来自流产布鲁氏菌和大肠杆菌的粗制脂多糖在RAW 264.7巨噬细胞样细胞中对肿瘤坏死因子α的相同丝裂原活化蛋白激酶信号通路有不同的激活作用。
Rough lipopolysaccharide from Brucella abortus and Escherichia coli differentially activates the same mitogen-activated protein kinase signaling pathways for tumor necrosis factor alpha in RAW 264.7 macrophage-like cells.
作者信息
Jarvis Bruce W, Harris Tajie H, Qureshi Nilofer, Splitter Gary A
机构信息
Animal Health and Biomedical Sciences Department, University of Wisconsin, Madison 53706, USA.
出版信息
Infect Immun. 2002 Dec;70(12):7165-8. doi: 10.1128/IAI.70.12.7165-7168.2002.
Abstract
The intracellular, gram-negative pathogen Brucella abortus establishes chronic infections in host macrophages while downregulating cytokines such as tumor necrosis factor alpha (TNF-alpha). When producing TNF-alpha, Brucella abortus rough lipopolysaccharide (LPS) activates the same mitogen-activated protein kinase signaling pathways (ERK and JNK) as Escherichia coli LPS, but Brucella LPS is a much less potent agonist.
摘要
细胞内革兰氏阴性病原体流产布鲁氏菌在宿主巨噬细胞中建立慢性感染，同时下调细胞因子，如肿瘤坏死因子α（TNF-α）。当产生TNF-α时，流产布鲁氏菌粗糙脂多糖（LPS）激活与大肠杆菌LPS相同的丝裂原活化蛋白激酶信号通路（ERK和JNK），但布鲁氏菌LPS是一种效力低得多的激动剂。
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