European Journal of Inflammation最新文献

{"title":"Activation of hydroxycarboxylic acid receptor 1 attenuates glutamate-induced excitotoxic neuronal injury","authors":"Xiaoqi Chu, Xuemin Wang, Bin Fu, Yuhao Li","doi":"10.1177/1721727x251398974","DOIUrl":"https://doi.org/10.1177/1721727x251398974","url":null,"abstract":"The aim of this study is to investigate the role of hydroxycarboxylic acid receptor 1 (HCAR1) in glutamate-induced excitotoxic neuronal injury. The effective and safe concentrations of an endogenous HCAR1 agonist (L-lactic acid) and an exogenous HCAR1 agonist (3,5-dihydroxybenzoic acid, 3,5-DHBA) were determined using a CCK-8 assay. An excitotoxic injury model was established by stimulating mouse hippocampal neuronal cells (HT22 cells) with 20 mM glutamate, followed by intervention with safe concentrations of L-lactic acid and 3,5-DHBA. Neuronal survival and apoptosis were assessed by NeuN immunofluorescence staining and a TUNEL assay. The effects of HCAR1 agonists on glutamate transport were evaluated using vesicular glutamate transporter 1 (VGLUT1) immunofluorescence staining and qRT‒PCR. Additionally, qRT‒PCR was performed to quantify the expression of a neuronal excitability marker gene ( c-fos ), inflammatory factors and hcar1 . The results showed that HCAR1 agonists (L-lactic acid and 3,5-DHBA) significantly improved neuronal survival, reduced glutamate-induced apoptosis and decreased neuronal excitability ( p < 0.05). The activation of HCAR1 inhibited the transport of the excitatory neurotransmitter glutamate ( p < 0.05). The upregulation of HCAR1 expression led to the significant downregulation of the expression of inflammatory factors ( il-1β , il-6 and tnf-α ) ( p < 0.05). In conclusion, HCAR1 activation effectively suppresses glutamate-induced neuronal apoptosis, reduces the uptake of excitatory neurotransmitters, and downregulates proinflammatory factor expression, thereby exerting neuroprotective effects.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147920534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of mitochondrial dysfunction and oxidative stress in chronic kidney disease","authors":"A. Blagov, V. Orekhova, Alexander D. Zhuravlev, Alexey A. Yakovlev, V. Sukhorukov, Alexander N. Orekhov","doi":"10.1177/1721727x241227349","DOIUrl":"https://doi.org/10.1177/1721727x241227349","url":null,"abstract":"Finding new pathogenic factors that affect the progression of chronic diseases is an important step in the fight against these diseases. In this review, the causes and role of mitochondrial dysfunction in the pathogenesis of chronic kidney disease (CKD) are considered. In this context, the importance of mitochondria for kidney cells in general and proximal tubule cells in particular, as well as the role of oxidative stress in the pathogenesis of CKD, are also discussed. The causes of mitochondrial dysfunction in CKD and the consequences of the development of pathological conditions as a result of impaired mitochondrial activity are analyzed in detail.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"78 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139639921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Co-expression of interleukin (IL)-17RA and IL-36γ in the hypothalamic paraventricular nucleus of the stress-induced hypertension rats","authors":"H Zhang, Tingyu Ding, Wenying Zhang, Changhao Wu, Yu‐Pin Chen, Jinjin Jiang, Jihu Sun, Qin Wu","doi":"10.1177/1721727x241237445","DOIUrl":"https://doi.org/10.1177/1721727x241237445","url":null,"abstract":"Objectives: The up-regulation of proinflammatory cytokines in the hypothalamic paraventricular nucleus (PVN) is well demonstrated to be involved in the development of neurogenic hypertension, including stress-induced hypertension (SIH). IL-17A has been found to be increased in the PVN of several hypertensive animal models and has been shown to play a key role in the development of hypertension. Although IL-36γ was found to be expressed in spinal neurons, its role in hypertension remains elusive. Here, we investigated the co-expression of IL-17 receptor A (IL-17RA) and IL-36γ in the PVN cells of SIH rats. Methods: The electric foot shock combined with buzzer noise stressors were used to make hypertensive rat model. The immunochemical staining or immunofluorescence staining was used to reveal cells as requested. The Western blot was used to detect the related protein levels. Results and Conclusion: In the PVN of the SIH rats, the number of CD3 + CD4 + T cells was significantly increased by the immunochemical staining. Additionally, the protein levels of RORγt and IL-17A were significantly upregulated by Western blot, confirming the infiltration of CD4 + T cells and differentiation into Th17 cells in the PVN of SIH rats. Immunofluorescence staining revealed abundant expression of IL-17RA in PVN neurons, with relatively less expression in astrocytes or microglia. Furthermore, IL-36γ positive cells and protein expression of IL-36R were significantly increased. Notably, this study demonstrates for the first time that most IL-36γ cells were strongly colocalized with IL-17RA positive cells in the PVN of SIH rats, and the colocalized cells were significantly higher in SIH rats. This suggests that IL-17A secreted by infiltrated Th17 cells may stimulate PVN neurons to produce IL-36γ via IL-17RA, indicating that the combination of IL-17 and IL-36γ might produce strong pro-inflammatory effects in the PVN of SIH rats.