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关键词： 下肢骨折   软组织损伤   白介素-6   前列腺素2   C反应蛋白  

摘要： 目的 分析下肢骨折伴软组织损伤患者血清白介素-6（IL-6）、前列腺素2（PGE2）及C反应蛋白（CRP）水平与软组织损伤严重程度的关联性，并评估IL-6、PGE2、CRP对软组织损伤严重程度的诊断效能。方法 选取2022年10月至2023年10月宜昌市中心人民医院收治的180例下肢骨折伴软组织损伤患者为研究对象，依据损伤的严重程度分为轻中度组（n=125）和重度组（n=55）。测定两组患者血清IL-6、PGE2及CRP水平；采用Spearman秩相关检验分析血清IL-6、PGE2及CRP水平与软组织损伤严重程度的相关性；采用受试者工作特征曲线（ROC曲线）分析血清IL-6、PGE2及CRP水平对软组织损伤严重程度的评估价值。结果 重度组患者血清IL-6、PGE2及CRP水平高于轻中度组（P<0.05）；血清IL-6、PGE2及CRP水平与下肢骨折患者软组织损伤严重程度均呈正相关（P<0.05）。ROC曲线分析结果显示，血清IL-6、PGE2及CRP水平联合评估下肢骨折患者软组织损伤严重程度的曲线下面积（AUC）为0.722，优于各指标单独评估（P<0.05）。结论 血清IL-6、PGE2及CRP水平与下肢骨折患者伴软组织损伤的严重程度密切相关，通过测定IL-6、PGE2、CRP水平可评估软组织损伤严重程度，以指导临床采取针对性治疗方案。

关键词： COPD   Exacerbations   Eosinophils  

摘要： BackgroundThe role of eosinophils in COPD and their utility as biomarkers for cytokine targeting monoclonal therapies remains unclear. We investigated the distribution of eosinophils across different tissue compartments in COPD and analysed gene expression to understand the possible mechanistic drivers of eosinophilic inflammation in *** and BAL from ex-smoking volunteers with mild/moderate COPD (n = 31) and healthy ex-smoking controls (n = 20), and bronchial biopsy tissue in a subcohort (n = 19 and n = 8, respectively) was analysed. Differentially-expressed genes (DEGs) were characterised using RNASeq. Proteomic analysis of BAL was conducted using *** subjects had more eosinophils in blood and lung tissue compared to controls, with increased eosinophil protein CLC/Galectin-10 in BAL. However, peripheral blood eosinophil counts related poorly to numbers in lung tissue (rho = -0.09192, p = 0.3541) or proportions in BAL (rho = 0.01762, p = 0.4632). Tissue IL-5R alpha expression was higher in frequent exacerbators and related to tissue eosinophils, but not peripheral blood *** blood eosinophils were associated with DEGs that differed with compartment. Higher tissue eosinophil levels were associated with IL-13-induced DEGs including POSTN in bronchial brushes and CCL26 in bronchial biopsies. Gene-set enrichment analysis on data from brushings revealed significant enrichment of IL-4/IL-13, but not IL-5, pathways associated with eosinophil *** subjects had more eosinophils in blood and lung tissue compared to controls, with increased eosinophil protein CLC/Galectin-10 in BAL. However, peripheral blood eosinophil counts related poorly to numbers in lung tissue (rho = -0.09192, p = 0.3541) or proportions in BAL (rho = 0.01762, p = 0.4632). Tissue IL-5R alpha expression was higher in frequent exacerbators and related to tissue eosinophils, but not peripheral blood *** blood eosinophils wer

关键词： 儿童病毒性肺炎   重组人干扰素α-2b   奥司他韦   血清免疫球蛋白   炎症因子   氧化损伤指标  

摘要： 目的:探讨重组人干扰素α-2b联合奥司他韦用于儿童病毒性肺炎治疗对血清免疫球蛋白、炎症因子和氧化损伤指标的影响.方法:选取2022年6月至2024年6月本院收治的病毒性肺炎患儿150例,按照随机数字表法分为对照组(采用奥司他韦治疗)75例,观察组(采用重组人干扰素α-2b联合奥司他韦治疗)75例,共两组.比较两组临床疗效,血清免疫球蛋白[免疫球蛋白A(IgA)、免疫球蛋白G(IgG)、免疫球蛋白M(IgM)]、炎症因子[降钙素原(PCT)、C反应蛋白(CRP)、白细胞介素-6(IL-6)]和氧化损伤指标[丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)]水平差异.结果:观察组治疗总有效率为93.33％(70/75),高于对照组的82.67％(62/75)(P＜0.05).与治疗前进行比较,两组治疗后免疫球蛋白IgA、IgG、IgM以及氧化损伤指标SOD、GSH-Px水平均呈上升趋势,MDA以及炎症因子CRP、PCT、IL-6水平均呈下降趋势(P＜0.05);治疗7d后与对照组进行比较,同期观察组IgA、IgG、IgM、SOD、GSH-Px水平更高,而MDA、CRP、PCT、IL-6水平更低(P＜0.05).结论:重组人干扰素α-2b联合奥司他韦治疗儿童病毒性肺炎能提高临床疗效,有效改善患儿免疫功能,调节炎症因子和氧化损伤指标,具有一定的临床应用价值.

