Journal of Inflammation Research最新文献

{"title":"Saikosaponin-d Attenuates Irinotecan-Induced Intestinal Toxicity via TAK1/NF-κB Pathway and Enhances Antitumor Efficacy.","authors":"Peng Zheng, Rui Ma, Xiaoya Liu, Luda Song, Bing Ma, Guijun Zou","doi":"10.2147/JIR.S504696","DOIUrl":"https://doi.org/10.2147/JIR.S504696","url":null,"abstract":"<p><strong>Purpose: </strong>Saikosaponin-d (SSD), a bioactive triterpenoid saponin derived from Bupleurum species (a traditional Chinese medicine), is recognized for its gastrointestinal protective properties. This study investigates the therapeutic potential and mechanisms of SSD against irinotecan (IRI)-induced intestinal mucositis.</p><p><strong>Methods: </strong>Using a CT26 colorectal cancer Syngeneic mouse model (BALB/c mice), we evaluated the synergistic antitumor efficacy of SSD combined with IRI. Concurrently, the protective effects of SSD against IRI-induced intestinal toxicity were assessed in vivo (BALB/c mice) and in vitro (lipopolysaccharide (LPS)-stimulated Caco-2 cells). In vivo evaluations included monitoring body weight changes, diarrhea severity, colon length, and histopathological alterations. Mechanistic insights into the anti-inflammatory and antioxidant effects were elucidated through RT-qPCR, Western blotting, immunohistochemistry, and oxidative stress marker analysis.</p><p><strong>Results: </strong>SSD significantly mitigated IRI-induced intestinal injury, as demonstrated by attenuated body weight loss, improved diarrhea scores, and preserved colon length. Histopathological examination revealed that SSD protected intestinal epithelial integrity and enhanced barrier function. Mechanistically, SSD reduced oxidative stress by modulating antioxidant enzyme activities (SOD, GSH-Px) and suppressing lipid peroxidation (MDA levels). Furthermore, SSD inhibited proinflammatory cytokine production (IL-6, TNF-α, IL-1β) via downregulation of the TAK1/NF-κB pathway in both IRI-treated mice and LPS-challenged Caco-2 cells.</p><p><strong>Conclusion: </strong>Our findings demonstrate that SSD alleviates IRI-induced intestinal mucositis through suppression of the TAK1/NF-κB signaling cascade, highlighting its potential as an adjuvant therapy to enhance the safety profile of IRI-based chemotherapy.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7973-7988"},"PeriodicalIF":4.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368979","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":"<i>Gegen Qinlian</i> Decoction Ameliorated DSS-Induced Colitis by Attenuating Inflammation, Restoring Intestinal Mucosal Barrier and Modulating Gut Microbiota.","authors":"Yao Wang, Ruikun Yan, Lijing Ye, Chao Tang, Haibo Zhou, Guojun Zhao","doi":"10.2147/JIR.S505423","DOIUrl":"https://doi.org/10.2147/JIR.S505423","url":null,"abstract":"<p><strong>Background: </strong><i>Gegen Qinlian</i> Decoction (GQD), a traditional Chinese medicine formula, has shown significant therapeutic potential for colitis. However, the specific mechanisms by which GQD exerts its effects remain poorly understood, limiting its application in UC treatment.</p><p><strong>Purpose: </strong>In this study, we utilized a dextran sodium sulfate-induced colitis model in mice to evaluate the efficacy of GQD and to elucidate its underlying mechanisms.</p><p><strong>Methods: </strong>Network pharmacology was employed to explore the potential targets and signaling pathways of GQD, which were subsequently validated using Western blot. The effects of GQD on gut barrier integrity, inflammation, and oxidative damage were assessed through immunofluorescence, immunohistochemistry, and ELISA. Additionally, 16S rRNA high-throughput sequencing was conducted to examine alterations in the gut microbiota composition.