: </strong>Our study identifies RRM2, LCE3D, CNFN, and SPRR2G as novel biomarkers for diagnosing AD in peripheral blood and lesional tissues, with potential for assessing disease severity, evaluating treatment efficacy, and serving as targets for diagnosis and treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7951-7972"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368966","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":"Establishment of a Novel in vitro Model of Sepsis-Induced Myocardial Injury Using Septic Serum: A Comprehensive Comparative Study.","authors":"Hang Yang, Lin Feng, Zhenjie Jiang, Ruiming Deng, Xiaodan Wu, Kai Zeng","doi":"10.2147/JIR.S523124","DOIUrl":"10.2147/JIR.S523124","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is a life-threatening systemic inflammatory syndrome, in which myocardial injury plays a key role in disease progression and poor outcomes. However, the precise mechanisms underlying sepsis-induced myocardial injury remain unclear, and the most appropriate in vitro model for its investigation remains to be established. This study aimed to systematically compare different in vitro models to determine the most appropriate model for studying the pathophysiological mechanisms of sepsis-induced myocardial injury.</p><p><strong>Materials and methods: </strong>AC16 cardiomyocytes were treated with lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α), or septic serum for 24 hours to induce myocardial injury. Cell viability, cytotoxicity, inflammatory response, oxidative stress, apoptosis, and myocardial injury biomarkers were assessed to evaluate model performance. The mRNA expression profiles were analyzed to identify differentially expressed genes (DEGs), followed by functional enrichment analysis. The diagnostic utility of each model was assessed using receiver operating characteristic (ROC) analysis.</p><p><strong>Results: </strong>While LPS and TNF-α-treated cardiomyocytes exhibited similar injury features, both only partially captured the complexity of the sepsis-induced myocardial injury phenotype. In contrast, cardiomyocytes exposed to septic serum demonstrated more pronounced inflammatory responses, oxidative stress, apoptosis, and myocardial damage. Transcriptomic analysis revealed that the septic serum model induced 706 DEGs, significantly more than LPS (262 DEGs) or TNF-α (237 DEGs), and enriched in a broader array of biological processes and signaling pathways. ROC analysis confirmed that the septic serum model (AUC=0.671, 0.610) had higher diagnostic accuracy for septic cardiomyopathy datasets compared to the LPS (AUC= 0.548, 0.426) and TNF-α (AUC= 0.470, 0.559) models.</p><p><strong>Conclusion: </strong>This study introduces a novel in vitro approach using septic serum to model sepsis-induced myocardial injury, providing a physiologically relevant platform that more accurately reflects the complex pathophysiology of the disease.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8015-8031"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368963","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":"Neural-Inflammation Mechanism of Spinal Palmitic Acid Promoting Atopic Dermatitis in Mice.","authors":"Jing Yang, Xiaoling Xue, Zhi Yang, Fei Hao, Bangtao Chen","doi":"10.2147/JIR.S525663","DOIUrl":"10.2147/JIR.S525663","url":null,"abstract":"<p><strong>Objective: </strong>To profile spinal medium- and long- chain fatty acids (ML-CFAs) and itch-related gene expressions (IRGEs) in dorsal root ganglion (DRG), and investigate the role of spinal palmitic acid (PA) in atopic dermatitis (AD), and its relationship with DRG and spinal extracellular signal-regulated kinase (ERK).</p><p><strong>Methods: </strong>MC903 was applied topically to the nape of C57BL/6 mice to induce AD. Two doses of PA were administered intrathecally during MC903 treatment, and several antagonists were administered intrathecally one day before PA challenge. Transcriptome sequencing was performed on DRGs, and 36 ML-CFAs in the spinal cord were analyzed.