关键词： diabetes   dyslipidemia   insulin resistance   obesity   cytokines   adipokines   cystatin C   oxidized LDL   vascular complications   atherosclerosis   endothelial dysfunction   inflammation  

摘要： In individuals with type 2 diabetes mellitus (T2DM), elevated levels of both plasma and urinary cystatin C (Cys-C) contribute to increased oxidation, which in turn accelerates the oxidation of low-density lipoprotein (LDL). This process may worsen the development of atherosclerosis and cardiovascular disease by promoting endothelial dysfunction and inflammation. Despite its potential significance, the relationship between Cys-C and oxidized LDL (ox-LDL) in T2DM remains poorly understood. This study investigated the relationship between plasma and urinary Cys-C and ox-LDL levels in T2DM patients. The cohort included 57 patients with T2DM (mean age 61.14 +/- 9.99 years;HbA1c 8.66 +/- 1.60% and BMI 35.15 +/- 6.65 kg/m(2)). Notably, 95% of the patients had hypertension, 82% had dyslipidemia, 59% had an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m(2), 14% had coronary artery disease (CAD), and 5% had a history of stroke. Plasma and urinary Cys-C and ox-LDL levels were measured using ELISA. Adipokine and cytokine levels were measured using the multiplex (R) MAP Human Adipokine Magnetic Bead Panels. Spearman's correlation analysis revealed a significant positive correlation of plasma and urinary Cys-C with ox-LDL (r = 0.569, p = 0.0001 and r = 0.485, p = 0.0001, respectively). Multivariable regression analysis indicated that both plasma and urinary Cys-C were independently associated with ox-LDL, after adjusting for confounding factors (beta = 0.057, p = 0.0001 and beta = 0.486, p = 0.003, respectively). Stepwise linear regression identified TNF alpha and adiponectin as the strongest predictors of the relationship between urinary Cys-C and ox-LDL (beta = 0.382, p = 0.0001;r(2) = 0.64), while adiponectin alone was the best predictor of the plasma Cys-C and ox-LDL association (beta = 0.051, p = 0.005;r(2) = 0.46). Furthermore, adiponectin partly mediated the relationship between plasma Cys-C and ox-LDL, explaining 18% of the variance in this association. In

关键词： helper T cells   IFN Upsilon   IL-21   PD1   PD-L1   regulatory B cells   rheumatoid arthritis  

摘要： Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disease. The pathomechanism of RA depends on both B and T cells. Regulatory B cells (Breg) have been shown to suppress T-cell immune responses and play a key role in modulating autoimmune processes. We aimed to investigate the possibility of utilizing PD-L1+ Breg cells in downregulating the Th cells' immune response in healthy individuals and RA patients. We hypothesized that the PD-1/PD-1L interaction plays a key role in this process, which may be defective in autoimmune diseases. We separated T and B cells from the peripheral blood of healthy volunteers and RA patients by magnetic cell sorting, and Th cells and Treg cells were isolated by fluorescence-activated cell sorting. The cytokine production by CD4+ Th cells was detected by intracellular flow cytometry. CpG and CD40L stimulations were applied to induce PD-L1hi expressing Breg cells. We found that the frequency of PD-L1hi cells is significantly lower in all B-cell subsets in RA compared to healthy controls. Functional analysis of induced PD-L1+ Breg cells in coculture with activated autologous Th cells has shown that healthy control samples containing higher levels of PD-L1hi Breg cells significantly inhibit IFN-gamma and IL-21 production by Th cells. In contrast, RA patients' samples with lower levels of PD-L1hi Breg cells failed to do so. Since the expression of PD-L1 on B cells can be modulated in vitro to induce Breg cell suppressive capacity, these data may provide new perspectives for future therapy for RA.

