Journal of Inflammation Research最新文献

{"title":"Qing-Luo-Yin Eases T Cells-Mediated Angiogenesis in Adjuvant-Induced Arthritis Rats by Activating PPARγ.","authors":"Meng-Ke Song, Meng-Qi Wang, Yu-Qing Ruan, Can Cui, Wen-Gang Chen, Opeyemi Joshua Olatunji, Yan Li, Jian Zuo","doi":"10.2147/JIR.S508316","DOIUrl":"https://doi.org/10.2147/JIR.S508316","url":null,"abstract":"<p><strong>Introduction: </strong>Qing-Luo-Yin (QLY) is an anti-rheumatic herbal formula potentially activating PPARγ. The study investigated if and how this property contributes to its anti-angiogenesis effects.</p><p><strong>Methods: </strong>Adjuvant-induced arthritis (AIA) rats were orally treated by QLY or rosiglitazone (a PPARγ agonist), and their monocytes and lymphocytes were co-cultured reciprocally in vitro with different sera. Healthy littermates received blood transfusion from QLY-treated or AIA model rats. Two days ahead of sacrifice, a matrigel plug was implanted in the recipients. AIA serum-incubated THP-1 monocytes and Jurkat T cells were treated by a mixture comprised sinomenine, berberine and palmatine. Jurkat T cells-related media and T0070907 were used to stimulate human umbilical vein endothelial cells (HUVECs).</p><p><strong>Results: </strong>QLY and rosiglitazone similarly alleviated joint injuries, synovial angiogenesis and metabolic disorders in AIA rats. Although QLY impaired inflammatory phenotype of AIA rat monocytes in vivo, it cannot be achieved or sustained in vitro. Lymphocytes of QLY-treated AIA rats had a weak inflammatory phenotype and failed to induce inflammatory polarization of monocytes. AIA blood-induced angiogenesis in the matrigel plug, a phenomenon invisible in QLY group. QLY therapy inhibited pathogenic functions of AIA rats' lymphocytes, shown by changes of cytokines network in the recipients' joints, where these cells accumulated. The related compounds affected secretion of Jurkat T cells cultured in AIA serum, which lost the potential in activating HUVECs. This effect disappeared in presence of T0070907, a PPARγ inhibitor.</p><p><strong>Conclusion: </strong>Angiogenesis amelioration during QLY therapy is an indirect result from PPARγ activation-caused functional changes of T cells.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3469-3484"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649272","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":"Tenascin-C Facilitates Microglial Polarization via TLR4/MyD88/NF-κB Pathway Following Subarachnoid Hemorrhage.","authors":"Zheng-Qing Hu, Ruijie Ma, Jia-Qing Sun, Min Peng, Jinlong Yuan, Niansheng Lai, Jiaqiang Liu, Dayong Xia","doi":"10.2147/JIR.S511378","DOIUrl":"https://doi.org/10.2147/JIR.S511378","url":null,"abstract":"<p><strong>Purpose: </strong>This study primarily aims to elucidate the underlying mechanism of Tenascin-C in neuroinflammation and microglia polarization in a mouse model of subarachnoid hemorrhage (SAH).</p><p><strong>Methods: </strong>The subarachnoid hemorrhage model was constructed by injecting blood into the anterior chiasmatic cistern and stimulating primary microglia with hemoglobin in vitro. Then, Imatinib mesylate was used to inhibit Tenascin-C. Through neurological function scoring, brain edema, primary cell extraction, immunofluorescence staining, CCK8, Tunel staining, Elisa, Western blot and other methods, the potential mechanism of Tenascin-C induced microglia cell polarization was explored.</p><p><strong>Results: </strong>The results of this study observed that the expression of Tenascin-C was up-regulated after subarachnoid hemorrhage. Inhibiting the increase of Tenascin-C by imatinib could significantly ameliorate neuroinflammation, neuronal apoptosis, blood brain barrier disruption and brain edema. When the level of Tenascin-C decreased, the numbers of TLR4 positive, MyD88 positive and NF-κB positive microglial cells decreased accordingly. Moreover, after subarachnoid hemorrhage, the number of microglial cells positive for M1-type markers increased significantly. After imatinib inhibited Tenascin-C, the number of M1-type microglial cells decreased and the number of M2-type microglial cells increased significantly.</p><p><strong>Conclusion: </strong>In summary, the elevated level of Tenascin-C after subarachnoid hemorrhage induces the activation of microglia, releasing a large number of inflammatory factors and aggravating early brain injury.