Journal of Inflammation Research最新文献

{"title":"Mechanisms of Hydromorphone-Mediated Protection Against Myocardial Ischemia-Reperfusion Injury via NLRP3 Inflammasome Inhibition.","authors":"Shiyue Zeng, Wei Xu, Fangyuan Ren, Qiangqiang Xiong, Qi Qing, Liu Luo, Xi Song, Yurong Tan, Zhujun Huang, Mingzhi Zheng","doi":"10.2147/JIR.S509328","DOIUrl":"10.2147/JIR.S509328","url":null,"abstract":"<p><strong>Background: </strong>Myocardial ischaemia/reperfusion, MI/R injury causes significant cardiac damage, leading to disability and mortality. Although hydromorphone attenuates MI/R injury in rat models, its underlying mechanisms remain unclear.</p><p><strong>Objective: </strong>This study aimed to investigate the protective effects of hydromorphone against MI/R injury and elucidate its mechanisms.</p><p><strong>Methods: </strong>A rat MIRI model was established by occluding the left coronary artery for 30 minutes followed by reperfusion for 120 minutes. Infarct size and cardiac function were assessed using hematoxylin-eosin, HE and Masson's staining. An in vitro model was established using H9C2 cells subjected to hypoxia/reoxygenation, and levels of cellular pyroptosis and pyroptosis-related proteins were quantified.</p><p><strong>Results: </strong>Hydromorphone significantly improved cardiac function in MIRI rats. Pre- and post-treatment with hydromorphone significantly improved cardiomyocyte morphology in MIRI rats. In addition, compared with the model group (IR), the hydromorphone-treated groups (HH+IR, IR+HH) significantly reduced the rna expression of NLRP3, ASC, caspase-1, IL-1β, and IL-18, as well as the protein levels of IL-1β, IL-18. In addition, transmission electron microscopy showed that hydromorphone attenuated CoCl2-induced cardiomyocyte injury.</p><p><strong>Conclusion: </strong>Pre- or post-treatment with hydromorphone exerts protective effects against MIRI by suppressing NLRP3 inflammasomes, potentially providing a theoretical basis for its use as a therapeutic agent in MIRI patients.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6853-6863"},"PeriodicalIF":4.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199380","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":"Muscone Ameliorates High-Altitude Hypoxia Gastrointestinal Stress via Modulation of Lactobacillus Murinus and Mitochondrial Metabolism.","authors":"Jin Zeng, Xinxin Yin, Yidan Pang, Jinglei Zhang, Changpeng Xie, Siai Chen, Liping Zhang, Xuejing Li, YuanMing Pan, Juan An","doi":"10.2147/JIR.S521991","DOIUrl":"10.2147/JIR.S521991","url":null,"abstract":"<p><strong>Purpose: </strong>This study is to investigate the previously unexamined mechanism through which muscone alleviates acute high-altitude gastrointestinal stress. Specifically, it focuses on the modulation of gut microbiota, emphasizing its role in promoting the abundance of <i>Lactobacillus murinus</i> and optimizing mitochondrial metabolic pathways.</p><p><strong>Patients and methods: </strong>A high-altitude hypoxia model mouse treated with muscone was established to assess routine blood indices, inflammatory factors, and inflammatory cell counts. Additionally, alterations in intestinal flora were analyzed using macrogenomics. To further investigate the relationship between muscone's mechanism of action and intestinal flora, the ABX hypoxia mice model was employed, alongside in vitro experiments to evaluate muscone's effect on the growth of <i>Lactobacillus murinus</i>. The ameliorative effects of <i>Lactobacillus murinus</i> on acute gastrointestinal stress induced by high-altitude conditions were validated through various methods, such as HE staining, immunohistochemistry, transmission electron microscopy, ELISA, and flow cytometry. Furthermore, the underlying mechanism was explored through transcriptomics and qPCR.</p><p><strong>Results: </strong>Muscone markedly alleviated hypoxia-induced inflammation improved hematological parameters, and reshaped gut microbiota composition, with a notable increase in the abundance of <i>Lactobacillus murinus</i>. In vitro, muscone directly stimulated the proliferation of <i>Lactobacillus murinus</i>. However, the protective effects of muscone were significantly diminished in ABX-treated mice, highlighting the critical role of the gut microbiota. Supplementation with <i>Lactobacillus murinus</i> alone effectively reduced serum inflammatory cytokines, alleviated intestinal oxidative stress, and restored mucosal integrity. Transcriptomic analysis and RT-qPCR findings suggest that these effects may be linked to the mitochondrial metabolic pathway.