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白色念珠菌和脂多糖诱导巨噬细胞肿瘤坏死因子所涉及的不同事件。

Different events involved in the induction of macrophage tumor necrosis factor by Candida albicans and lipopolysaccharide.

作者信息

Blasi E, Pitzurra L, Puliti M, Mazzolla R, Barluzzi R, Saleppico S, Bistoni F

机构信息

Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.

出版信息

Cell Immunol. 1994 Sep;157(2):501-9. doi: 10.1006/cimm.1994.1245.

DOI:10.1006/cimm.1994.1245
PMID:8069929
Abstract

Using an in vitro experimental model, we have recently demonstrated that Candida albicans in its hyphal form (H-Candida), similarly to lipopolysaccharide (LPS), enhances tumor necrosis factor (TNF) secretory response in the cloned macrophage (M phi) population ANA-1. Here we show that H-Candida and LPS each differ in their requirements for intact protein kinase functions, susceptibility to 0.4-microns micropore-size membranes, and sensitivity to polymyxin B. These results, together with the synergistic effect occurring between H-Candida and LPS in inducing TNF response, indicate the existence of different receptor(s) and/or signal-transduction pathway(s) through which the two stimuli act.

摘要

利用体外实验模型,我们最近证明,白色念珠菌的菌丝形态(H-念珠菌)与脂多糖(LPS)类似,可增强克隆巨噬细胞(M phi)群体ANA-1中的肿瘤坏死因子(TNF)分泌反应。在此我们表明,H-念珠菌和LPS在对完整蛋白激酶功能的需求、对0.4微米微孔尺寸膜的敏感性以及对多粘菌素B的敏感性方面各有不同。这些结果,连同H-念珠菌和LPS在诱导TNF反应中产生的协同效应,表明存在两种刺激作用所通过的不同受体和/或信号转导途径。

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Different events involved in the induction of macrophage tumor necrosis factor by Candida albicans and lipopolysaccharide.白色念珠菌和脂多糖诱导巨噬细胞肿瘤坏死因子所涉及的不同事件。
Cell Immunol. 1994 Sep;157(2):501-9. doi: 10.1006/cimm.1994.1245.
2
Heterogeneous secretory response of phagocytes from different anatomical districts to the dimorphic fungus Candida albicans.来自不同解剖区域的吞噬细胞对双相真菌白色念珠菌的异质性分泌反应。
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Cytokine responses to fungal pathogens in Kupffer Cells are Toll-like receptor 4 independent and mediated by tyrosine kinases.库普弗细胞中细胞因子对真菌病原体的反应不依赖于Toll样受体4,而是由酪氨酸激酶介导的。
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The Candida albicans phospholipomannan induces in vitro production of tumour necrosis factor-alpha from human and murine macrophages.白色念珠菌磷脂甘露聚糖可在体外诱导人和小鼠巨噬细胞产生肿瘤坏死因子-α。
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Ketamine inhibits tumor necrosis factor-alpha and interleukin-6 gene expressions in lipopolysaccharide-stimulated macrophages through suppression of toll-like receptor 4-mediated c-Jun N-terminal kinase phosphorylation and activator protein-1 activation.氯胺酮通过抑制Toll样受体4介导的c-Jun氨基末端激酶磷酸化和激活蛋白-1激活,抑制脂多糖刺激的巨噬细胞中肿瘤坏死因子-α和白细胞介素-6的基因表达。
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Regulation of inducible nitric oxide synthase messenger RNA expression and nitric oxide production by lipopolysaccharide in vivo: the roles of macrophages, endogenous IFN-gamma, and TNF receptor-1-mediated signaling.体内脂多糖对诱导型一氧化氮合酶信使核糖核酸表达及一氧化氮生成的调节:巨噬细胞、内源性γ干扰素及肿瘤坏死因子受体-1介导的信号传导的作用
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Tumor necrosis factor-alpha production induced by viruses and by lipopolysaccharides in macrophages: similarities and differences.病毒和脂多糖诱导巨噬细胞产生肿瘤坏死因子-α:异同点
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[Effects of RNA interference on expression of tumor necrosis factor-alpha in lipopolysaccharide-activated mouse macrophages].RNA干扰对脂多糖激活的小鼠巨噬细胞中肿瘤坏死因子-α表达的影响
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Macrophage TNF mRNA expression is modulated by protease inhibitors.巨噬细胞肿瘤坏死因子信使核糖核酸的表达受蛋白酶抑制剂调控。
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Increased susceptibility of TNF-alpha lymphotoxin-alpha double knockout mice to systemic candidiasis through impaired recruitment of neutrophils and phagocytosis of Candida albicans.肿瘤坏死因子-α 淋巴毒素-α 双敲除小鼠因中性粒细胞募集受损和白色念珠菌吞噬作用减弱而对全身性念珠菌病易感性增加。
J Immunol. 1999 Aug 1;163(3):1498-505.

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