Journal of Inflammation Research最新文献

{"title":"Predictive Role of Blood Cell-Derived Inflammatory Markers for the Risk of Asymptomatic Cerebral Infarction in Essential Hypertension: A Population-Based Cross-Sectional Study in Central China.","authors":"Qinghui Zhang, Menglin Wang, Huiyu Du, Huiyun Qu, Kai Liu, Wenyong Dong, Dehui Kong, Dandan Tian, Xiaojian Zhao, Yibin Hao, Min Liu","doi":"10.2147/JIR.S505385","DOIUrl":"https://doi.org/10.2147/JIR.S505385","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the relationship between ACI and blood cell-derived inflammatory markers including platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), systemic immune inflammation index (SII) and systemic inflammation response index (SIRI) in an essential hypertensive (EH) cohort, and assess the predictive value of these inflammatory markers for ACI risk in this population.</p><p><strong>Methods: </strong>A total of 583 EH patients were included and categorized into ACI (123 patients) and non-ACI (NACI) (460 patients) groups. Multivariate logistic regression analysis was performed to explore the relationship of PLR, NLR, SII and SIRI to ACI risk in EH population. We also used receiver operating characteristic curve analysis to assess the discriminative ability of four inflammatory markers in predicting ACI risk in EH population.</p><p><strong>Results: </strong>ACI group exhibited higher levels of inflammatory markers (PLR, NLR, SII, and SIRI) compared to NACI group (<i>P</i> < 0.05). PLR (odds ratio (OR): 1.006, 95% confidence interval (CI): 1.001-1.011, <i>P</i> = 0.023), NLR (OR: 1.573, 95% CI: 1.225-2.021, <i>P</i> < 0.001), SII (OR: 1.002, 95% CI: 1.001-1.003, <i>P</i> < 0.001) and SIRI (OR: 1.851, 95% CI: 1.290-2.656, P = 0.001) were independent factors for ACI risk in EH patients. The odds ratios of the highest versus lowest quartile of PLR, NLR, SII and SIRI were 2.090 (95% CI 1.085-4.024), 3.049 (95% CI 1.509-6.161),2.464 (95% CI 1.278-4.749) and 3.372 (95% CI 1.709-6.652), respectively. PLR, NLR, SII, SIRI were characterized by area under the curve (0.586, 0.632, 0.591, 0.617) and cut-off value (125.834, 2.468, 532.011, 0.934), respectively.</p><p><strong>Conclusion: </strong>The findings suggested that PLR, SII, SIRI, especially NLR were of significant value biomarkers to positively predict ACI risk in EH population.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3523-3534"},"PeriodicalIF":4.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649266","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":"Transcriptomic Insights Into Electroacupuncture Using Different Acupoint Combinations to Repair Mucosal Inflammatory Injury Induced in a Rat Model of Gastric Ulcer.","authors":"Qi Zhang, Tie Li, Hailin Jiang, Jiazhen Cao, He Wang, Zhongke Wang, Qingqing Tang, Ning Yang, Jinying Zhao, Fuchun Wang","doi":"10.2147/JIR.S504930","DOIUrl":"https://doi.org/10.2147/JIR.S504930","url":null,"abstract":"<p><strong>Background: </strong>Electroacupuncture (EA) is a promising treatment for gastrointestinal disorders, yet the efficacy of different acupoint combinations remains mechanistically undefined. We evaluated the therapeutic effects of different acupoint combinations on mucosal inflammatory injury induced in a rat model of gastric ulcer (GU) and dissected its molecular mechanisms through transcriptomic profiling.</p><p><strong>Methods: </strong>A GU rat model was established using hypothermic restrained water immersion stress. EA therapy was administered to the He-Mu (ST36-CV12), Shu-Mu (BL21-CV12), and Yuan-Luo (ST42- ST40) acupoint combinations for 5 days. EA therapeutic effects were evaluated by coat score, fecal moisture percentage, pain threshold, body mass, organ index, histopathological changes, serum level of oxidative stress, and inflammatory cytokine levels in gastric tissue. A transcriptome analysis identified the related differentially expressed genes (DEGs) and central signaling pathway. Real-time quantitative PCR and Western blot were performed to verify the mRNA and protein expression levels of the main genes in the central pathway.</p><p><strong>Results: </strong>EA using different acupoint combinations differentially alleviated gastric mucosal injury in GU rats, with the He-Mu group exhibiting superior tissue damage alleviation, as well as inflammation and oxidative stress reductions. A Venn diagram transcriptome analysis revealed a shared central pathway among the three groups, corresponding to focal adhesion. Quantitative validation confirmed that the mRNA, protein, and phosphorylated protein expression of FAK, VCL, and EGFR-the core signal transduction factors of the focal adhesion pathway activated in gastric tissue after EA treatment-were upregulated, consistent with their therapeutic efficacy.</p><p><strong>Conclusion: </strong>Our results demonstrated that the He-Mu acupoint combination exhibited superior therapeutic efficacy among the three acupoint combinations. EA using different acupoint combinations improved gastric mucosal injury to varying degrees, and was related to the focal adhesion pathway. The <i>FAK, VCL</i>, and <i>EGFR</i> are promising targets, and further studies are needed to elucidate their functional consequences in GU.