</p><p><strong>Results: </strong>A global upregulation of IRGEs in DRGs and increases in major ML-CFAs including PA in the spinal cord were observed in adult AD model. MC903 resulted in less severe dermatitis with weaker IRGEs in DRGs and lower spinal ML-CFAs in senile than adult mice. In adult mice, intrathecal PA injection caused acute scratches, aggravated AD, and induced stronger IRGEs in DRGs. Intrathecal injection of transient receptor potential vanilloid-1 channel (TRPV1) antagonist capsazepine or Mas-related G protein-coupled receptor D (MRGPRD) antagonist d-Pro7-ANG-(1-7) remarkably halted PA/MC903-induced dermatitis and PA-induced scratching. Administration of histamine h4 receptor antagonist JNJ7777120 only moderately alleviated dermatitis, with no notable effect on scratches. Intrathecal pan-palmitoylation inhibitor 2-Bromopalmitate moderately alleviated MC903/PA-induced lesions and spinal ERK phosphorylation. Intrathecal lidocaine markedly suppressed both lesions and ERK phosphorylation, along with a global reduction in IRGEs in DRGs. Finally, PA-induced scratches were significantly improved by intrathecal lidocaine but not 2-Bromopalmitate.</p><p><strong>Conclusion: </strong>MC903-induced AD develops more readily in adult than senile mice, with consistent changes in IRGEs in DRG and spinal ML-CFA levels, including PA. Spinal PA promotes AD involving spinal TRPV1 and MRGPRD signaling, and IRGEs increments in DRG. Intrathecal lidocaine suppresses AD aggravated by PA via inhibiting spinal ERK phosphorylation and reducing IRGEs in DRG.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7907-7919"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368977","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":"Neutrophil Extracellular Traps (NETs) in Sterile Inflammatory Diseases.","authors":"Yin-Min Ji, Tao Li, Yu-Hui Qin, Shu-Yan Xiao, Ya-Hui Lv, Yi Dong, Xiao-Ran Cui, Yi Hu","doi":"10.2147/JIR.S526936","DOIUrl":"10.2147/JIR.S526936","url":null,"abstract":"<p><p>Neutrophil Extracellular Traps (NETs) are fibrous web-like structures released by neutrophils in response to pathogenic infections or inflammatory stimuli. Composed of decondensed chromatin DNA, histones, and granular proteins, NETs primarily function to eliminate pathogens through physical entrapment and biochemical cytotoxicity. However, they may also contribute to the pathogenesis of inflammatory diseases. While NETs played an important role in pathogen defense, their non-specific components can also damage surrounding tissues, exacerbating inflammation. The role and mechanisms of NETs in various diseases have been well-documented, including autoimmune diseases, cancer, and infectious diseases. This review aims to elaborate on the mechanisms by which NETs mediate sterile inflammation.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7989-8004"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368978","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":"Dynamic Neutrophil-to-Lymphocyte Ratio at 3-4 weeks of Intensity-Modulated Radiotherapy Combined with Normal Liver Volume Predicts Radiation-Induced Hepatic Toxicity in Hepatocellular Carcinoma: A Retrospective Study.","authors":"Lijun Chen, Jizhou Li, Xiaoting Wang, Shenshen Chen, Yi Wu, Jianxu Li, Shixiong Liang","doi":"10.2147/JIR.S523065","DOIUrl":"10.2147/JIR.S523065","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate whether early dynamic variation in circulating neutrophil-to-lymphocyte ratio(NLR) during intensity-modulated radiotherapy (IMRT) can predict radiation-induced hepatic toxicity (RIHT) in patients with hepatocellular carcinoma(HCC).</p><p><strong>Patients and methods: </strong>Neutrophil and lymphocyte counts of 103 HCC patients were measured every 2 weeks before, during and after completion of IMRT.Generalized estimating equations analyses was used to analyze the dynamic changes of neutrophil and lymphocyte counts. The prognostic significant factors were assessed through logistic regression analyses. Statistical power was assessed using power analysis, and the model was adjusted for multiple comparisons via the Bonferroni correction. Receiver operating characteristic (ROC) curves and calibration curves were used to evaluate the prediction accuracy.The predictive model was internally validated using 5-fold cross-validation.</p><p><strong>Results: </strong>Radiation-induced liver disease(RILD) is a type of RIHT and is a relatively severe phenomenon of hepatic toxicity.Overall, 23 patients (22%) developed RILD. In RILD group, NLR were significantly changed in the first 3 to 4 weeks during IMRT (p=0.006).In multivariate analysis, NLR in first 3-4 weeks(NLR 4), the ratio of NLR in first 3-4 weeks to 1-2 weeks(NLR 4/2),and normal liver volume(NLV) were independent predictive factors for RILD. The area under the curve(AUC) was 0.860 (95% CI, 0.783-0.937).Larger NLV correlated with a lower likelihood of developing RILD(p = 0.041).The mean AUC values was 0.86 in the training set and 0.81 in the test sets across 5-fold cross-validation (p=0.41).