</p><p><strong>Conclusion: </strong>Muscone may alleviate acute high-altitude gastrointestinal stress by enhancing the abundance of <i>Lactobacillus murinus</i> within the intestinal tract. Its mechanism of action appears to be associated with mitochondrial metabolic pathways.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6683-6701"},"PeriodicalIF":4.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199383","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 Predictive Role of FGF21 in Acute Liver Injury Caused by Bacterial Infectious Diseases in Critical Care: A Retrospective Cohort Study.","authors":"Zhijun Zhang, Li Yuan, Junqing Zhang, Qiang Gu, Fang Yan","doi":"10.2147/JIR.S521327","DOIUrl":"10.2147/JIR.S521327","url":null,"abstract":"<p><strong>Background: </strong>Acute liver injury (ALI) is a common complication in critically ill patients and has been strongly associated with adverse clinical outcomes. Early detection and timely management of ALI in these patients are crucial for implementing effective therapeutic strategies to prevent disease progression and improve patient outcomes.</p><p><strong>Methods: </strong>In this study, 112 critically ill patients with bacterial infectious diseases were categorized into two groups based on the presence or absence of ALI within 24 hours of the intensive care unit (ICU) admission. Serum concentrations of fibroblast growth factor 21 (FGF21), interleukin(IL)-6, IL-22, IL-10, liver enzymes, hypersensitive C-reactive protein (hs-CRP), and D-Dimer (D2) were measured within 24 hours of ICU admission. Demographic and clinical data were recorded. Logistic regression analysis was performed to identify potentially predictive biomarkers for ALI. Receiver operating characteristic (ROC) curve analysis was employed to determine the optimal model for predicting ALI in critically ill patients.</p><p><strong>Results: </strong>Patients in the ALI group exhibited significantly higher serum levels of IL-6, IL-10, IL-22, FGF21, liver enzymes, lactic acid, procalcitonin, D2, APACHE II scores, shorter survival time and higher 28-day mortality compared to those in the non-ALI group. Logistic regression analysis indicated that age, gender, plasma D2, and serum levels of direct bilirubin (DBIL), IL-22 and FGF21 were valuable predictors of ALI among critically ill patients. ROC curve revealed that this predictive model achieved a high area under the curve of 0.885, demonstrating excellent discriminatory ability.</p><p><strong>Conclusion: </strong>Elevated levels of serum FGF21 in the early stages of critical illness may represent a promising novel biomarker for predicting ALI.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6795-6806"},"PeriodicalIF":4.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199387","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":"HMGB1 Inhibition Alleviates Chronic Nonbacterial Prostatitis by Suppressing M1 Polarization of Macrophages.","authors":"Jilong Zhou, Lihui Ding, Juan Chen, Chen Chen, Ping Jiang, Zongwei Mei, Qing Jiang, Xiaoliang Hua","doi":"10.2147/JIR.S502616","DOIUrl":"10.2147/JIR.S502616","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background and objective: &lt;/strong&gt;Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) poses a significant threat to male urinary health and has an unclear pathogenesis. High-mobility group box 1 (HMGB1), a danger-associated molecular pattern that has been identified as a key mediator in various inflammatory diseases. However, its role in CP/CPPS remains unclear. This study aimed to investigate HMGB1's potential contributions to the pathogenesis of CP/CPPS, offering new perspectives for innovative treatments.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Materials and methods: &lt;/strong&gt;We have successfully extracted prostate antigens from Sprague-Dawley rat prostate tissue and established an experimental autoimmune prostatitis (EAP) mouse model in non-obese diabetic (NOD) mice. Subsequently, EAP mice were treated with recombinant HMGB1 protein (rmHMGB1) or the HMGB1-specific inhibitor glycyrrhizin for 14 days. Behavioral test was performed to assess the chronic pelvic pain. Hematoxylin and eosin (H&E) staining was employed to assess the extent of inflammatory cell infiltration in the prostate, and enzyme-linked immunosorbent assay (ELISA) was performed to assess levels of inflammatory cytokines. Co-immunofluorescence was used to analyze the functional phenotype of macrophages and spatial localization of HMGB1 in prostate of EAP