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3555-3570"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649286","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 and Comparison of Systemic Inflammation Indicators and Myocardial Injury After Noncardiac Surgery in Older Patients.","authors":"Bingbing Meng, Kai Zhang, Chang Liu, Siyi Yao, Zhao Li, Jingsheng Lou, Qiang Fu, Yanhong Liu, Jiangbei Cao, Weidong Mi, Hao Li","doi":"10.2147/JIR.S500795","DOIUrl":"https://doi.org/10.2147/JIR.S500795","url":null,"abstract":"<p><strong>Objective: </strong>To identify the association between preoperative inflammatory state and myocardial injury after noncardiac surgery (MINS) in older patients using systemic inflammation indicators neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) and to compare their clinical predictive values.</p><p><strong>Methods: </strong>This study included patients aged ≥65 years who underwent noncardiac surgery between January 2017 and August 2019. The relationship between preoperative inflammatory state and MINS was investigated using univariate and multivariate logistic regression analyses. The predictive values of NLR, PLR, and SII were determined by receiver operating characteristic (ROC) curve analysis. Based on the basic model we constructed, the predictive values were compared through separately adding NLR, PLR and SII.</p><p><strong>Results: </strong>Among 12464 patients, 965 (7.74%) developed MINS. The optimal cut-off values of NLR, PLR, and SII were 597×10⁹, 2.59, and 923. Univariate and multivariate analyses show that preoperative inflammatory state is associated with MINS. In the multivariate analysis, the OR values for NLR, PLR, and SII were (OR: 1.61, 95% CI: 1.36-1.89, p<0.001), (OR: 1.28, 95% CI: 1.07-1.52, p=0.006), and (OR: 1.43, 95% CI: 1.20-1.70, p<0.001). ROC curve analysis indicated that NLR was more predictive of MINS (area under the curve [AUC]: 0.671, 95% CI: 0.652-0.689) than PLR (AUC: 0.635, 95% CI: 0.616-0.655) and SII (AUC: 0.648, 95% CI: 0.628-0.667). The addition of the NLR to a basic prediction model improved its predictive ability to a greater extent than the addition of PLR and SII.</p><p><strong>Conclusion: </strong>Higher preoperative inflammation levels are associated with an increased risk of MINS. The NLR, PLR, and SII are independent risk factors for MINS and NLR demonstrated better predictive value than that of PLR and SII.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3499-3510"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649190","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>HDAC1</i> Mediates Immunosuppression of the Tumor Microenvironment in Non-Small Cell Lung Cancer.","authors":"Yongfei Fan, Xiang Ji, Kai Yuan, Qiyong Wu, Ming Lou","doi":"10.2147/JIR.S509316","DOIUrl":"10.2147/JIR.S509316","url":null,"abstract":"<p><strong>Background: </strong>Studies have demonstrated that histone deacetylase 1 (<i>HDAC1</i>) enables cancer cells to evade killing mediated by cytotoxic T lymphocytes. However, there are no studies on the immunological aspects of <i>HDAC1</i> in non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>In this research, we used the Cancer Genome Atlas (TCGA) public database combined with tissue microarray (TMA) to investigate <i>HDAC1</i> expression and prognosis in NSCLC. According to the median value of <i>HDAC1</i> expression in the TCGA dataset, samples of patients with NSCLC were classified into high- and low-expression cohorts. Subsequently, the biological characteristics of <i>HDAC1</i> in high- and low-expression cohorts in terms of signaling pathways, immune cell infiltration, immune cell function, and genomic stability were investigated to better understand the effect of <i>HDAC1</i> in the tumor microenvironment (TME) of NSCLC. Additionally, we selected tissue samples with <i>HDAC1</i> overexpression in TMA2 and performed immunohistochemical staining of CD8⁺ T cells to observe the distribution of CD8⁺ T cells in the tumor.</p><p><strong>Results: </strong>The findings revealed that overexpression of <i>HDAC1</i> in NSCLC was associated with poor prognosis. Analysis of signaling pathway enrichment indicated that <i>HDAC1</i> downregulated immune-related signaling pathways in NSCLC. Immune cell infiltration, immune cell function, and genomic stability analyses suggested that the TME alteration mediated by <i>HDAC1</i> in the high-expression cohort was consistent with the \"immune desert\" phenotype. Furthermore, CD8⁺ T immunohistochemical staining experiments of tissue samples with <i>HDAC1</i> overexpression in NSCLC revealed few CD8⁺ T cells distributed in the tumor parenchyma and interstitium.</p><p><strong>Conclusion: </strong>Conclusively, our findings from several biological analyses revealed that <i>HDAC1</i> is overexpressed in NSCLC and induces TME immunosuppression.