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://journals.sagepub.com/doi/pdf/10.1177/1721727X241237445","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of shared mechanisms and targets between immune checkpoint inhibitor-associated myocarditis and autoimmune myocarditis","authors":"Kai Yang, Min Zhang, Dong Li, Yuandong Yu, Fengjun Cao, Guoxing Wan","doi":"10.1177/1721727x231223578","DOIUrl":"https://doi.org/10.1177/1721727x231223578","url":null,"abstract":"This study aimed to explore the shared mechanisms and targets between immune checkpoint inhibitor-associated myocarditis (ICIM) and autoimmune myocarditis. Relevant data were retrieved from public datasets and Gene Expression Omnibus (GEO) database. Gene set enrichment analysis (GSEA) of differentially expressed genes (DEGs) was used to identify significant shared signaling pathways between ICIM and non-ICI associated autoimmune myocarditis (NICIAM) represented by ICIM model and experimental autoimmune myocarditis (EAM) model, respectively. Cell type enrichment analysis and immune infiltration analysis by clusterProfiler and ImmuCellAI were performed to identify critical immune cell component involved in ICIM and NICIAM. Additionally, core shared genes across ICIM and NICIAM were identified and validated by various models and methods. Interferon-γ response, inflammatory response and allograft rejection signaling were identified as the shared signaling pathways associated with ICIM and NICIAM. Enrichment analysis of cell type supported an important role of increased infiltration of T cells and macrophages in both ICIM and NICIAM. However, the predominant increase of infiltrated T cells was CD4+ T cells in NICIAM, while that were CD8+ T cells in ICIM. Core shared genes Lck and Cd3d expression were found increased in both ICIM and NICIAM, and Lck inhibition was further identified and validated as potential therapeutic approach. Our study initially established a comorbidity model to identify potential molecular mechanism including interferon-γ response, inflammatory response and allograft rejection signaling accounting for the concerns of myocarditis risk in patients with preexisting autoimmune disease (PAD) receiving ICI treatment, and supported the therapeutic potential of targeting Lck or Cd3d.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139639495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and immunological aspects of gingival retraction systems in fixed dental prostheses: A systematic review","authors":"M. A. Alarcón-Sánchez, G. Minervini, A. Heboyan","doi":"10.37766/inplasy2024.1.0005","DOIUrl":"https://doi.org/10.37766/inplasy2024.1.0005","url":null,"abstract":"To describe the existing knowledge on the efficacy of the different gingival retraction systems (GRSs) in gingival displacement, to know their effects on biological functions of human gingival fibroblasts (HGFs), and on the expression of inflammatory mediators (TNF-α and MCP-1) in gingival crevicular fluid (GCF), and saliva. The protocol used for this systematic review was registered in INPLASY: 202410005. A digital search was performed in the databases PubMed/MEDLINE, Scopus, Science Direct, Web of Science, and Google Scholar of the literature published in the English language in the last 17 years (from December 10th, 2006, to May 15th, 2023), and included retrospective randomized clinical studies, prospective, and in vitro experimental studies. In addition, PRISMA criteria were followed. The methodological validity of the selected articles was assessed using Joanna Briggs Institute (JBI) critical appraisal tool, and the modified Consolidated Standards of Reporting Trials checklist (CONSORT). 27 articles published between 2006 and 2023 were evaluated. Six hundred 32 subjects, aged between 18 and 65, participated in the clinical studies. 93.7% of the studies assessed periodontally healthy patients, and only 6.3% evaluated patients with mild gingivitis. Also, 882 teeth were samples, of which the majority were posterior teeth (54%). The most commonly used GRSs was aluminum chloride gingival retraction paste (74%). The GCF samples were taken in 67% of the studies, and ELISA was used in all studies (100%) to determine inflammatory mediators. The most frequently analyzed marker was TNF-α (67%). The system Merocel Strips (Mystic, conn, USA) achieved the highest level of gingival displacement (1.66 ± 3.7 mm). In addition, the braided cords produced the lowest TNF-α levels (0.43 ± 0.08pg/mL). Astringent systems such as ferric sulfate had higher toxicity in HGFs.