Novel Risk Factors for Progression of Diabetic and Nondiabetic CKD: Findings From the Chronic Renal Insufficiency Cohort (CRIC) Study

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Cytokine Expression in Human Osteoblasts After Antiseptic Treatment: A Comparative Study Between Polyhexanide and Chlorhexidine

Purpose/Aim of the study: Chlorhexidine and polyhexanide are frequently used antiseptics in clinical practice and have a broad antimicrobial range. Both antiseptics are helpful medical agents for septic wound treatment with a high potential for defeating joint infections. Their effect on human osteoblasts has, so far, not been sufficiently evaluated. The aim of this study was to investigate the activating potential of polyhexanide and chlorhexidine on inflammatory cytokines/chemokines in human osteoblasts in vitro. Materials and Methods: Human osteoblasts were isolated and cultivated in vitro and then treated separately with 0.1% and 2% chlorhexidine and 0.04% polyhexanide as commonly applied concentrations in clinical practice. Detection of cell structure and cell morphology was performed by light microscopic inspection. Cytokine and chemokine secretion was determined by using a multiplex suspension array. Results: Cell shrinking, defective cell membrane, and the loss of cell adhesion indicated cell damage of human osteoblasts after treatment with both antiseptics was evaluated by using light microscopy. Polyhexanide, but not chlorhexidine, caused human osteoblasts to secrete various interleukins (1β, 6, and 7), interferon γ, tumor necrosis factor α, vascular endothelial growth factor, eotaxin, fibroblast growth factor basic, and granulocyte macrophage colony-stimulating factor as quantified by multiplex suspension array. Conclusions: Both antiseptics induced morphological cell damage at an optimum exposure between 1 and 10 min. But only polyhexanide mediated a pronounced secretion of inflammatory cytokines and chemokines in human osteoblasts. Therefore, we recommend a preferred usage of chlorhexidine in septic surgery to avoid the induction of an inflammatory reaction.     

牙周炎和趋化因子的研究新进展

趋化因子(chemokines)是一类一级结构相似,对白细胞具有化学趋化作用等多种生物学效应的小分子蛋白,在机体的防御和炎症反应等方面起着重要的调节作用.近年来许多研究发现,趋化因子在牙周炎的免疫发病机制中发挥着重要作用.深入研究趋化因子和牙周炎的关系,对牙周炎的预防、诊断、治疗以及治疗后疗效监测有重要意义.     

Differential in situ distribution of interleukin-8, monocyte chemoattractant protein-1 and Rantes in human chronic periapical granuloma

In situ distribution of three prototype chemokines interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1 and Rantes was determined in chronic human periapical granulomas by immunohistochemistry using monoclonal antibodies. IL-8 was found primarily in the cytoplasm of the Malassez epithelial cells. MCP-1 immunoreactivity was confined to the endothelial cells that lined small venules. Each of the three investigated chemokines, including Rantes, exhibited a characteristic binding pattern to the extracellular matrix of the lesion. The observed chemokines may play a role in establishing the cellular composition of chronic apical periodontitis, thus augmenting the intensity of local inflammation and tissue damage.     

趋化因子IL-8及其受体基因的多态性和肺结核易感性的相关性研究

目的探讨IL-8+781C/T位点与它的受体CXCR1+2608G/C的基因多态性和结核病易感性之间的关系。方法采用病例对照研究方法,应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)对78例结核病患者和97例健康对照者的IL-8+781C/T位点和它的受体CXCR1+2608G/C位点进行基因分型,χ2检验分析这两个位点多态性与结核病发生的相关性。结果 IL-8+781C/T位点CC、CT和TT基因型在病例组的分布频率分别为82.0%,15.4%和2.6%,在对照组的分布频率分别为85.6%,13.4%和1.0%。2组间CC、CT、TT三种基因型频率分布用行×列表χ2检验比较,差异无统计学意义(χ2=0.72,P>0.05);同时C、T等位基因在2组间分布频率差异无统计学意义(χ2=0.68,P>0.05)。CXCR1+2608G/C位点GG、GC和CC基因型在病例组的分布频率分别为83.3%,15.4%和1.3%,在对照组的分布频率分别为79.4%,20.6%和0。2组间GG、GC、CC三种基因型频率分布用行×列表χ2检验比较,差异无统计学意义(χ2=1.89,P>0.05);同时G、C等位基因在2组间分布频率差异无统计学意义(χ2=0.18,P>0.05)。结论 IL-8+781C/T位点和CXCR1+2608G/C位点的单核苷酸多态性(SNP)与肺结核感染的易感性不相关。     

High predictive value of immune-inflammatory biomarkers for schizophrenia diagnosis and association with treatment resistance

Objectives. Recent schizophrenia (SCZ) research aims to establish biomarkers with high predictive value for the diagnosis, severity of illness or treatment resistance. SCZ is accompanied by activated immune-inflammatory pathways, including increased levels of cytokines and chemokines, but few studies tried to identify predictive properties of such measures. Methods. We included 54 medicated SCZ patients and 118 healthy controls and examined 15 cytokines and chemokines. Possible associations between these immune-inflammatory biomarkers and the diagnosis of SCZ, severity of illness and treatment resistance were investigated. Results. SCZ is associated with a specific cytokine – chemokine profile, i.e., increased CCL11, MIP-1α, sTNF-R1 and sTNF-R2 levels, and decreased levels of IP-10, TNF-α, IL-2 and IL-4. The combination of five biomarkers (sTNF-R1, sTNF-R2, CCL11, IP-10, IL-4) may predict the diagnosis of SCZ with a sensitivity of 70.0% and a specificity of 89.4%. There was a weak association between the negative symptoms and biomarkers, i.e., IL-2 (inversely) and CCL11 (positively). Patients with treatment resistance showed increased levels of sTNF-R1, sTNF-R2 and MCP-1. Conclusions. The findings of this study reinforce that SCZ is associated with a pro-inflammatory profile and suggest that some immune mediators may be used as reliable biomarkers for the diagnosis of SCZ and treatment resistance.     

CXCL10 induces the recruitment of monocyte-derived macrophages into kidney,which aggravate puromycin aminonucleoside nephrosis

The mechanism responsible for trafficking of monocyte-derived macrophages into kidney in the puromycin aminonucleoside model of nephrotic syndrome in rats (PAN-NS), and the significance of this infiltration, remain largely unknown. CXCL10, a chemokine secreted in many T helper type 1 (Th1) inflammatory diseases, exhibits important roles in trafficking of monocytes and activated T cells. We hypothesized that induction of circulating interferon (IFN)-γ and glomerular tumour necrosis factor (TNF)-α during PAN-NS would stimulate the release of CXCL10 by podocytes, leading to infiltration of activated immune cells and greater glomerular injury. We found that serum IFN-γ, glomerular Cxcl10 mRNA and intra- and peri-glomerular macrophage infiltration were induced strongly during the late acute phase of PAN-NS in Wistar rats, but not in nude (Foxn1^rnu/rnu) rats lacking functional effector T lymphocytes. Wistar rats also developed significantly greater proteinuria than nude rats, which could be abolished by macrophage depletion. Stimulation of cultured podocytes with both IFN-γ and TNF-α markedly induced the expression of Cxcl10 mRNA and CXCL10 secretion. Together, these data support our hypothesis that increased circulating IFN-γ and glomerular TNF-α induce synergistically the production and secretion of CXCL10 by podocytes, attracting activated macrophages into kidney tissue. The study also suggests that IFN-γ, secreted from Th1 lymphocytes, may prime proinflammatory macrophages that consequently aggravate renal injury.