关键词： Head and neck squamous cell carcinoma   Regulatory T cell   Interleukin-1 receptor 2   Cytotoxic T lymphocyte-associated antigen-4  

摘要： Regulatory T cells (Tregs) play an immunosuppressive role in tumor microenvironment (TME) in various of cancer types. However, how different Treg subsets influence and effect on head and neck squamous cell carcinoma (HNSCC) remain unclear. Here, using single-cell RNA sequencing (scRNA-seq), we identified an IL1R2+Treg subset which promoted the progression of HNSCC. Via tissue microassay (TMA) and enzyme-linked immunosorbent assay (ELISA), we verified the clinical diagnostic value of the IL1R2+Treg and soluble IL1R2 (sIL1R2). In addition, we constructed tumor-bearing mouse models to explore the antitumor effects of combined targeting IL1R2 and CTLA4. For mechanism, we found IL-1 beta promoted the expression of IL1R2 and CTLA4 in Tregs, and upregulated CTLA4 though NR4A1 translocation. These results revealed that IL1R2+Treg and serum IL1R2 level had potential diagnostic and prognostic value of HNSCC and combined targeting of IL1R2 and CTLA4 might be an effective strategy to inhibit tumor progression.

关键词： inflammation   mitochondria   ATP   aging   gp130   IL6   HIF1A   HIF1α   ESRRA   ERRα   PPARGC1A   PGC1α   PPARGC1B   PGC1β  

摘要： Chronic inflammation and a decline in mitochondrial function are hallmarks of aging. Here, we show that the two mechanisms may be linked. We found that interleukin-6 (IL6) suppresses mitochondrial function in settings where PGC1 (both PGC1a and PGC1b) expression is low. This suppression is mediated by the JAK1/ STAT1/3 axis, which activates HIF1a through non-canonical mechanisms involving upregulation of HIF1A and ERRa transcription, and subsequent stabilization of the HIF1A protein by ERRa. HIF1a, in turn, inhibits ERRa, which is a master regulator of mitochondrial biogenesis, thus contributing to the inhibition of mitochondrial function. When expressed at higher levels, PGC1 rescues ERRa to boost baseline mitochondrial respiration, including under IL6-treated conditions. Our study suggests that inhibition of the IL6 signaling axis could be a potential treatment for those inflammatory settings where mitochondrial function is compromised.

关键词： copper nanoclusters   high GC content PCR   HLA-B*5801gene   fluorescence   visualization analysis  

摘要： The optimal sequence for synthesizing copper nanoclusters is a promising research area. Initially, random dsDNA sequences yielded low fluorescence intensity, which constrained visual detection under UV light. Poly-AT dsDNA sequences later produced visible fluorescence, but it caused significant interference in negative samples when combined with gene amplification techniques. This interference occurs because the single-stranded poly-AT primer can self-anneal into a double-stranded AT sequence, efficiently synthesizing copper nanoclusters. To mitigate this, we designed a poly-AAT sequence at the primer's 5 ' end, creating a single base pair mismatch every three nucleotides during self-annealing. This adjustment reduced synthesis efficiency of copper nanoclusters in negative samples, improving the visual distinction between negative and positive results. We applied this method to identify the HLA-B*5801 gene, thereby demonstrating its efficacy even within a GC-rich region of human genomic DNA. Our method showed 100% agreement with a commercial qPCR kit, with results distinguishable under UV light. We conclude that the poly-AAT sequence is more suitable for integrating copper nanoclusters synthesis with nucleic acid amplification detection techniques, with potential applications in microelectronics, biosensing, and catalysis.

摘要： Intraepithelial lymphocytes expressing the γδ T cell receptor (γδ IEL) provide continuous surveillance of the intestinal epithelium. We report that mice harboring a microbiota-specific hyperproliferative γδ IEL (γδ ) phenotype also upregulate the expression of the ectonucleotidase CD39, a marker of regulatory γδ T cells. Enhanced TCR and IL-15 signaling correlates with a progression from a naïve-like CD39 γδ IEL to a more mature, tissue-adapted CD39 IEL population. We found that TCRγδ activation drives CD122-mediated CD39 upregulation on γδ IELs and increased mucosal IL-15 further amplifies CD39 expression in these cells. Further investigation revealed that CD39 induction requires sustained exposure to the γδ -associated microbiota. Moreover, CD39 γδ IELs exhibit a reduced capacity to produce pro-inflammatory cytokine, which may explain the lack of histopathology in γδ mice. Overall, our study identifies a previously unappreciated mechanism by which an altered microbiota amplifies CD39 expression on γδ IELs, leading to the expansion of γδ IELs with regulatory potential.