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3333-3347"},"PeriodicalIF":4.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615578","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":"Prediction of Flares in Systemic Lupus Erythematosus During Post-Remission Follow-up.","authors":"Yu Bai, Jiuliang Zhao, Qian Wang, Dong Xu, Xiaofeng Zeng, Xinping Tian, He-Jun Li, Mengtao Li","doi":"10.2147/JIR.S504995","DOIUrl":"10.2147/JIR.S504995","url":null,"abstract":"<p><strong>Purpose: </strong>Patients at high risk of SLE flares benefit from being identified before flares; this can be done by predictors of flares. This study aimed to explore the predictive factors and model of SLE flares after remission, providing basis for clinical decision-making.</p><p><strong>Patients and methods: </strong>SLE patients recruited at the Peking Union Medical College Hospital (PUMCH), were all registered in the Chinese SLE treatment and research (CSTAR) registry cohort and had experienced at least one remission before December 31, 2020. Demographic, clinical, and laboratory parameters were collected through CSTAR online registry. The predictive effects of variables were analyzed using a Cox proportional hazards model. A nomogram was formulated to predict flares.</p><p><strong>Results: </strong>A total of 359 patients were included in the analysis, among which, 108 (30.1%) patients had at least one flare. Multivariate Cox regression model showed that younger age (hazard ratio [HR], 0.97; 95% CI, 0.95-0.99), positive anti-dsDNA at remission (HR, 1.64; 95% CI, 1.08-2.51), significantly low levels of C3 and C4 (HR, 2.09; 95% CI, 1.17-3.73) were independent risk factors associated with flares. A nomogram was established based on the multivariate analysis. The internal bootstrap resampling approach suggested the nomogram has a certain degree of discriminatory power with a C-index of 0.654 (95% CI, 0.601-0.707). The calibration plots also showed good consistency between the prediction and the observation.</p><p><strong>Conclusion: </strong>This study highlights that SLE patients with significantly low levels of C3 and C4, younger age, and elevated anti-dsDNA levels may require closer monitoring and follow-up after remission. Identifying these predictors allows clinicians to better assess the risk of flare and tailor therapeutic strategies accordingly for more effective long-term management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3377-3384"},"PeriodicalIF":4.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605131","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 Outcomes of Hospitalized Immunocompromised Patients With COVID-19 and the Impact of Hyperinflammation: A Retrospective Cohort Study.","authors":"Xinxin Zhang, Xiaobo Han, Chenglong Li, Junchang Cui, Xin Yuan, Jiguang Meng, Zhihai Han, Xinjie Han, Wei Chen, Junchen Xiong, Wuxiang Xie, Lixin Xie","doi":"10.2147/JIR.S482940","DOIUrl":"10.2147/JIR.S482940","url":null,"abstract":"<p><strong>Purpose: </strong>Immunocompromised patients are at increased risk for severe outcomes from COVID-19 due to their altered immune responses, yet their inflammatory profiles and the interplay between immunosuppression remain poorly understood. We aimed to illustrate the inflammation profile and clinical outcomes of hospitalized immunocompromised patients with COVID-19.</p><p><strong>Methods: </strong>We conducted a retrospective study using a multicenter database and included adult hospitalized patients with Corona virus disease 2019 (COVID-19) in China's late 2022 COVID-19 wave. Crude and adjusted 28- and 60-day mortality was compared between the two groups. Inflammatory phenotypes were evaluated by serum interleukin-6 (IL-6) and C-reactive protein (CRP) level. The interplay between overt inflammation and immunosuppression was analyzed.</p><p><strong>Results: </strong>Among the 4078 included patients, 348 (8.5%) were immunocompromised. Immunocompromised patients had lower crude mortality but higher adjusted mortality at 28-day (hazard ratio [HR] = 1.55; 95% CI 1.08 to 2.23) and 60-day (HR = 1.47; 95% CI 1.05 to 2.06). Besides, immunocompromised patients had a higher risk of developing hyperinflammation (odd ratio [OR] =1.92; 95% CI 1.47 to 2.50, p <0.001). Moreover, hyperinflammation mediated a major part of the deleterious survival effect of immunosuppression on COVID-19.</p><p><strong>Conclusion: </strong>Immunodeficiency not only increases short-term mortality risk but also predisposes patients to hyperinflammation. The complex interplay between immunosuppression, hyperinflammation, and COVID-19 outcomes warrants more detailed profiling of inflammation and immunity in this population.