Reference Database

In vitro adrenergic modulation of cellular immune functions in experimental autoimmune encephalomyelitis.
Haerter, Katharina
Vroon, Anne
Kavelaars, Annemieke
Heijnen, Cobi J
Limmroth, Volker
Espinosa, Enrique
Schedlowski, Manfred
Elsenbruch, Sigrid
Journal of neuroimmunology 2004 Jan;146: 126-32

OBJECTIVE: To analyze the effects in vitro of alpha- and beta-adrenoceptor agonists on splenocyte proliferation and on proinflammatory cytokine production in splenocytes and peritoneal macrophages (MF) in different stages of EAE.

METHODS: Splenocytes and peritoneal macrophages were harvested in the acute phase of EAE and in remission, and from controls. The beta-agonist terbutaline, the alpha(1)-agonist methoxamine, and the alpha(2)-agonist UK-14304 were added with ConA or lipopolysaccharide (LPS). TNF-alpha and IFN-gamma contents in supernatant and splenocyte proliferation were determined.

RESULTS: Terbutaline and UK-14304 significantly suppressed TNF-alpha production by MF. However, EAE acute phase rats were resistant to the suppressive effect of UK-14304. Terbutaline significantly suppressed IFN-gamma and TNF-alpha production by splenocytes. EAE acute phase and remission animals showed reduced terbutaline-induced inhibition of IFN-gamma production.

CONCLUSIONS: Disturbed sympathetic-immune communication in EAE is characterized by alterations in adrenergic sensitivity via both alpha- and beta-adrenergic pathways.

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