Journal of Inflammation Research最新文献

{"title":"Comprehensive Analysis of RNA Modifications Related Genes in the Diagnosis and Subtype Classification of Dilated Cardiomyopathy.","authors":"Cuixiang Xu, Xiangrong Zhao, Huiting Li, Yaping Li, Yangmeng Feng, Guoan Zhang, Xiaoyan Huang","doi":"10.2147/JIR.S498496","DOIUrl":"10.2147/JIR.S498496","url":null,"abstract":"<p><strong>Background: </strong>RNA modifications are associated to various human diseases. However, the functions of RNA modification-related genes have yet to be thoroughly investigated in dilated cardiomyopathy (DCM). This study sought to conduct a comprehensive analysis of RNA modification-associated genes for the diagnosis and subtype classification of DCM.</p><p><strong>Methods: </strong>We collected DCM and control sample RNA modification-related genes from Gene Expression Omnibus (GEO) microarray datasets. Differential expression analysis was performed on these using the \"Limma\" package in R. Univariate logistic regression, and the LASSO algorithm were used to identify optimal genes for diagnostic model establishment. Furthermore, ConsensusClusterPlus was used to identify RNA modification-molecular subtypes. Lastly, the expression of the hub RNA modification-related genes and their connection to DCM were confirmed using the clinical samples and mouse models.</p><p><strong>Results: </strong>Twenty-six RNA modification-related genes were identified as dysregulated in DCM, with strong connections noted among these genes. A diagnostic model based on 13 genes (<i>TRMT61B, MBD2, YTHDC2, NOP2, TRMT10C, WDR4, CPSF2, CSTF3, ZBTB4, UNG, NSUN6, TET1</i>, and <i>DNMT3B</i>) with an AUC of 0.980 predicted DCM well. Infiltrating plasma B cells, eosinophils, CD8 T cells, and regulatory T cells correlated strongly with <i>TRMT61B, MBD2, YTHDC2</i>, and <i>CPSF2</i>. Two RNA modification-molecular subtypes (clusters 1 and 2) were identified. Cluster 1 had greater RNA modification scores, lower immune ratings, and lower HLA-DRB1 and HLA-DPB1 expression than Cluster 2. Cluster 2 engaged metabolism-related pathways, while Cluster 1 activated renin-angiotensin system pathways.We further found a substantial link between lower cardiac function and up-regulation of <i>TET1, DNMT3B</i>, and down-regulation of <i>MBD2, TRMT61B</i> in the 13 hub RNA modification-related genes.</p><p><strong>Conclusion: </strong>In conclusion, our RNA modification-related diagnostic model predicts DCM well. The discovery of two RNA modification-molecular subgroups and four key pivotal genes may assist stratify DCM patients by risk.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6331-6345"},"PeriodicalIF":4.2,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12089261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110762","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 Lactate Dehydrogenase/Albumin Ratio and in-Hospital Mortality in Patients with Acute Aortic Dissection.","authors":"Saimire Mutailifu, Qing Zhu, Menghui Wang, Delian Zhang, Shuaiwei Song, Nanfang Li","doi":"10.2147/JIR.S515010","DOIUrl":"10.2147/JIR.S515010","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have identified the lactate dehydrogenase/albumin ratio (LAR) as an independent prognostic marker, significantly predicting in-hospital mortality in patients with inflammation and cancer. Building on this, the current study is designed to explore the association between LAR and mortality during hospitalization in patients with acute aortic dissection (AAD).</p><p><strong>Methods: </strong>This retrospective study included patients diagnosed with AAD between January 1, 2010, and March 1, 2023. Patients were categorized into three groups based on LAR tertiles: T1 (<5.01), T2 (5.01-6.43), and T3 (>6.43). Multivariable logistic regression analysis was used to calculate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). In addition, subgroup analysis, receiver operating characteristic (ROC) curves, decision curve analysis (DCA), clinical impact curve analysis, Boruta algorithm, and the Kaplan-Meier analysis were applied to analyze the data.</p><p><strong>Results: </strong>A total of 2083 patients were enrolled in the study, with an average age of 53.20 ± 12.35 years, and male patients constituted 77%. After adjusting for relevant variables, ORs for in-hospital mortality were found to be 2.12 (95% CI: 1.34-3.36, p=0.001) for T2 and 2.30 (95% CI: 1.44-3.68, p<0.001) for T3, compared to T1. The ROC curve, DCA analysis, Boruta algorithm, and Kaplan-Meier analysis demonstrated that the LAR exhibited a high level of concordance and practical applicability in forecasting in-hospital mortality.</p><p><strong>Conclusion: </strong>Elevated LAR is significantly associated with an increased risk of in-hospital mortality in patients with AAD. The results indicate that LAR may serve as a valuable predictor of adverse outcomes during hospitalization for these patients.