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

被引：29

作者：

Jarvis, BW ^{[1
]}

Harris, TH ^{[1
]}

Qureshi, N ^{[1
]}

Splitter, GA ^{[1
]}

机构：

[1] Univ Wisconsin, Anim Hlth & Biomed Sci Dept, Madison, WI 53706 USA

来源：

INFECTION AND IMMUNITY | 2002年 / 70卷 / 12期

关键词：

D O I：

10.1128/IAI.70.12.7165-7168.2002

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The intracellular, gram-negative pathogen Brucella abortus establishes chronic infections in host macrophages while downregullating 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.

引用

页码：7165 / 7168

页数：4

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