Long-Term Dietary Vitamin E Retards Development of Retrovirus-Induced Disregulation in Cytokine Production

Yuejian Wang, Dennis S. Huang, Cleamond D. Eskelson, Ronald R Watson

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

A 15-fold increase in dietary vitamin E (160 IU/liter) normalized hepatic and serum levels of vitamin E normally reduced by retrovirus infection. It also significantly retarded development of splenomegaly and hypergammaglobulinemia induced by retrovirus infection, while significantly restoring release of interleukin-2 (IL) and interferon-γ by splenocytes which are suppressed by retrovirus infection. Retrovirus infection elevated production of IL-4 and IL-6 by splenocytes, but this elevation was inhibited by vitamin E. Increased levels of IL-6 and tumor necrosis factor-α produced by splenocytes during progression to murine AIDS were also inhibited by vitamin E. Vitamin E supplementation also helped restore retrovirus-suppressed splenocyte proliferation. These data indicate that vitamin E supplementation can help overcome retrovirus-induced reduction in tissue vitamin E, modulate cytokine release, and normalize immune dysfunctions during progression to murine AIDS.

Original languageEnglish (US)
Pages (from-to)70-75
Number of pages6
JournalClinical Immunology and Immunopathology
Volume72
Issue number1
DOIs
StatePublished - Jul 1994

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Retroviridae
Vitamin E
Retroviridae Infections
Cytokines
Interleukin-2
Murine Acquired Immunodeficiency Syndrome
Interleukin-6
Hypergammaglobulinemia
Tocopherols
Splenomegaly
Interleukin-4
Interferons
Tumor Necrosis Factor-alpha
Liver
Serum

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Immunology and Allergy
  • Immunology

Cite this

Long-Term Dietary Vitamin E Retards Development of Retrovirus-Induced Disregulation in Cytokine Production. / Wang, Yuejian; Huang, Dennis S.; Eskelson, Cleamond D.; Watson, Ronald R.

In: Clinical Immunology and Immunopathology, Vol. 72, No. 1, 07.1994, p. 70-75.

Research output: Contribution to journalArticle

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