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6281-6292"},"PeriodicalIF":4.2,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094013","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":"Si-Ni Decoction as a Potential Treatment for Ulcerative Colitis: Modulation of Gut Microbiota and AKT1 Inhibition Through Network Pharmacology and in vivo Validation.","authors":"Lihao Shi, Leilei Chen, Guiyuan Jin, Yonghong Yang, Fengqin Zhu, Guangxi Zhou","doi":"10.2147/JIR.S516556","DOIUrl":"10.2147/JIR.S516556","url":null,"abstract":"<p><strong>Background: </strong>Sini Decoction (SND), a time-honored formulation in traditional Chinese medicine, consists of three key ingredients: aconite, licorice, and ginger rhizome. It has been used for more than a thousand years to relieve symptoms associated with acute gastroenteritis, dyspepsia, and abdominal discomfort, but its therapeutic efficacy in ulcerative colitis (UC) and the mechanisms involved have not been validated. In this study, a comprehensive approach integrating network pharmacology, molecular docking, molecular dynamics simulation and experimentation was used to assess the efficacy of SND in the treatment of UC and to explore its molecular mechanisms.</p><p><strong>Methods: </strong>The bioactive compounds associated with ulcerative colitis (UC) were identified using the TCMSP database, with potential targets predicted via the Swiss Target Prediction database. Protein-protein interaction networks were constructed using the STRING database and Cytoscape and the most important genes were identified. Subsequently, molecular docking was combined with molecular dynamics simulations using molecular docking to assess the binding affinity of the main active ingredient of SND to AKT1. To evaluate the therapeutic effects of SND, we utilized a dextran sodium sulfate-induced UC mouse model. Additionally, fecal samples were collected for analysis of the intestinal microbiota to explore the influence of SND on gut flora composition.</p><p><strong>Results: </strong>Fifteen bioactive components from SND were identified, and their activities were validated. The results indicated that AKT serine/threonine kinase 1 is a core target of SND for the treatment of UC. The anti-inflammatory, intestinal barrier-protective, and microbiota-regulating effects of SND were confirmed in animal models, alongside evidence of its inhibitory effect on AKT1.</p><p><strong>Conclusion: </strong>The active ingredients of SND were screened, with a focus on AKT1 inhibition, to reduce inflammation in UC, protect the intestinal barrier, and regulate the intestinal microbiota, demonstrating significant therapeutic potential.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6263-6280"},"PeriodicalIF":4.2,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12087465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101842","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":"Integrative Analysis and Experimental Validation Reveal FCGR1A and ITGAL as Key Inflammatory Biomarkers in Proliferative Diabetic Retinopathy.","authors":"Han Yu, Lvyin Luo, Rui Zhang, Fabao Xu, Xueying Yang, Yuhan Wu, Dechang Han, Xuanzhe Chu, Jianqiao Li","doi":"10.2147/JIR.S519725","DOIUrl":"10.2147/JIR.S519725","url":null,"abstract":"<p><strong>Purpose: </strong>Diabetic retinopathy (DR), one of the most common severe complications of diabetes, has become a leading cause of blindness among the working population without a fundamental treatment. Proliferative DR (PDR) is the advanced stage of DR. Recent studies have shown that inflammation is closely related to PDR, as it promotes leukocyte adhesion, breakdown of the blood-retinal barrier, and pathological neovascularization, but the key regulatory genes involved remained unclear. We aim to identify inflammation-related biomarkers in PDR.</p><p><strong>Methods: </strong>We downloaded and merged PDR-related datasets GSE102485, GSE94019, and GSE60436, comprising a total of 13 control samples and 37 samples from PDR patients, and conducted a joint analysis of inflammation-related genes (IRGs). Differential analysis, functional enrichment analysis, WGCNA and LASSO were used to identify key genes and their functions in the pathogenesis of PDR. Dataset GSE241239, which contains retinal sequencing data from mice, was used for external validation. Additionally, single-cell RNA analysis using GSE165784, which includes five human-derived PDR samples, was conducted to investigate the cellular expression of Fc Gamma Receptor IA (FCGR1A) and Integrin Subunit Alpha L (ITGAL). Finally, the expression of FCGR1A and ITGAL was validated in DR mouse models and high glucose-induced cell models.</p><p><strong>Results: </strong>Nine key genes associated with the pathogenesis of PDR were identified. Further screening identified FCGR1A and ITGAL as potential therapeutic targets, with single-cell analysis showing their primary distribution in microglia. In vivo and in vitro experiments confirmed localization of FCGR1A and ITGAL in microglia and significant elevation within DR mouse models.