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.
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.
Jarvis
Bruce W
BW
Animal Health and Biomedical Sciences Department, University of Wisconsin, Madison 53706, USA.
Harris
Tajie H
TH
Qureshi
Nilofer
N
Splitter
Gary A
GA
D000818:Animals; D002003:Brucella abortus / Q000276:immunology* / Q000472:pathogenicity*; D002460:Cell Line; D015536:Down-Regulation; D004789:Enzyme Activation; D004926:Escherichia coli / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology*; D008264:Macrophages / Q000382:microbiology; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D020928:Mitogen-Activated Protein Kinases