Lipopolysaccharide pretreatment modulates the disease course in experimental autoimmune encephalomyelitis

被引:38
作者
Buenafe, Abigail C.
Bourdette, Dennis N.
机构
[1] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA
[2] Vet Affairs Med Ctr, Neurol Serv, Portland, OR 97239 USA
关键词
EAE; multiple sclerosis; LPS; anti-inflammatory mediators; antigen presentation; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; NECROSIS-FACTOR-ALPHA; MYELIN BASIC-PROTEIN; TOLL-LIKE RECEPTOR; ISCHEMIC TOLERANCE; LEWIS RATS; T-CELLS; MICE; MACROPHAGES;
D O I
10.1016/j.jneuroim.2006.09.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Treatment with the bacterial product lipopolysaccharide (LPS) prior to the induction of experimental autoimmune encephalomyelitis (EAE) consistently led to a delayed onset of disease but not to a reduction in disease severity. T cell proliferation was reduced in LPS-treated mice, due at least in part to a loss in antigen presenting cell function. T cell and macrophage infiltration into the CNS was delayed and TNF alpha production was diminished in LPS pre-treated mice, consistent with the delay in disease onset. Real-time PCR analysis of gene expression in the CNS of LPS or saline pre-treated mice demonstrated an early induction of TNF alpha, TGF alpha, IFN beta, and SOCS3 in the LPS pre-treated mice. Thus, exposure to LPS prior to EAE induction affects antigen presentation and may modulate the expression of inflammatory regulators that impact the autoimmune disease course. (c) 2006 Elsevier B.V All rights reserved.
引用
收藏
页码:32 / 40
页数:9
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