Central catecholamine neurotoxin administration. 1. Immunological changes associated with the suppression of experimental autoimmune encephalomyelitis

Journal of Neuroimmunology
W J KarpusJ A Killen

Abstract

Central nervous system (CNS) depletion of norepinephrine (NE) using 6-hydroxydopamine (6-OHDA) prior to disease induction suppressed the clinical signs of experimental autoimmune encephalomyelitis (EAE). This treatment did not have an effect on the degree of mononuclear cell infiltration when spinal cord sections were examined and stained with hematoxylin and eosin, nor on serum levels of anti-myelin basic protein antibodies. However, investigation of the subpopulations of lymphoid cells within the perivascular lesions showed an increase in cells bearing the T suppressor cell phenotype, OX8+, in the 6-OHDA-treated EAE rats when compared to saline-control-treated EAE rats. Examination of other cellular subsets showed no differences in the numbers of T helper cells, macrophages, or B cells within the lesions of the two groups. Furthermore, histofluorescent estimation of catecholamines in spinal cord sections from 6-OHDA- and saline-control-treated EAE rats demonstrated that catecholamines were indeed depleted in the rats with suppressed clinical EAE. These findings suggest that 6-OHDA depletion of CNS NE may remove an effector amplification mechanism, or trigger a T suppressor cell mechanism, or both, leading to suppression of th...Continue Reading

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Citations

Oct 18, 2012·Journal of Neuroimmune Pharmacology : the Official Journal of the Society on NeuroImmune Pharmacology·Marco Cosentino, Franca Marino
Aug 15, 2002·Neurochemistry International·Douglas L FeinsteinElena Galea
Sep 11, 2009·Journal of Leukocyte Biology·Sourojit BhowmickRobert E Cone
Feb 25, 2009·Annals of the New York Academy of Sciences·Istvan BercziKalman Kovacs
Nov 1, 1992·The International Journal of Neuroscience·B D Janković, J Radulović
Mar 12, 2017·Journal of Neural Transmission·Mia LeviteMarco Cosentino
May 29, 2021·Translational Neuroscience·Majid GhareghaniKazem Zibara

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