</p><p><strong>Conclusion: </strong>Comprehensive analysis indicates, for the first time, that FCGR1A and ITGAL are key inflammation-related genes involved in the pathogenesis of PDR mediated by microglia. FCGR1A and ITGAL are promising therapeutic targets for PDR.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6229-6243"},"PeriodicalIF":4.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093639","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":"Nomogram for Predicting Sepsis After Percutaneous Transhepatic Cholangioscopic Lithotripsy.","authors":"Lve Cheng, Xiong Ding, Jie Liu, Mengjia Shi, Shijia Huang, Junwei Niu, Shengwei Li, Yao Cheng","doi":"10.2147/JIR.S513678","DOIUrl":"10.2147/JIR.S513678","url":null,"abstract":"<p><strong>Purpose: </strong>Sepsis is a possible complication of percutaneous transhepatic cholangioscopic lithotripsy (PTCSL) for hepatolithiasis, but risk assessment tools are lacking. This study aimed to identify predictors of sepsis after PTCSL and develop a predictive nomogram.</p><p><strong>Patients and methods: </strong>In this nested case‒control study, the data from 298 patients who underwent 528 PTCSL sessions between 1 January 2016 and 1 July 2024 were retrospectively reviewed. All sessions demonstrating sepsis complications were included in the sepsis group. For each session in the sepsis group, two treatment date-matched sessions not demonstrating sepsis were randomly selected via a nested case‒control design. All the matched sessions were divided into training and validation sets. Least absolute shrinkage and selection operator (LASSO) analysis was conducted to preliminarily select predictors of sepsis complications. Multivariable logistic regression was performed to identify factors for constructing the nomogram.</p><p><strong>Results: </strong>Sepsis was diagnosed in 46 patients (53 sessions), for an incidence of 10.69% (53 among 496 sessions). Three characteristic variables were included in the model: operation technique (odds ratio [OR]=0.170, 95% confidence interval [CI]: 0.048-0.599, P=0.006), cirrhosis (OR=3.769, 95% CI: 1.474-9.638, P=0.006), and postoperative prophylactic dexamethasone (OR=0.267, 95% CI: 0.101-0.703, P=0.008). The area under the curve (AUC) for the nomogram was 0.756 (95% CI, 0.658-0.853) in the training set and 0.762 (95% CI, 0.618-0.906) in the validation set, demonstrating relatively high discriminability. The calibration curves demonstrated the consistency between the predicted and actual values. Decision curve analysis indicated that the nomogram offers net clinical benefits.</p><p><strong>Conclusion: </strong>The operation technique, cirrhosis, and postoperative prophylactic dexamethasone may predict the occurrence of sepsis after PTCSL. We developed a nomogram to predict sepsis complications following PTCSL and demonstrated its relatively strong performance.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6203-6216"},"PeriodicalIF":4.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093714","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":"PANoptosis in Sepsis: A Central Role and Emerging Therapeutic Target.","authors":"Qiqi Wu, Siyuan Qi, Zhaofeng Kang, Xiangjun Bai, Zhanfei Li, Jing Cheng, Xijie Dong","doi":"10.2147/JIR.S513367","DOIUrl":"10.2147/JIR.S513367","url":null,"abstract":"<p><p>The pathogenesis of sepsis is intricately linked to regulated cell death. As a novel form of regulated cell death, PANoptosis plays a critical role in driving the inflammatory response, impairing immune cell function, and contributing to multi-organ dysfunction in sepsis. This review explores the molecular mechanisms underlying PANoptosis and its involvement in sepsis. By activating multiple pathways, PANoptosis promotes the release of inflammatory cytokines, triggering a cytokine storm that disrupts immune cell homeostasis and exacerbates organ damage. Emerging therapeutic strategies targeting PANoptosis, including chemotherapeutic agents and herbal remedies, are showing potential for clinical application. The concept of targeting PANoptosis offers a promising avenue for developing innovative treatments for sepsis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6245-6261"},"PeriodicalIF":4.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093749","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 Pan-Immune-Inflammation Value and Dipper/Non-Dipper Status in Newly Diagnosed Hypertensive Patients.","authors":"Muhammet Salih Ateş, Alp Yıldırım, Erdoğan Sökmen","doi":"10.2147/JIR.S522032","DOIUrl":"10.2147/JIR.S522032","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the association between the pan-immune-inflammation value (PIV) and dipper/non-dipper status in newly diagnosed hypertensive (HT) patients. Given the role of systemic inflammation in circadian blood pressure (BP) pattern, we hypothesized that elevated PIV levels would be linked to an impaired nocturnal BP decline.