</p><p><strong>Conclusion: </strong>Circulating NLR in first 3 to 4 weeks and its relatively change during IMRT were significantly associated with RIHT.The model based on early dynamic variation of NLR and dosimetric factors NLV can predict RIHT with high accuracy in HCC patients.It can timely assist clinician to take preventive measures and adjusting treatment plans.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7879-7892"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368962","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-33 Participates in <i>G. Vaginalis</i>-Induced Bacterial Vaginosis: Involvement of Intravaginal IgA.","authors":"Min Zhou, Lili Zhou, Junbo Liu, Shaohui Yu","doi":"10.2147/JIR.S523880","DOIUrl":"10.2147/JIR.S523880","url":null,"abstract":"<p><strong>Introduction: </strong>Bacterial vaginosis (BV) is a common gynecological disease characterized by an abnormal increase in vaginal secretions, odor and itching. The pathogenesis of BV is not fully understood, but it is believed that the disruption of the mucosal immune system plays a key role. We investigated the role of IL-33 in preventing BV and explored the mechanism by which IL-33 regulates intravaginal IgA.</p><p><strong>Methods: </strong>Protein levels of IL-33 and IgA, and the pH value of vaginal secretions in healthy donors and patients with BV (14 vs 14) were determined by ELISA. <i>G. vaginalis</i>-induced bacterial vaginosis mouse model was established using wild-type (WT) and IL-33 knockout (KO) mice. Protein levels of IL-33, IgA and TGF-β, the pH value of vaginal secretions, and Gram-staining were measured in vivo and in vitro to investigate the role of IL-33 in BV progression.</p><p><strong>Results: </strong>IL-33 and IgA were significantly decreased in vaginal secretions of patients with BV. IL-33 deficiency aggravated BV induced by <i>G. vaginalis</i> in a mouse model, while IL-33 supplementation prevented it. IL-33 modulated intravaginal IgA expression through the TGF-β signaling pathway in B cells.</p><p><strong>Conclusion: </strong>IL-33 prevents <i>G. vaginalis</i>-induced BV by modulating intravaginal IgA expression through the TGF-β signaling pathway in B cells.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8005-8013"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368964","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":"Landscape of Histone Posttranslational Modifications in Osteoarthritis.","authors":"Siyu Zhao, Jia Zheng, Songkai Yue, Xiaoyang Chen, Yonghui Dong","doi":"10.2147/JIR.S514599","DOIUrl":"10.2147/JIR.S514599","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a complex, progressive, and age-associated disease characterized by aberrant epigenetic expression. Epigenetic analysis has helped clarify the role of histone post-translational modifications (PTMs) in OA. PTMs affect histone structure and function and, therefore, regulate the expression of genes implicated in various biological processes. The roles of histone methylation and acetylation in OA progression-including extracellular collagen degradation and matrix destruction-have been thoroughly analyzed. Though several studies have shown that histone PTMs are related to OA, summative investigations in this area are lacking. The present literature review examines the relationships between histone PTMs and OA. It focuses mainly on methylation, acetylation, phosphorylation, lactylation, ubiquitination, and the roles of the histone methyltransferase (HMT)/histone demethylase (HDMT) and histone acetyltransferase (HAT)/histone deacetylase (HDAC) families in OA development. We used epigenetic tools for discovering new OA treatments. This review offers new perspectives for future studies on OA pathogenesis and treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7893-7906"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368967","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 Combined Diagnostic Value of Serum Trefoil Factor 2 and microRNA-186-5p for Evaluating Disease Severity in Patients with Acute Pancreatitis.","authors":"Zhijian Fang, Hong Zhao, Yongpeng Cheng, Long Yu","doi":"10.2147/JIR.S527630","DOIUrl":"10.2147/JIR.S527630","url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the association of serum Trefoil Factor 2 (TFF2) and microRNA-186-5p (miR-186-5p) levels with the severity and prognosis of acute pancreatitis (AP).