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3385-3397"},"PeriodicalIF":4.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605020","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":"Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.","authors":"Fan Gu, Delan Huang, Ruiqi Li, Linlin Peng, Tingting Huan, Kaili Ye, Zhuan Bian, Wei Yin","doi":"10.2147/JIR.S507198","DOIUrl":"10.2147/JIR.S507198","url":null,"abstract":"<p><p>Pyroptosis is a type of programmed cell death that induces proinflammatory cytokine release and is closely related to inflammatory diseases. Pulpitis and apical periodontitis are common inflammatory diseases that lead to alveolar bone destruction and tooth loss. Recent studies have revealed that pyroptosis is crucial in the progression of pulpitis and apical periodontitis, which involves various cell types and leads to different results. Odontoblasts are located at the periphery of dental pulp tissue and are susceptible to various irritants, the lysates from odontoblasts act as alerts and induce immune reactions in the inner pulp after pyroptosis. The expression levels of inflammasomes in dental pulp cells (DPCs) change with the progression of pulpitis, which may serve as a diagnostic marker of pulpitis. Periodontal ligament fibroblasts (PDLFs) undergo pyroptosis when stimulated by bacterial infection or cyclic stretch and are associated with both infection-induced and trauma-induced apical periodontitis. Immune cells can undergo pyroptosis directly after infection or are influenced by the pyroptotic secretome of other cells, which changes their composition. In this review, we briefly introduce the location and function of different cell types involved in the progression of pulpitis and apical periodontitis, summarize the roles of pyroptosis in different cells, and discuss the effects of drugs targeting pyroptosis in the treatment of pulpitis and apical periodontitis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3361-3375"},"PeriodicalIF":4.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624967","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":"Preoperative SII Can Predict Postoperative Recurrence and Serious Complications in Patients with Hepatolithiasis.","authors":"Tianyang Mao, Xin Zhao, Kangyi Jiang, Qingyun Xie, Manyu Yang, Hongyuan Wang, Peng Zheng, Zehua Lei, Fengwei Gao","doi":"10.2147/JIR.S506442","DOIUrl":"10.2147/JIR.S506442","url":null,"abstract":"<p><strong>Purpose: </strong>The occurrence and progression of hepatolithiasis are related to inflammatory reactions and immune proteins. This study aims to evaluate the relationship between systemic immune index (SII) in recurrence-free survival (RFS), as well as the incidence of severe postoperative complications in hepatolithiasis patients.</p><p><strong>Patients and methods: </strong>We retrospectively analyzed 177 patients with hepatolithiasis. The optimal cut-off values of SII, systemic inflammatory response index (SIRI), neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), platelet/lymphocyte ratio (PLR) and prognostic nutritional index (PNI) were evaluated by the analysis of the receiver operating characteristic (ROC) curve. The relationship between SII, SIRI, NLR and clinical results was tested with <i>χ</i>²-test. Logical regression analysis is used to evaluate the risk factors of postoperative serious complications. The Kaplan-Meier survival curve and Cox regression analyses are used to evaluate the impact of SII, SIRI, NLR on RFS.</p><p><strong>Results: </strong>The analysis of the ROC curve determines the optimal cut-off value and the area under the curve (AUC) of SII, SIRI, NLR, MLR, PLR and PNI, and then grouped. In the multivariate analysis, surgical method (HR=3.331, 95% CI: 1.360-8.158, p=0.008) and SII (HR=2.883, 95% CI: 1.084-7.668, p=0.034) were identified as independent risk factors for serious postoperative complications; the multivariate cox regression analysis demonstrated that a history of gallstones (HR=1.965, 95% CI: 1.206-3.201, p=0.007), SII (HR=2.818, 95% CI: 1.340-5.926, p=0.006), and MLR (HR=3.240, 95% CI: 1.158-9.067, p=0.025) were independent risk factors for RFS; survival analysis results show that patients with low levels of SII (p<0.001), SIRI (p=0.005), and NLR (p<0.001) had significantly higher RFS compared to those in the high-level group.</p><p><strong>Conclusion: </strong>Preoperative high levels of SII, SIRI, and NLR are associated with postoperative recurrence in patients with hepatolithiasis, with SII identified as an independent risk factor for both postoperative RFS and serious complications.