mice. To further validate these findings, we conducted in vitro experiments. In these experiments, lipopolysaccharide (LPS) was used to induce an inflammatory environment in RAW264.7 cells. Interventions included administering rmHMGB1, silencing HMGB1 gene expression with siRNA, and treating cells with the TRAF6 inhibitor C25-140. After interventions, Western blot and immunofluorescence were employed to evaluate the impact on M1 macrophage polarization and inflammation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In this study, we demonstrate that HMGB1 is highly expressed in the prostate tissues of EAP mice. Treating EAP mice with rmHMGB1 significantly increased prostate histological scores (2.83 vs 1.83, p &lt; 0.05) and the sensitivity to pain stimuli, as evidenced by a higher response frequency to von Frey filament stimulation at 4 g (68.33% vs 53.33%, p &lt; 0.05). This treatment also increased the levels of inflammatory proteins IL-6 and TNF-α. In contrast, suppressing HMGB1 with glycyrrhizin significantly reduced inflammation, as indicated by decreased histological scores (0.50 vs 2.17, p &lt; 0.05), and attenuated pain sensitivity, as evidenced by a lower response frequency to von Frey filament stimulation at 4 g (30.83% vs 52.50%, p &lt; 0.05). Glycyrrhizin treatment also reduced IL-6 and TNF-α levels. Furthermore, the proportion of CD11b&lt;sup&gt;+&lt;/sup&gt;iNOS&lt;sup&gt;+&lt;/sup&gt; cells, indicative of M1 macrophage polarization, was significantly reduced after glycyrrhizin treatment. In vitro, HMGB1 can regulate the activity of TRAF6 by partially modulating its ubiquitination and degradation, thereby amplifying TRAF6-mediated NF-κB activation, promoting M1 macrophag","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6735-6748"},"PeriodicalIF":4.2,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12123095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199378","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":"Using Olink Proteomics to Identify Inflammatory Biomarkers in the Cerebrospinal Fluid in Guillain-Barré Syndrome.","authors":"Shuanghong Sun, Meng Li, Jihe Song, Di Zhong","doi":"10.2147/JIR.S507515","DOIUrl":"10.2147/JIR.S507515","url":null,"abstract":"<p><strong>Purpose: </strong>The precise etiology of Guillain-Barré syndrome (GBS) is uncertain; however, it is linked to immunological and inflammatory processes. Thus, this research aims to investigate new inflammatory biomarkers for GBS diagnosis.</p><p><strong>Patients and methods: </strong>In this work, Olink proteomics was used to compare the expression levels of 92 inflammation-related proteins in the cerebrospinal fluid (CSF) of patients with non-inflammatory neurological diseases (n=14) and GBS (n=23). Differentially expressed proteins (DEPs) were then analyzed biologically and in terms of their relationship to clinical features, and logistic regression models were built. We also downloaded GEO data to validate DEPs at the mRNA level.</p><p><strong>Results: </strong>We identified twenty DEPs. The PPI network screened six key DEPs (including TNF, CCL20, IL8, MCP-1, IL10, and IL5). These DEPs were enriched in the chemokine signaling pathway, the IL-17 signaling pathway, cytokines and their receptor interactions, and other pathways. TNFRSF9 and IL-10RB showed the strongest correlation of expression in CSF. CCL20 and IL5 could be used as potential independent predictors for the diagnosis of GBS. Seven DEPs (MCP-1, CXCL1, MCP-4, MMP-10, CXCL10, CCL28, and CCL20) had some predictive value for the severity of GBS. Based on the validation of the GEO data, the mRNA expression of MCP-1 and CXCL9 was found to be upregulated at the peak of EAN, and the enriched pathways at the gene transcription level were consistent with the results of this study.</p><p><strong>Conclusion: </strong>DEPs linked to inflammation (such as TNF, CCL20, IL8, MCP-1, IL10, and IL5) could be useful biomarkers for GBS diagnosis. More research is required to determine their precise mechanisms in GBS.