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3399-3417"},"PeriodicalIF":4.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647931","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 Value of Soluble Fms-Like Tyrosine Kinase-1 for Prognosis in COVID-19 Patients.","authors":"Chunlian Lai, Yingfei Wang, Fengwei Shi, Nan Geng, Zhao Liu, Wen Pan, Hongbo Shi, Yingmin Ma, Bo Liu","doi":"10.2147/JIR.S504751","DOIUrl":"https://doi.org/10.2147/JIR.S504751","url":null,"abstract":"<p><strong>Background: </strong>Coronavirus Disease 2019 (COVID-19), caused by the novel coronavirus, has posed a significant threat to global public health, leading to substantial morbidity, mortality, and strain on healthcare resources. Despite the availability of vaccines and treatments, effective biomarkers for predicting disease progression remain limited. This study aimed to investigate the prognostic value of soluble fms-like tyrosine kinase-1 (sFlt-1) in COVID-19 patients.</p><p><strong>Methods: </strong>A prospective cohort study was conducted involving 154 COVID-19 patients, with comprehensive clinical data and laboratory parameters analyzed to evaluate the effectiveness of sFlt-1 in determining disease severity and prognosis.</p><p><strong>Results: </strong>The results revealed that sFlt-1 levels correlated significantly with disease severity, showing higher levels in severe/critical cases compared to mild cases (P<0.05). In the deceased group, sFlt-1 levels were notably higher compared to survivors, with an area under the curve (AUC) of 0.840, showing good predictive power for 28-day mortality. Multivariable logistic regression identified sFlt-1, respiratory rate, and albumin as independent prognostic factors, with a combined AUC of 0.938 (95% CI: 0.886-0.991) for predicting mortality risk.</p><p><strong>Conclusion: </strong>These findings underscore the potential of sFlt-1 as a valuable biomarker for clinical decision-making in managing COVID-19 patients. Future studies should focus on the clinical application of sFlt-1 and explore its underlying mechanisms to enhance patient management strategies.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3511-3522"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649293","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":"Identification of Senescence-Related Genes for the Prediction of Ulcerative Colitis Based on Interpretable Machine Learning Models.","authors":"Jingjing Ma, Chen Chen, Nian Wang, Ting Fang, Yinghui Liu, Pengzhan He, Weiguo Dong","doi":"10.2147/JIR.S508396","DOIUrl":"https://doi.org/10.2147/JIR.S508396","url":null,"abstract":"<p><strong>Background: </strong>Cellular senescence, a hallmark of aging, significantly contributes to the pathology of ulcerative colitis (UC). Despite this, the role of senescence-related genes in UC remains largely undefined. This study seeks to clarify the impact of cellular senescence on UC by identifying key senescence-related genes and developing diagnostic models with potential clinical utility.</p><p><strong>Methods: </strong>Clinical data and gene expression profiles were obtained from the Gene Expression Omnibus (GEO) database. Senescence-related differentially expressed genes (sene-DEGs) between patients with UC and healthy controls were identified using various bioinformatics techniques. Functional enrichment and immune infiltration analyses were performed to understand subtype characteristics derived from sene-DEGs through consensus clustering. Machine learning algorithms were employed to select feature genes from sene-DEGs, and their expression was validated across multiple independent datasets and human specimens. A nomogram incorporating these feature genes was created and assessed, with its diagnostic performance evaluated using receiver operating characteristic (ROC) analysis on independent datasets.</p><p><strong>Results: </strong>Fourteen senescence-related differential genes were identified between patients with UC and healthy controls. These genes enabled the classification of patients with UC into molecular subtypes via unsupervised clustering. ABCB1 and LCN2 emerged as central hub genes through machine learning and feature importance analysis. ROC analysis verified their diagnostic value across various datasets. Validation in independent datasets and human specimens supported the bioinformatics findings. Furthermore, the expression levels of ABCB1 and LCN2 showed significant associations with immune cell profiles. The logistic regression (LR) model based on these genes demonstrated accurate UC prediction, as confirmed by ROC curve analysis. The nomogram model, constructed with feature genes, exhibited outstanding prediction capabilities, supported by DCA, C index, and calibration curve assessments.