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(Journal of Leukocyte Biology. 2002;71:981-986.)
© 2002 by Society for Leukocyte Biology

Eicosapentaenoic acid inhibits CSF-induced human monocyte survival and maturation into macrophage through the stimulation of H2O2 production

Sachiyo Terada*, Mari Takizawa{dagger}, Shigeru Yamamoto{ddagger}, Osamu Ezaki*, Hiroshige Itakura* and Kiyoko S. Akagawa§

* Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan;
{ddagger} Department of Nutrition, School of Medicine, University of Tokushima, Japan; and
{dagger} AIDS Research Center and
§ Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan

Correspondence: Dr. Kiyoko S. Akagawa, Department of Immunology, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan. E-mail: akagawak{at}nih.go.jp

Human studies suggest a beneficial effect of eicosapentaenoic acid (EPA)-supplemented diets on atherosclerotic and atherothrombotic disorders as well as autoimmune and inflammatory diseases and tumors. The effects of EPA on human monocyte survival and maturation into macrophage are not yet known. We studied the effects of EPA on the survival and development into macrophage of human monocyte treated with colony-stimulating factor (CSF). We have found that EPA induces cell death of the monocyte via apoptosis, even in the presence of M-CSF or GM-CSF, and inhibits differentiation from the monocyte to macrophage by inducing H2O2 production. In contrast to the effect of EPA on monocytes, EPA did not induce cell death of monocyte-derived macrophages. Such an apoptosis inducing effect on monocytes by EPA may contribute to the efficacy of EPA in atherosclerosis and autoimmune diseases.

Key Words: apoptosis • cell-surface antigens • atherosclerosis • autoimmune disease




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