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Journal of Histochemistry and Cytochemistry, Vol. 51, 1241-1244, September 2003, Copyright © 2003, The Histochemical Society, Inc.

BRIEF REPORT

Intravenous Liposomal Prednisolone Downregulates In Situ TNF-{alpha} Production by T-cells in Experimental Autoimmune Encephalomyelitis

Jens Schmidta, Josbert M. Metselaarb, and Ralf Golda
a Department of Neurology, University of Würzburg, Würzburg, Germany
b Department of Pharmaceutics, Utrecht University, Utrecht, The Netherlands

Correspondence to: Jens Schmidt, Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 4N 252, 10 Center Drive, MSC 1382, Bethesda, MD 20892. E-mail: schmidtj@ninds.nih.gov

Multiple sclerosis (MS) relapses are treated with high-dose IV glucocorticosteroids. Here we investigated mechanisms of long-circulating polyethylene glycol-coated liposomes encapsulating prednisolone (PL) in adoptive transfer experimental autoimmune encephalomyelitis. Rats received IV 10 mg/kg PL 6, 18, or 42 hr before sacrifice at disease maximum. In formalin-fixed, paraffin-embedded spinal cord we employed a nonfluorescent immunohistochemical (IHC) double labeling. We stained for tumor necrosis factor-{alpha} (TNF-{alpha}) in combination with a T-cell antigen. Compared with PBS-containing liposomes, PL at 18 hr, and more at 42 hr, significantly reduced the rate of TNF-{alpha} double-labeled T-cells. This correlated with an ameliorated disease score at day 5 after PL 42 hr. Our results help to further understand mechanisms of action of drug targeting by liposomal steroids, with possible implications for treatment of autoimmune disorders such as MS.

(J Histochem Cytochem 51:1241–1244, 2003)

Key Words: glucocorticosteroids, drug targeting, long-circulating liposomes, multiple sclerosis, EAE, neuroinflammation, autoimmunity, immunohistochemical double, labeling


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