</p><p><strong>Methods: </strong>A retrospective analysis was conducted on 380 AP patients, classified into mild to moderately severe (mild acute pancreatitis (MAP) and moderately severe acute pancreatitis (MSAP), n=205) and severe (SAP, n=175) groups. Serum TFF2 levels were measured by enzyme-linked immunosorbent assay (ELISA), and miR-186-5p expression was quantified via reverse transcription quantitative polymerase chain reaction (RT-qPCR). Correlations with inflammatory markers (high-sensitivity C-reactive protein (hs-CRP), interleukin-18 (IL-18), and tumor necrosis factor-α (TNF-α)) and Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were assessed using Pearson analysis. Diagnostic performance was evaluated using receiver operating characteristic (ROC) curves, and logistic regression was used to identify risk factors for SAP.</p><p><strong>Results: </strong>Compared with the MAP&MSAP group, the SAP group showed significantly elevated TFF2, hs-CRP, IL-18, TNF-α levels, and APACHE II scores, while miR-186-5p levels were significantly reduced (P < 0.05). TFF2 levels were positively correlated with inflammatory markers and APACHE II scores (r = 0.427-0.546), whereas miR-186-5p levels showed negative correlations (r = -0.431 to -0.570; all P < 0.05). TFF2 and miR-186-5p levels were inversely correlated (r = -0.483, P < 0.05). ROC analysis yielded AUCs of 0.804 for TFF2, 0.832 for miR-186-5p, and 0.895 for their combination in predicting SAP. Logistic regression identified TFF2 as an independent risk factor and miR-186-5p as a protective factor for SAP (P < 0.05).</p><p><strong>Conclusion: </strong>Elevated serum TFF2 level and reduced miR-186-5p level were found to be associated with increased AP severity. These biomarkers may serve as useful indicators for assessing disease severity and prognosis in AP.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7921-7931"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368980","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":"Impact of Pan-Immune Inflammation Value on Short-Term Outcomes and Long-Term Prognosis in Patients with Type A Aortic Dissection.","authors":"Hao Cai, F M Shourav, Yue Shao, Sun Shuangling, Changzhu Duan, Cheng Zhang, Qing-Chen Wu","doi":"10.2147/JIR.S522998","DOIUrl":"10.2147/JIR.S522998","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory responses are closely linked to the onset and progression of aortic dissection. The Pan-Immune Inflammation Value (PIV), a composite index derived from peripheral blood cell counts, has demonstrated prognostic relevance in multiple clinical conditions. However, its predictive value in acute Type A Aortic Dissection (TAAD) has not been well established. This study aims to investigate the relationship between preoperative PIV and both short-term and long-term outcomes in patients with acute TAAD.</p><p><strong>Methods: </strong>This retrospective study included acute TAAD patients who underwent surgical repair between September 2017 and December 2020. The optimal cutoff value for PIV was determined using receiver operating characteristic (ROC) curve analysis. Patients were then divided into low and high PIV groups based on this threshold. Short-term outcomes, including prolonged ICU stay (>7 days) and postoperative complications were compared between groups using univariate and multivariate logistic regression analyses. Cox regression analyses were performed to identify independent predictors of long-term survival.</p><p><strong>Results: </strong>A total of 171 acute TAAD patients were included and stratified into low (n = 75) and high (n = 96) PIV groups based on preoperative values. In the high PIV group, patients had significantly longer surgery time, increased blood loss, greater volumes of red blood cell and plasma transfusions, longer ICU stays, and higher incidence of both overall and major complications (p=0.007, p=0.010, p=0.001, p=0.040, p=0.048, p<0.001, p=0.003, respectively). Multivariate logistic regression analysis identified high preoperative PIV as an independent risk factor for prolonged ICU stay (>7 days) (OR = 0.686, 95% CI, 0.303-0.954, p = 0.027), overall complications (OR = 0.037, 95% CI, 0.005-0.210, p = 0.002), and major complications (OR = 0.085, 95% CI, 0.026-0.173, p = 0.017). Additionally, lower preoperative PIV levels were significantly associated with improved long-term survival (HR = 0.757, 95% CI, 0.378-0.859, p = 0.020).</p><p><strong>Conclusion: </strong>PIV was identified as an independent predictor of prolonged ICU stay, overall and major postoperative complications, and long-term survival in patients with acute TAAD. As an integrative biomarker reflecting systemic immune-inflammatory status, PIV may serve as a valuable tool for early risk stratification and prognostic management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7855-7866"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368965","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}