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"157 4-5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140523250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive value of early measurement of cytokine levels for persistent inflammation-immunosuppression-catabolism syndrome in ICU patients: A retrospective study","authors":"Yongxia Hu, Yun Wang, Shan Guo, Weimin Zhang","doi":"10.1177/1721727x231224604","DOIUrl":"https://doi.org/10.1177/1721727x231224604","url":null,"abstract":"Investigating cytokine levels in ICU patients reveals their potential in predicting the occurrence of Persistent Inflammatory Response-Immunosuppression-Catabolic Syndrome (PICS). Our study encompassed clinical data from ICU patients admitted between December 2020 and January 2022. The cohort was divided based on the incidence of PICS, and a comparative analysis was conducted on their clinical data. Using logistic regression, we identified independent factors influencing PICS. Among 132 patients meeting our inclusion criteria, 39 (31.70%) developed PICS. Significant differences were observed between the PICS and non-PICS groups in terms of average age, APACHE II scores, hospital stay duration, mortality, and infection rates. Notably, laboratory parameters indicated lower pre-albumin and IL-4 levels, alongside higher IL-6, IL-10, IL-17, and IFN-y levels in the PICS group. Multivariate analysis pinpointed pre-albumin, IL-4, IL-6, and IL-10 as independent risk factors for PICS in ICU settings. Our findings underscore the importance of IL-4, IL-6, and IL-10 as key cytokines in the early detection and management of PICS, offering significant insights for clinical practice.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":" 18","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139393353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between 25 (OH) D levels in aqueous humor and the patients with ARC","authors":"Gang Huang, Wen Qi Suo, Jian Ying Du, Xiong Zhang","doi":"10.1177/1721727x231217802","DOIUrl":"https://doi.org/10.1177/1721727x231217802","url":null,"abstract":"Age-related cataract (ARC) is an eye disease characterized by lens opacity. This study analyzed the correlation between 25 hydroxyvitamin D [25 (OH) D] levels and Interleukin 6 (IL-6) levels in aqueous humor from the patients with ARC, as well as between 25 (OH) D levels and lens opacity, and explored the effect of 25 (OH) D on the pathogenesis of ARC. A retrospective analysis was performed, which included the clinical data from 120 ARC patients and 40 healthy individuals. They were divided into three groups based on the objective scattering index (OSI): 40 healthy individuals (control group), 84 patients with the early cataract (EC group), and 36 patients with the mature cataract (MC group). An electrochemical luminescence method was used to detect the levels of 25 (OH) D and IL-6 in aqueous humor, the OSI of the eye was measured using a visual quality analysis system. The correlation between the changes in the above indicators and ARC was analyzed. The OSI and IL-6 levels in the control group, EC group, and MC group increased sequentially (all p < .001), while the levels of 25 (OH) D showed an opposite trend (all p < .001). The decrease in 25 (OH) D levels is related to the occurrence and development of ARC, and the relationship between 25 (OH) D deficiency and the pathological mechanism of ARC needs further research.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"33 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139251342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between rs968697 genetic polymorphism and gastric cancer susceptibility, TNM stage and survival prognosis","authors":"Jun Hu, Xiaoting Wang","doi":"10.1177/1721727x231216202","DOIUrl":"https://doi.org/10.1177/1721727x231216202","url":null,"abstract":"HMGA2 can promote the development of multiple malignancies. This study aimed to determine whether a putative functional genetic polymorphism (rs968697 T>C) in the HMGA2 gene promoter region was associated with malignancy susceptibility in the Chinese population. The rs968697 genetic polymorphism was genotyped using the SNaPshot method in the case-control study. The odds ratios and 95% confidence intervals were calculated using a logistic regression model. STATA software was used to conduct the meta-analysis. The rs968697 genetic polymorphism was associated not only with susceptibility to malignant tumors [CC versus TT: OR = 0.45, 95%CI = 0.28–0.73, p = .001; CC versus (CT + TT): OR = 0.47, 95%CI = 0.29–0.75, p = .003] including gastric cancer (GC), but also with TNM stage and survival prognosis of GC patients. Genotype-tissue expression analysis, luciferase assay and bioinformatics analysis revealed that the rs968697 genetic polymorphism might affect the binding of transcription factors, especially POLR2A, which in turn regulate the expression of HMGA2. The current research suggests that the rs968697 genetic polymorphism may be used as a biomarker for malignancy susceptibility and GC prognosis in the Chinese population.","PeriodicalId":502292,"journal":{"name":"European Journal of Inflammation","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139261458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}