</p><p><strong>Patients and methods: </strong>A total of 725 newly diagnosed hypertensive patients and 343 normotensive controls were prospectively included in the study. The HT patients were further classified as dipper (n=339) or non-dipper (n=386) based on 24-hour ambulatory BP monitoring (ABPM). PIV was calculated as (neutrophil count × platelet count × monocyte count) / lymphocyte count. Multivariate logistic regression analysis was performed to assess the independent association between PIV quartiles and non-dipper status. Receiver operating characteristic (ROC) curve analysis was conducted to determine the predictive value of PIV.</p><p><strong>Results: </strong>PIV was significantly higher in non-dipper hypertensive patients compared with dipper hypertensive patients (p<0.001). In multivariate regression models adjusted for age, sex, body mass index (BMI), smoking, diabetes mellitus, and echocardiographic parameters, the highest PIV quartile (Q4) was independently associated with non-dipper status (OR: 12.56, 95% CI: 7.31-21.56, p<0.001). ROC analysis demonstrated that a PIV cutoff of 326.96 predicted non-dipper status with a sensitivity of 70.5% and specificity of 65.5% (AUC: 0.725, p<0.001).</p><p><strong>Conclusion: </strong>Elevated PIV levels were significantly associated with non-dipper hypertension, reinforcing the contribution of systemic inflammation to circadian BP dysregulation. These findings suggest that PIV may serve as a potential biomarker for risk stratification and personalized treatment approaches in hypertensive patients.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6217-6228"},"PeriodicalIF":4.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094031","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 Metabolic and Inflammatory Biomarkers and Prognosis in Traumatic Brain Injury: A Focus on Short- and Medium-Term Mortality.","authors":"Hua Liu, Jinrong Wang, Wenming Wang, Min Ruan, Jiangang Liu","doi":"10.2147/JIR.S519606","DOIUrl":"10.2147/JIR.S519606","url":null,"abstract":"<p><strong>Background: </strong>Traumatic brain injury (TBI) is a leading cause of disability and death worldwide, involving complex pathophysiological responses such as metabolic disturbance and systemic inflammation. This study aimed to evaluate the prognostic value of selected metabolic and inflammatory biomarkers in predicting short- and medium-term mortality in patients with moderate-to-severe TBI.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of patients with TBI admitted between March 29, 2018, and July 31, 2023. Clinical data, including a panel of metabolic (eg, triglyceride-glucose index [TYG], APOB/A1 ratio) and inflammatory biomarkers (eg, neutrophil-to-platelet ratio [NPR]), were collected within 24 hours of admission. Mortality was assessed at 14 days, 30 days, and hospital discharge. Multivariate Cox regression models and ROC curve analysis were used to assess prognostic associations and model performance.</p><p><strong>Results: </strong>A total of 2555 patients were enrolled, of whom 579 (22.67%) underwent surgical treatment. Multivariate Cox proportional hazards regression analysis revealed that the triglyceride-glucose index (TYG) was an independent predictor of short-term mortality in TBI patients, while the neutrophil-to-platelet ratio (NPR) and apolipoprotein B/A1 (APOB/A1) ratio were independent predictors of both short- and mid-term mortality. In addition, surgical treatment was associated with an increased risk of mid-term mortality, while tracheostomy significantly reduced mortality risk across all time points. Receiver operating characteristic (ROC) curve analysis showed that the regression model incorporating inflammatory markers had the highest areas under the curve (AUCs) of 0.904, 0.897, and 0.897, demonstrating superior performance in predicting short- and mid-term mortality. Additionally, in the subgroup analysis of non-operation patients, TYG and NPR had a more significant impact on mortality risk.</p><p><strong>Conclusion: </strong>Metabolic and inflammatory biomarkers, including TYG, NPR, and APOB/A1 ratio, provide valuable prognostic information in patients with TBI. These markers may assist clinicians in early risk stratification and personalized treatment planning.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6149-6165"},"PeriodicalIF":4.2,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12083500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094027","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":"Integration of Multi-Omics and Network Pharmacology Analysis Reveals the Mechanism of Qingchang Huashi Jianpi Bushen Formula in Repairing the Epithelial Barrier of Ulcerative Colitis.","authors":"Yulai Fang, Shichen Min, Yuguang Wu, Feng Xu, Hongxin Chen, Yanan Li, Yizhou Lu, Jingyi Hu, Lei Zhu, Hong Shen","doi":"10.2147/JIR.S510966","DOIUrl":"10.2147/JIR.S510966","url":null,"abstract":"<p><strong>Purpose: </strong>Derivation of Qingchang Huashi formula, named Qingchang Huashi Jianpi Bushen (QCHS_JPBS) formula, has shown significant therapeutic effect on patients with ulcerative colitis (UC). In this study, the potential mechanism of QCHS_JPBS formula in repairing mucosal damage was explored from the perspective of intestinal stem cell (ISCs) differentiation, and potential targets of the QCHS_JPBS formula to improve UC were predicted using network pharmacology analysis.