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6703-6717"},"PeriodicalIF":4.2,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180898","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":"Advances in Research on the Release of von Willebrand Factor from Endothelial Cells through the Membrane Attack Complex C5b-9 in Sepsis.","authors":"Yi Liu, Weili Zhao, Qingqing Huang, Linjun Wan, Zongfang Ren, Bangting Zhang, Chen Han, Jin Yang, Haoling Zhang, Jingjing Zhang","doi":"10.2147/JIR.S520726","DOIUrl":"10.2147/JIR.S520726","url":null,"abstract":"<p><p>Sepsis, a lethal organ dysfunction syndrome driven by aberrant host responses to infection, intertwines excessive inflammatory responses and dysregulated coagulation processes in its pathophysiology. Emerging research reveals the complement terminal membrane attack complex C5b-9 orchestrates ultralarge von Willebrand factor (ULVWF) release from vascular endothelial cells (ECs) through multifaceted mechanisms: C5b-9 compromises EC membrane integrity, activates calcium influx cascades, and provokes NLRP3 inflammasome signaling, triggering massive exocytosis of ULVWF stored within Weibel-Palade bodies (WPBs). When ADAMTS13 activity falters, undegraded ULVWF complexes with platelets to spawn microthrombi, precipitating microvascular occlusion and multiorgan collapse. Strikingly, elevated plasma von Willebrand factor (vWF) antigen levels in sepsis patients correlate robustly with endothelial injury, thrombocytopenia, and mortality-underscoring C5b-9-driven vWF release as a linchpin of septic coagulopathy. Current therapeutic strategies targeting these pathways, including recombinant ADAMTS13 (rhADAMTS13), N-acetylcysteine (NAC), and complement inhibitors like eculizumab, face limitations in clinical translation, necessitating further validation of their efficacy. Additionally, investigating complement regulatory molecules such as CD59 may unlock novel therapeutic avenues. Deciphering the intricate interplay within the C5b-9-vWF axis and advancing precision therapies hold transformative potential for ameliorating sepsis outcomes.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6719-6733"},"PeriodicalIF":4.2,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174126","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":"MPO-ANCA-Associated Hypertrophic Pachymeningitis Mimicking IgG4-Related Disease: A Case Report and Literature Review.","authors":"Yuxue Chen, Lu Liu, Cuihong Xie","doi":"10.2147/JIR.S521138","DOIUrl":"10.2147/JIR.S521138","url":null,"abstract":"<p><p>Hypertrophic pachymeningitis (HP) is a rare and chronic clinical disease characterized by thickening of the dura mater, leading to persistent headache, cranial neuropathy, seizures, and other neurological symptoms. Immune-mediated causes, particularly antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis and IgG4-related disease (IgG4-RD), are among the most common etiologies. We report a case of a 54-year-old female with recurrent headache, blepharoptosis, hearing loss, and markedly elevated inflammatory markers. Blood tests, and serum levels of IgG4 were within normal ranges. Contrast enhanced cranial MRI revealed thickening and enhancement of bilateral cerebral hemispheres and tentorial dural maters. Additional findings included mild left lacrimal gland enlargement, bilateral middle ear mastoiditis, and tympanic tegmen destruction. Abdominal high-resolution computed tomography (CT) showed enlarged retroperitoneal lymph nodes. Histopathology demonstrated dense lymphoplasmacytic and neutrophilic infiltration with 80 IgG4-positive plasma cells per high-power field and an IgG4⁺/IgG⁺ cell ratio of 20%. An initial diagnosis of possible IgG4-RD was made. However, the patient's symptoms responded poorly to prednisolone (20 mg/day), and fever ensued. P<i>seudomonas aeruginosa, nocardia malleis</i>, and <i>leptocyclus virus</i> were found in the cerebrospinal fluid measured by NGS. Subsequent laboratory testing showed positive p-ANCA and anti-myeloperoxidase antibodies (anti-MPO), with a negative anti-nuclear antibodies panel, leading to a revised diagnosis of MPO-ANCA-associated HP. Treatment was escalated to intravenous methylprednisolone (40 mg/day), cyclophosphamide, and anti-infectious agents, leading to improved symptoms and decreased inflammatory markers. However, there was a recurrence during the taper of prednisolone. The addition of rituximab achieved complete remission. MPO-ANCA-associated HP is a rare inflammatory disorder that brings diagnostic challenges and requires comprehensive differential diagnosis. In relapsed or refractory cases, rituximab may be a valuable therapeutical option.