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Central catecholamine depletion inhibits peripheral lymphocyte responsiveness in spleen and blood
Author(s) -
PachecoLópez Gustavo,
Niemi MajBritt,
Kou Wei,
Bildhäuser Andre,
Gross Claus M.,
Goebel Marion U.,
Del Rey Adriana,
Besedovsky Hugo O.,
Schedlowski Manfred
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2003.01914.x
Subject(s) - catecholamine , splenocyte , immune system , spleen , endocrinology , medicine , cytokine , lymphocyte , cd8 , peripheral blood lymphocyte , glucocorticoid , biology , peripheral , sympathectomy , immunology
Experimental and clinical evidence has demonstrated extensive communication between the CNS and the immune system. To analyse the role of central catecholamines in modulating peripheral immune functions, we injected the neurotoxin 6‐hydroxydopamine (6‐OHDA) i.c.v. in rats. This treatment significantly reduced brain catecholamine content 2, 4 and 7 days after injection, and in the periphery splenic catecholamine levels were reduced 4 days after treatment. Central catecholamine depletion induced an inhibition of splenic and blood lymphocyte proliferation and splenic cytokine production and expression (interleukin‐2 and interferon‐γ) 7 days after injection. In addition, central treatment with 6‐OHDA reduced the percentage of spleen and peripheral blood natural killer (CD161 +) cells, and T‐cytotoxic (CD8 +) cells in peripheral blood. The reduction in splenocyte proliferation was not associated with a glucocorticoid alteration but was completely abolished by prior peripheral sympathectomy. These data demonstrate a crucial role of central and peripheral catecholamines in modulating immune function.