Lipopolysaccharide pretreatment modulates the disease course in experimental autoimmune encephalomyelitis

Abstract 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 lea...

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Bibliographic Details
Published in:Journal of neuroimmunology 2007-01, Vol.182 (1), p.32-40
Main Authors: Buenafe, Abigail C, Bourdette, Dennis N
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Anti-inflammatory mediators
Antigen presentation
Antigen-Presenting Cells - drug effects
Cell Movement
Cell Proliferation - drug effects
Central Nervous System - pathology
EAE
Encephalomyelitis, Autoimmune, Experimental - pathology
Encephalomyelitis, Autoimmune, Experimental - physiopathology
Gene Expression - drug effects
Gene Expression Regulation
Interferon-beta - genetics
Lipopolysaccharides - pharmacology
LPS
Macrophages - pathology
Male
Mice
Mice, Inbred C57BL
Multiple sclerosis
Neurology
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins - genetics
T-Lymphocytes - pathology
Time Factors
Transforming Growth Factor beta - genetics
Tumor Necrosis Factor-alpha - antagonists & inhibitors
Tumor Necrosis Factor-alpha - genetics
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Summary:Abstract 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 TNFα 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 TNFα, TGFβ, IFNβ, 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.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2006.09.004