Early-life exposure to lipopolysaccharide reduces the severity of experimental autoimmune encephalomyelitis in adulthood and correlated with increased urine corticosterone and apoptotic CD4+ T cells

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DOIResolve DOI: http://doi.org/10.1016/j.neuroscience.2011.07.047
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TypeArticle
Journal titleNeuroscience
ISSN0306-4522
Volume193
Pages283290; # of pages: 8
Subjectcorticosterone; lipopolysaccharide; allergic encephalomyelitis; animal cell; animal experiment; animal model; animal tissue; antigen presenting cell; article; CD3+ T lymphocyte; CD4+ T lymphocyte; controlled study; correlation analysis; disease predisposition; disease severity; drug exposure; immune response; immunization; immunohistochemistry; immunoregulation; lymphocyte proliferation; neuroprotection; nonhuman; priority journal; rat; regulatory T lymphocyte; upregulation; urinalysis; Analysis of Variance; Animals; Animals, Newborn; Annexin A5; Antigens, CD; Apoptosis; CD4-Positive T-Lymphocytes; Cell Proliferation; Corticosterone; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Flow Cytometry; Freund's Adjuvant; Histocompatibility Antigens Class II; Lipopolysaccharides; Rats; Rats, Sprague-Dawley; Severity of Illness Index; Spinal Cord; Statistics, Nonparametric; Time Factors
AbstractEarly-life exposure to bacterial endotoxins, such as lipopolysaccharides (LPS), can provide neuroprotection against experimental autoimmune encephalomyelitis (EAE) during adulthood, possibly through altering the responsiveness of the immune system. Here, we show that exposure of LPS to neonatal rats resulted in a sustained elevation of corticosterone level in urine when compared with saline-treated rats, and that the high level of urine corticosterone was maintained during the progression of EAE (P<0.05). This high level of production of corticosterone plays an important role in altering the predisposition to EAE-induced neuroinflammation, as a positive correlation occurred between the concentration of urine corticosterone and the increased apoptotic CD4 + T cells from the peripheral blood. LPS-treated rats also showed a reduced number of CD3 + T cells in the spinal cord. The splenic antigen-presenting cells showed a reduced expression of MHC II during EAE development in LPS-exposed rats when compared with rats exposed to the saline-treated control. Together, these findings suggest that treating neonatal rats with LPS evokes a sustained elevation of glucocorticoid, which may suppress immune response during EAE by increasing apoptosis of CD4 + T cells and reducing the expression of MHC II on antigen-presenting cells. Therefore, exposing neonates to bacterial endotoxin may further be developed as an immunization strategy to prevent human multiple sclerosis and other inflammatory brain diseases. © 2011.
Publication date
LanguageEnglish
AffiliationNational Research Council Canada (NRC-CNRC); NRC Institute for Biological Sciences (IBS-ISB)
Peer reviewedYes
NPARC number21271459
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Record identifierd2ffbf44-5e13-4030-945c-f19a05aa00f9
Record created2014-03-24
Record modified2016-05-09
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