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Nicotinamide Decreases Cytokine-Induced Activation of Orbital Fibroblasts from Patients with Thyroid-Associated Ophthalmopathy

Division of Endocrinology and Metabolism (Y.H., D.Y., I.M., M.K., J.K., M.S., K.N.), Department of Medicine, Kurume University School of Medicine, Fukuoka, 830 Japan; and Eye Division of Olympia Clinic (Y.I.), 150 Tokyo, Japan

Address all correspondence and requests for reprints to: Dr. Yuji Hiromatsu, Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine, 67 Asahimachi, Kurume, Fukuoka, 830 Japan.

We used flow cytometry to investigate the effects of nicotinamide, an inhibitor of poly (ADP ribose) synthetase, on the cell-surface expression of cytokine-induced human leukocyte antigen (HLA)-A,B,C antigen, HLA-DR antigen, intercellular adhesion molecule 1, CD44, and Fas expression in cultured orbital fibroblasts from patients with thyroid-associated ophthalmopathy. After two to seven passages, cultured orbital fibroblasts were incubated for 3 days with interferon or tumor necrosis factor in the presence of nicotinamide. Nicotinamide inhibited the induction of both HLA-DR and intercellular adhesion molecule 1 expression by cytokines on fibroblasts but did not interfere with induction of HLA-A,B,C, or CD44 expression. Nicotinamide also inhibited the proliferation of orbital fibroblasts, as assessed by a [³H]-thymidine incorporation assay and cell counts. Nicotinamide also enhanced the expression of the apoptosis-mediating protein Fas on fibroblasts. Our data suggest that nicotinamide inhibits cytokine-induced activation of fibroblasts and thus may decrease the autoimmune injury to the orbit in thyroid-associated ophthalmopathy.

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