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脂多糖诱导的白细胞介素-6产生是通过鸡血小板中ERK 1/2、p38丝裂原活化蛋白激酶、丝裂原活化蛋白激酶激酶和核因子κB的激活介导的。

Lipopolysaccharide induced Interleukin-6 production is mediated through activation of ERK 1/2, p38 MAPK, MEK, and NFκB in chicken thrombocytes.

作者信息

Winkler C, Ferdous F, Dimmick M, Scott T

机构信息

Department of Biological Sciences, College of Agriculture, Forestry and Life Sciences, Clemson University, United States.

Department of Animal and Veterinary Sciences, College of Agriculture, Forestry and Life Sciences, Clemson University, United States.

出版信息

Dev Comp Immunol. 2017 Aug;73:124-130. doi: 10.1016/j.dci.2017.03.017. Epub 2017 Mar 23.

DOI:10.1016/j.dci.2017.03.017
PMID:28344171
Abstract

Thrombocytes express Toll-like receptor 4 and apparently use both mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB) pathways for nuclear signaling. However, it is not well known if the same enzyme systems found in mammalian cells are fully functional in chickens. Therefore, kinase inhibitors were used with thrombocytes to block kinases in lipopolysaccharide (LPS) stimulated cells to determine if interleukin (IL)-6 expression and production would be diminished. Results demonstrated that extracellular-signal-regulated kinase (ERK)1/2 and p38 MAPK pathways influence gene expression of IL-6 through treatment with either ERK or p38 MAPK inhibitor. In addition, thrombocyte lysates from cells treated with ERK, p38, mitogen-activated protein kinase kinase (MEK)1/2 and inhibitor of nuclear factor kappa-B kinase (IKK) inhibitor showed different levels of the phosphorylated form of ERK1/2, p38 and NFκB. Furthermore, IL-6 gene expression and production were significantly upregulated in LPS stimulated thrombocytes relative to all inhibitor-treated cells.

摘要

血小板表达Toll样受体4,显然利用丝裂原活化蛋白激酶(MAPK)和活化B细胞核因子κ轻链增强子(NFKB)途径进行核信号传导。然而,在哺乳动物细胞中发现的相同酶系统在鸡体内是否完全发挥功能尚不清楚。因此,激酶抑制剂与血小板一起用于阻断脂多糖(LPS)刺激细胞中的激酶,以确定白细胞介素(IL)-6的表达和产生是否会减少。结果表明,细胞外信号调节激酶(ERK)1/2和p38 MAPK途径通过用ERK或p38 MAPK抑制剂处理来影响IL-6的基因表达。此外,用ERK、p38、丝裂原活化蛋白激酶激酶(MEK)1/2和核因子κB激酶(IKK)抑制剂处理的细胞的血小板裂解物显示出不同水平的ERK1/2、p38和NFκB的磷酸化形式。此外,相对于所有抑制剂处理的细胞,LPS刺激的血小板中IL-6基因表达和产生显著上调。

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