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.
Original language | English (US) |
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Pages (from-to) | 32-40 |
Number of pages | 9 |
Journal | Journal of Neuroimmunology |
Volume | 182 |
Issue number | 1-2 |
DOIs | |
State | Published - Jan 1 2007 |
Keywords
- Anti-inflammatory mediators
- Antigen presentation
- EAE
- LPS
- Multiple sclerosis
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology