Prevention of retrovirus-induced aberrant cytokine secretion, excessive lipid peroxidation, and tissue vitamin E deficiency by T cell receptor peptide treatments in C57BL/6 mice.

To test whether T cell receptor (TCR) peptide treatment can prevent immune dysfunction, excessive lipid peroxidation, and malnutrition caused by retrovirus infection, female C57BL/6 mice were infected with LP-BM5 retrovirus. Infection with retrovirus inhibited lymphocyte proliferation, cytokine release T helper 1 cells, stimulated cytokine secretion by T helper 2 cells, induced abnormal hepatic and cardiac lipid profiles, and produced excessive tissue lipid peroxidation with hepatic and cardiac vitamin E deficiency. Two weeks after infection, TCR peptides Vbeta5.2, Vbeta8.1, Vbeta8.1 + Vbeta5.2, Vbeta8.1(N), and Vbeta8.1 were injected to the mice at dose of 200 microg/mouse. Vbeta8.1 and Vbeta5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-gamma release, and prevented excessive IL-6, IL-10, and TNF-alpha secretion. Concomitantly, these treatments normalized hepatic and cardiac lipid profiles, reduced tissue lipid peroxidation, and thereby significantly maintained vitamin E in the liver and heart. Vbeta8.1 segments treatment did not prevent the immune dysfunction, abnormal lipid profile and lipid peroxidation, and vitamin E deficiency caused by the retrovirus infection. In conclusion, injection of intact TCR peptides during murine retrovirus infection largely prevented immune dysfunction by blocking the excessive stimulation of a T cell subset caused by retroviral superantigens. It also ameliorated malnutrition status by normalizing lipid profile, lipid peroxidation, and vitamin E deficiency. T cell immune dysfunction and its prevention by TCR peptide treatment is important in the therapy of vitamin E deficiency induced by retrovirus infection.

Antioxidant activity of dioscorea and dehydroepiandrosterone (DHEA) in older humans.

Dioscorea is a yam steroid extract used in commercial steroid synthesis and consumed by people. DHEA is a steroid which declines with age, but without known activity. This study was designed to determine whether dioscorea supplementation could increase serum dehydroepiandrosterone sulfate (DHEAS) in humans and modulate lipid levels in older people. The subjects were selected volunteers aged 65-82 years. The serum DHEAS level, lipid peroxidation and lipid profile were assessed. Three weeks of dioscorea supplementation had no affect on serum DHEAS level. However DHEA intake of 85 mg/day increased serum DHEA levels 100.3%. DHEA and dioscorea significantly reduced serum lipid peroxidation, lowered serum triglycerides, phospholipid and increased HDL levels. Both DHEA and the steroid yam extract, dioscorea, have significant activities as antioxidant to modify serum lipid levels.

Vitamins and immunomodulation in AIDS.

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a retrovirus infection and represents the end point in a progressive sequence of immunosuppressive changes. Vitamins can enhance disease resistance in animals and humans. As such they are important co-factors in optimal functioning of the immune systems. In this article, the immunological and nutritional modifications caused by AIDS are summarized. The effects of murine and human retrovirus infection on vitamin status are analyzed as co-factors in the development of severe immune dysfunction, AIDS. The properties of immunoenhancing antioxidative vitamins, vitamin A, B6, B12, C, E, and beta-carotene, which are frequently low in AIDS patients, are evaluated relative to the development of immunodeficiency during retrovirus infection. Vitamin A, E, and B12 deficiency accelerated the development of AIDS with low T cells, whereas their normalization retarded the development of immune dysfunction. The interactions between these vitamins and the immune system in human AIDS patients and animal models of AIDS are reviewed. Our purpose is to provide data on how retrovirus infection can cause nutritional deficiencies that accentuate immune damage and to evaluate the potential therapeutic role of vitamins in the treatment of immune dysfunctions in AIDS patients.

Immunomodulation by pycnogenol in retrovirus-infected or ethanol-fed mice.

Pycnogenol is a commercial mixture of bioflavonoids that exhibits antioxidative activity. The effects of dietary pycnogenol on immune dysfunction in normal mice as well as those fed ethanol or infected with the LP-BM5 murine retrovirus were determined. The ethanol consumption and retrovirus infection caused abnormalities in the function and/or structure of a broad array of cells involved in humoral and cellular immunity. Pycnogenol enhanced in vitro IL-2 production by mitogen-stimulated splenocytes if its production was suppressed in ethanol-fed or retrovirus-infected mice. Mitogenesis of splenocytes did not show a significant change in mice treated with pycnogenol. It reduced the elevated levels of interleukin-6 produced in vitro by cells from retrovirus infected mice and IL-10 secreted by spleen cells from mice consuming ethanol. Natural killer cell cytotoxicity was increased with pycnogenol treatment.