Vitamin E is thought to enhance immunity by increasing interleukin-1 (IL-1) production and by downregulating prostaglandin E2 (PGE2) synthesis. In an effort to understand the mechanism(s) whereby the form of vitamin E known as RRR-alpha-tocopheryl succinate [also called vitamin E succinate (VES)] ameliorates retrovirus-induced immune dysfunctions, peritoneal exudate cells (PECs) derived from normal chickens and avian and murine macrophage cell lines were used as in vitro model systems to test the effects of VES treatments on PGE2 and IL-1 production. Supernatants from PECs that were exposed to avian erythroblastosis virus (AEV) for 45 minutes exhibited a 256% increase in PGE2 levels compared with supernatants from replica cultures of PECs not exposed to AEV. Pretreatment of PECs with VES before exposure to AEV maintained PGE2 levels at normal control levels. VES treatment enhanced IL-1 production by avian (HD11) and murine (P388D1) macrophage cells, respectively. Supernatants from VES-treated HD11- and P388D1-stimulated cells contained IL-1 activity 196% and 385%, respectively, greater than that observed with supernatants from untreated control cells. On the basis of these studies, downregulation of retrovirus-induced PGE2 production and/or upregulation of IL-1 production by VES are potential mechanisms for VES amelioration of retrovirus-induced immune suppression.
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