</p><p><strong>Results: </strong>The results demonstrated that GQD alleviated the colitis symptoms in mice, as evidenced by an increase in goblet cell numbers, upregulation of ZO-1, MUC-2, and Occludin expression, and a decrease in apoptosis in intestinal epithelial cells. GQD effectively suppressed the expression of pro-inflammatory and oxidative mediators, including interleukin-6, tumor necrosis factor-α, interleukin-1β, nitric oxide, malondialdehyde, and myeloperoxidase, with inhibition rates ranging from 47% to 66%. According to the results from Western blot, the phosphorylation levels of p53, Akt, STAT3, and MAPK inflammatory signaling pathway-related proteins (p38, ERK, and JNK) were significantly inhibited with GQD treatment. Furthermore, GQD re-regulated composition of gut microbiota, including inhibiting the harmful bacteria (<i>Proteobacteria, Bacteroides</i>, and <i>Romboutsia</i>) enrichment and restoring the probiotics (<i>Lactobacillus</i> and <i>Allobaculum</i>). The correlation analysis revealed that the abundances of gut microbiota were closely related to the key protein expression in colon.</p><p><strong>Conclusion: </strong>This study revealed GQD can alleviate colitis by attenuating inflammation, restoring intestinal mucosal barrier and modulating gut microbiota.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"8065-8084"},"PeriodicalIF":4.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368951","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":"Circulating Neutrophil Extracellular Traps as Diagnostic and Prognostic Markers for Inflammatory Bowel Disease: A Case-Control Study.","authors":"Fen-Ying Lu, Xia Huang, Ke Zhang, Xin Yin, Yang Lv, Yue-Chen Du, Qian Zhou, Jing-Yu Min, Cui-E Cheng","doi":"10.2147/JIR.S519545","DOIUrl":"https://doi.org/10.2147/JIR.S519545","url":null,"abstract":"<p><strong>Objective: </strong>Current challenges in inflammatory bowel disease (IBD) treatment include the invasive nature of endoscopic evaluation, the gold standard for diagnosis, and the limited prognostic value of traditional inflammatory markers such as CRP and IL-6. This study aimed to explore the potential role of neutrophil extracellular traps (NETs) as biomarkers for the diagnosis, disease monitoring, and prognosis of IBD.</p><p><strong>Methods: </strong>A total of 100 patients with Crohn's disease or ulcerative colitis and 100 healthy controls were recruited between June 2020 and September 2022. Clinical and laboratory data were collected, and patients with inactive IBD were followed for two years to assess factors influencing disease relapse.</p><p><strong>Results: </strong>Significant differences were observed in the levels of NETs markers and inflammatory cytokines among the three groups. Cell-free DNA (cfDNA), myeloperoxidase (MPO)-DNA complexes, and citrullinated histone 3 (CitH3) levels were significantly elevated in the active IBD group compared to the inactive IBD and healthy control groups (P < 0.001). Additionally, inflammatory cytokines such as C-reactive protein (CRP), vascular endothelial growth factor (VEGF), IL-1β, and IL-6 were also higher in the active IBD group (P < 0.001). A positive correlation was observed between circulating NETs markers and inflammatory cytokines. Multivariate analysis identified cfDNA (OR = 1.045), MPO-DNA (OR = 1.084), and CitH3 (OR = 2.871) as independent risk factors for IBD. Furthermore, patients with higher NETs scores experienced more frequent relapses. At the 1-year follow-up, the high-NETs group had 13 relapses compared to 5 in the low-NETs group (P = 0.026), and at the 2-year follow-up, 22 versus 14 relapses (P = 0.044).</p><p><strong>Conclusion: </strong>These findings suggest that NETs biomarkers may serve as effective diagnostic and prognostic tools for IBD, enabling early intervention and improved long-term management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"7867-7877"},"PeriodicalIF":4.2,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368960","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":"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":"https://doi.org/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":"https://doi.org/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":"https://doi.org/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":"https://doi.org/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":"https://doi.org/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":"https://doi.org/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":"https://doi.org/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}