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6673-6680"},"PeriodicalIF":4.2,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174156","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":"Towards Precision Diagnosis: Thoughts and Suggestions on Enhancing the Nomogram for Ventilator-Associated Pneumonia [Response to Letter].","authors":"Jiajia Yang, Yuancheng Li, Ying Wang","doi":"10.2147/JIR.S537758","DOIUrl":"10.2147/JIR.S537758","url":null,"abstract":"","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6681-6682"},"PeriodicalIF":4.2,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174160","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":"Clinical Characteristics of CARD14-Associated Papulosquamous Eruption and Evaluation of Therapeutic Efficacy of Secukinumab.","authors":"Xinrong Zhao, Zhaoyang Wang, Yunliu Chen, Xin Xiang, Yuanxiang Liu, Chaoyang Miao, Zigang Xu","doi":"10.2147/JIR.S519554","DOIUrl":"10.2147/JIR.S519554","url":null,"abstract":"<p><strong>Background: </strong><i>CARD14</i>-associated papulosquamous eruption (CAPE) is a spectrum of disease exhibited by patients with <i>CARD14</i> mutations, which are rare and have a wide variety of clinical manifestations. Patients usually have limited response to traditional therapies.</p><p><strong>Methods: </strong>We retrospectively analyzed a case series of 8 patients with CAPE in China. Whole-exome sequencing (WES) was performed in all patients to identify the mutation type. Three patients received the treatment of secukinumab with a 52-week follow-up period. They achieved 84.6%, 76.9%, and 68.8% improvement in PASI score, respectively.</p><p><strong>Results: </strong>The study identified three new variants in <i>CARD14</i> that had not been previously reported: c.392_397del, c.391_392delinsTT, and c.-280C>T. Three patients with different clinical manifestations showed good response to secukinumab.</p><p><strong>Conclusion: </strong>The mutation types in <i>CARD14</i>-associated papulosquamous eruption were various. IL-17A inhibitors, such as secukinumab, can be an alternative treatment option for pediatric patients with CAPE.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6597-6605"},"PeriodicalIF":4.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144159641","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":"Correlation Between Systemic Immune Inflammation Index(Sll) and Outcome After Occlusion in Patients with Post-Infarction Ventricular Septal Rupture.","authors":"Qingwang Hou, Yipin Zhao, Zebin Lin, Tongfeng Chen, Xinlong Di, Xiaohu Wang, Jiangtao Cheng, Xiaoyan Guo, Chong Chen, Dan Hu, Chang Liu, Yapeng Jiang, Yancun Liu, Ying Li, Mai Su, Yuhao Liu","doi":"10.2147/JIR.S518540","DOIUrl":"10.2147/JIR.S518540","url":null,"abstract":"<p><strong>Background: </strong>The Systemic Immune-Inflammation Index (SII) is a key indicator for assessing inflammatory status. This study aims to determine the association between SII and prognosis following occlusion in patients with post-infarction ventricular septal rupture (PIVSR).</p><p><strong>Methods: </strong>A total of 130 patients admitted to Fuwai Central China Cardiovascular Hospital between 2018 and 2023 were included in this retrospective study. Based on the tertiles of the Systemic Inflammatory Index (SII), the patients were categorized into two groups: 65 patients in the low SII group and 65 in the high SII group. Variable screening was performed using the Least Absolute Shrinkage and Selection Operator (LASSO) analysis. We conducted multivariable logistic regression analyses to rigorously assess the independent association between SII and short-term outcomes in PIVSR patients. After variable selection, a nomogram was constructed using R, and Restricted Cubic Splines (RCS) were employed to flexibly model nonlinear relationships. Subsequently, the predictive abilities of the screened variables and SII for the outcome were independently evaluated using Receiver Operating Characteristic (ROC) curve analysis.</p><p><strong>Results: </strong>A nomogram model incorporating ALT, UREA, NT-proBNP, and SII was developed to predict the short-term prognosis of PIVSR patients following occlusion surgery. ROC curve analysis demonstrated that the area under the curve (AUC) for SII level was 0.702 (95% CI: 0.599-0.804, <i>P</i> < 0.001). Incorporating the Systemic Immune-Inflammation Index (SII) significantly improved prognostic accuracy, with Model 2 demonstrating superior discriminatory power (AUC 0.845 vs 0.828) over Model 1.</p><p><strong>Conclusion: </strong>The Systemic Immune-Inflammation (SII) is a convenient and effective prognostic indicator, and the model incorporating SII can facilitate personalized prognostic assessment for patients with post-infarction ventricular septal rupture (PIVSR).</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"6641-6652"},"PeriodicalIF":4.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174129","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}