</p><p><strong>Methods: </strong>The therapeutic efficacy of QCHS_JPBS formula was evaluated in a mouse model of 2.5% dextran sulfate sodium (DSS) induced colitis. The effect of this formula on the ISC differentiation was evaluated using tissue transmission electron microscopy, immunofluorescence, and RT-qPCR. The cecal contents were subjected to 16s RNA sequencing analysis and non-target metabolomics analysis using LC-MS/MS. The fecal microbiota transplantation method verified the essential role of gut microbiota in promoting ISC differentiation and repairing mucosal damage.</p><p><strong>Results: </strong>The results indicated that QCHS_JPBS formula suppressed the inflammatory response and repaired the damaged intestinal epithelial barrier in DSS-induced colitis mice. QCHS_JPBS formula promoted ISC differentiation, particularly in the direction of goblet cells. QCHS_JPBS formula restored gut dysbiosis and regulated metabolic disorders in DSS-induced colitis mice. And then, the results of fecal microbiota transplantation indicated that QCHS_JPBS formula promoted differentiation of intestinal stem cells to repair mucosal damage through gut microbiota. Finally, a total of 79 active ingredients of QCHS_JPBS formula were identified based on LC-MS analysis and EGFR, STAT3, SRC, AKT1, and HSP90AA1 were considered as potential therapeutic UC targets of QCHS_JPBS formula based on network pharmacology analysis.</p><p><strong>Conclusion: </strong>The present study demonstrated that QCHS_JPBS formula promoted the differentiation of ISCs through gut microbiota to repair the damaged intestinal epithelial barrier in UC mice.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6167-6189"},"PeriodicalIF":4.2,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12083493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094033","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":"Seasonal Proteomic Variations and Biomarkers in Seasonal Allergic Rhinitis: Insights from Olink Inflammation Profiling.","authors":"Jiaqi Shen, Xinliang Zheng, Mohan Yan, Minqian Feng, Chan Ding, Shuanghua Xie, Huadong Xu","doi":"10.2147/JIR.S519126","DOIUrl":"10.2147/JIR.S519126","url":null,"abstract":"<p><strong>Purpose: </strong>Seasonal allergic rhinitis (SAR) is a prevalent inflammatory condition, yet its molecular mechanisms and reliable biomarkers remain incompletely understood. This study aimed to identify key inflammation-related proteins and pathways associated with SAR by investigating seasonal proteomic profile variations and their correlations with SAR symptoms.</p><p><strong>Patients and methods: </strong>Serum samples were collected from nineteen SAR patients during both allergy (in-season, IS) and non-allergy (out-of-season, OS) periods. Differentially expressed proteins (DEPs) were identified using the Olink Target 96 Inflammation panel, which were further analyzed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Spearman correlation analysis was conducted to explore associations between DEPs and SAR symptoms, including sneezing, rhinorrhea, nasal blockage, itchy nose, and itchy eye.</p><p><strong>Results: </strong>A total of 36 inflammation-related DEPs were identified, all significantly upregulated in the allergy season. Notable proteins such as glial cell line-derived neurotrophic factor (GDNF), interleukin-18 receptor 1 (IL-18R1), and interleukin-15 receptor alpha (IL-15RA) showed strong correlations with SAR symptoms. Sneezing was associated with IL-2 receptor beta (IL-2RB) (<i>r</i> = 0.415, <i>p</i> = 0.013), rhinorrhea with FMS-related tyrosine kinase 3 ligand (Flt3L) (<i>r</i> = 0.455, <i>p</i> = 0.004), and nasal blockage with osteoprotegerin (OPG) (<i>r</i> = 0.493, <i>p</i> = 0.002). GO analysis revealed enrichments in Ras signaling and small GTPase pathways, while KEGG analysis highlighted immune-related pathways, including PI3K-Akt signaling and cytokine-cytokine receptor interactions.</p><p><strong>Conclusion: </strong>This study identified key inflammation-related proteins and pathways that vary seasonally in SAR, offering insights into potential biomarkers and therapeutic targets for SAR management. Further studies are recommended to validate these findings in larger and more diverse populations.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6191-6202"},"PeriodicalIF":4.2,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12083496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093753","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}