</p><p><strong>Conclusion: </strong>This integrated bioinformatics approach identified ABCB1 and LCN2 as significant biomarkers associated with cellular senescence. These findings enhance the understanding of cellular senescence in UC pathogenesis and propose its potential as a valuable diagnostic biomarker.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3431-3447"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649238","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":"Caffeic Acid Alleviates Chronic Sleep Deprivation-Induced Intestinal Damage by Inhibiting the IMD Pathway in <i>Drosophila</i>.","authors":"Dan Yang, Minghui Xiu, Xiaolin Jiang, Qian Kang, Jinyu Fu, Shihong Zhou, Yongqi Liu, Jianzheng He","doi":"10.2147/JIR.S500892","DOIUrl":"https://doi.org/10.2147/JIR.S500892","url":null,"abstract":"<p><strong>Background: </strong>Sleep is vital for maintaining the health of the organism. Chronic sleep deprivation (CSD) is a key contributor to significant health risks, including the induction of gastrointestinal disorders. However, the mechanism of CSD caused intestinal damage remains unclear.</p><p><strong>Methods: </strong><i>Drosophila melanogaster</i> as an in vivo model was used to investigate the mechanism of CSD-induced intestinal injury, as well as the ameliorative effect of caffeic acid.</p><p><strong>Results: </strong>CSD resulted in reduced survival and severely affected intestinal homeostasis in flies, as evidenced by disruption of intestinal acid-base homeostasis, increased feeding, increased intestinal permeability and shortened intestinal length. Meanwhile, the expressions of the immune deficiency (IMD) pathway-related genes <i>PGRP-SB1, Dpt, AttA, AttB</i> and <i>Mtk</i> were significantly up-regulated in the intestine of CSD flies. On the other hand, Caffeic acid supplementation restored intestinal acid-base homeostasis and intake, while improving intestinal barrier permeability and intestinal length, and effectively reducing intestinal damage. In addition, administration of caffeic acid decreased the expressions of <i>PGRP-SB1, Dpt, AttA</i> and <i>Mtk</i> genes in the CSD flies gut.</p><p><strong>Discussion: </strong>These results suggested that CSD could disrupt gut homeostasis in adult flies by overactivating the IMD pathway, while Caffeic acid has an obvious protective role on the gut homeostasis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3485-3498"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649229","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 Analysis of Ferroptosis and Immune Infiltration in Ulcerative Colitis Based on Bioinformatics.","authors":"Daxing Cai, Weitao Hu, Yanliang Cai, Taiyong Fang, Xiaoqing Chen","doi":"10.2147/JIR.S501651","DOIUrl":"https://doi.org/10.2147/JIR.S501651","url":null,"abstract":"<p><strong>Introduction: </strong>Ulcerative colitis (UC) is an inflammatory bowel disease influenced by genetic, immune, and environmental factors. This study investigates the link between ferroptosis, a cell death process related to oxidative stress and iron metabolism, and immune infiltration in UC.</p><p><strong>Materials and methods: </strong>We analyzed UC patient transcription data from the Gene Expression Omnibus (GEO) and identified ferroptosis-related genes using FerrDB. Using STRING and Cytoscape, we analyzed protein-protein interactions to identify hub UC Differentially Expressed Genes (UCDEGs) and performed functional enrichment with GO and KEGG pathways. Machine learning helped further identify key UC Differentially Expressed Ferroptosis-related genes (UCDE-FRGs), which were validated using additional GEO datasets and immunohistochemical staining.</p><p><strong>Results: </strong>A total of 11 hub UCDEGs (<i>CCL2, ICAM1, TLR2, CXCL9, MMP9, CXCL10, IL1B, CXCL8, PTPRC, FCGR3A</i>, and <i>IL1A</i>) and 3 key UCDE-FRGs (<i>DUOX2, LCN2</i> and <i>IDO1</i>) were identified. GO and KEGG functional enrichment indicates that these genes play a role in immunity and ferroptosis. Analysis of immune cell infiltration showed that there were a large number of Plasma cells, Monocytes, M0/M1 Macrophages and Neutrophils in the UC. Correlation analysis revealed 3 key UCDE-FRGs associated with immune-infiltrated cells in UC. IHC results showed that the expression levels of 3 key UCDE-FRGs in UC were all higher than that in the healthy controls.</p><p><strong>Conclusion: </strong>In summary, this study identified three key genes related to UC ferroptosis and immunity, namely <i>DUOX2, IDO1</i> and <i>LCN2</i>. These findings suggest that immune infiltration plays an important role in UC caused by ferroptosis, and that there is mutual regulation between UC and immune-infiltrated cells. Our research revealed the potential application of immune and ferroptosis in the diagnosis, treatment and prognosis of UC, providing new strategies for clinical management.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"3535-3549"},"PeriodicalIF":4.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649262","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":"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}