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3321-3331"},"PeriodicalIF":4.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605132","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":"From Inflammasomes to Pyroptosis: Molecular Mechanisms in Chronic Intestinal Diseases - Opportunity or Challenge?","authors":"Jintao Fang, Weihan Zhu, Dian Yu, Lujian Zhu, Haorui Zha, Jingyi Tang, Yujia Li, Xiaxin Zhu, Ting Zhao, Wei Zhang","doi":"10.2147/JIR.S498703","DOIUrl":"10.2147/JIR.S498703","url":null,"abstract":"<p><p>Pyroptosis is a unique form of programmed cell death characterized by intense inflammation. It involves the activation of Gasdermin proteins, which form membrane pores, leading to rapid cell rupture and the release of inflammatory molecules. Unlike other types of cell death, pyroptosis has distinct activation mechanisms and plays a complex role in chronic intestinal diseases, including inflammatory bowel disease, intestinal fibrosis, chronic infectious enteritis, and colorectal cancer. This review comprehensively examines how pyroptosis influences disease development and progression while exploring the therapeutic potential of targeting pyroptosis-related pathways. Moreover, the complex interplay between gut microbiota and pyroptosis is summarized, highlighting its critical role in the pathogenesis of chronic intestinal disorders. A deeper understanding of pyroptosis-related mechanisms in these diseases may provide valuable insights for future research and contribute to the development of innovative therapeutic strategies in gastroenterology.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3349-3360"},"PeriodicalIF":4.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605180","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 Systemic Immune-Inflammatory Indices and Severity of Coronary Artery Lesions in Patients With Coronary Artery Disease in Different Glucose Metabolic States.","authors":"Xiandu Jin, Yue Liu, Wenjun Jia, Ruohang Xu, Xiuju Guan, Min Cui, Hanmo Zhang, Hao Wu, Liping Wei, Xin Qi","doi":"10.2147/JIR.S507696","DOIUrl":"10.2147/JIR.S507696","url":null,"abstract":"<p><strong>Background: </strong>The systemic immune-inflammatory index (SII) serves as a comprehensive indication of systemic inflammation. However, the relationship between SII and the severity of coronary artery lesions in participants with coronary artery disease (CAD) in different glucose metabolic states has not been fully elucidated.</p><p><strong>Methods: </strong>A total of 2727 patients with CAD were enrolled between January 2018 and April 2022. SII was calculated as (platelet count × neutrophil count)/lymphocyte count. Participants were grouped by SII quartiles. Glucose metabolic status was classified as normal glucose regulation (NGR), pre-diabetes mellitus (Pre-DM) and diabetes mellitus (DM) according to World Health Organization guidelines. Logistic regression and restricted cubic spline models were applied to estimate the relationship between SII and severity of coronary artery lesions in different glucose metabolic states with further adjustments for confounders.</p><p><strong>Results: </strong>Logistic regression analysis indicated a significant association between SII and coronary lesion severity (<i>P</i> < 0.05). Regardless of glucose metabolic status, Participants in the highest SII quartile (Q4) had a markedly higher risk of severe coronary lesions than those in the lowest quartile (Q1). After adjusting for confounders, a significant association between SII and coronary lesion severity was observed in the Pre-DM and DM individuals (<i>P</i> < 0.05), whereas not in the NGR individuals (<i>P</i> > 0.05). Subgroup analyses revealed that the association between SII and coronary lesion severity was consistent across age, gender, hypertension, antihypertensive drugs, hyperlipidemia, antilipidemic drugs, smokingand drinking (<i>P</i> > 0.05). Furthermore, restricted cubic spline modeling indicated a significant linear correlation between SII and coronary artery lesion severity.</p><p><strong>Conclusion: </strong>The SII is a relatively stable indicator of inflammation and is positively correlated with coronary lesion severity. This study highlights the potential of SII as a novel inflammatory biomarker for assessing the coronary lesion severity among patients in different glucose metabolic states.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3295-3309"},"PeriodicalIF":4.2,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596858","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}