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首页> 外文期刊>Cytokine >Neutrophilic granule protein (NGP) attenuates lipopolysaccharide-induced inflammatory responses and enhances phagocytosis of bacteria by macrophages
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Neutrophilic granule protein (NGP) attenuates lipopolysaccharide-induced inflammatory responses and enhances phagocytosis of bacteria by macrophages

机译:中性粒细粒蛋白(NGP)衰减脂多糖诱导的炎症反应,并通过巨噬细胞增强细菌的吞噬作用

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Neutrophilic granule protein (NGP) belongs to the cystatin superfamily. Even though this superfamily is critically involved in cancer biology and adaptive immunity, the relationship of macrophage NGP to inflammation and phagocytosis remains poorly understood. In this study, we observed a significant increase of NGP in peritoneal macrophages (PMs) isolated from mice challenged with E. con or lipopolysaccharide (LPS), as judged by NGP mRNA microarray. We also found changes in NGP to be mainly Toll-like receptor 4 (TLR4)-dependent. By western blot and electrophoretic mobility shift assay, we demonstrated NGP overexpression to reduce TNF-alpha and IL-1 beta production by LPS-induced RAW264.7 cells (RAW) via suppression of the NF-kappa B (p65 and p50) signalling pathway, rather than the JNK1/AP-1 (fos and jun) signalling pathway. NGP overexpression by LPS-induced RAW also induced IL-10, an anti-inflammatory cytokine, which was partially involved in the anti-inflammatory effect produced by NGP overexpression. Moreover, upregulated NGP enhanced the phagocytosis of E. coli by RAW. Taken together, these results demonstrated NGP to be an important host defense component that regulates inflammatory responses and phagocytosis by activated macrophages. As such, NGP may be useful for the treatment of inflammatory based disease.
机译:中性粒细粒蛋白(NGP)属于胱抑素超家族。尽管这一超级家族批判性地参与了癌症生物学和适应性免疫,但巨噬细胞NGP与炎症和吞噬作用的关系仍然很差。在这项研究中,我们观察到由NGP mRNA微阵列判断,从小鼠攻击的小鼠中分离的小鼠中分离的腹膜巨噬细胞(PMS)中NGP的显着增加。我们还发现NGP的变化主要是收费类似的受体4(TLR4) - 依赖性。通过蛋白质印迹和电泳迁移率转变测定,我们证明了通过抑制NF-Kappa B(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号通路(P65和P50)信号传导途径降低为NGP过表达,以减少TNF-α和IL-1β生产,而不是JNK1 / AP-1(FOS和Jun)信号通路。 LPS诱导的RAG的NGP过表达也诱导IL-10,抗炎细胞因子,其部分参与NGP过表达产生的抗炎作用。此外,上调的NGP通过原料增强了大肠杆菌的吞噬作用。总之,这些结果证明了NGP是一种重要的宿主防御组分,通过活化的巨噬细胞调节炎症反应和吞噬作用。因此,NGP可用于治疗炎症的疾病。

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