The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression

Mediators Inflamm. 2017:2017:4024672. doi: 10.1155/2017/4024672. Epub 2017 Jan 22.

Abstract

Cellular immunosuppression appears to be involved in sepsis and sepsis-induced multiple organ dysfunction syndrome (MODS). Recent evidence showed that parenteral vitamin C (Vit C) had the ability to attenuate sepsis and sepsis-induced MODS. Herein, we investigated the impact of parenteral Vit C on cellular immunosuppression and the therapeutic value in sepsis. Using cecal ligation and puncture (CLP), sepsis was induced in WT and Gulo-/- mice followed with 200 mg/Kg parenteral Vit C administration. The immunologic functions of CD4+CD25+ regulatory T cells (Tregs) and CD4+CD25- T cells, as well as the organ functions, were determined. Administration of parenteral Vit C per se markedly improved the outcome of sepsis and sepsis-induced MODS of WT and Gulo-/- mice. The negative immunoregulation of Tregs was inhibited, mainly including inhibiting the expression of forkhead helix transcription factor- (Foxp-) 3, cytotoxic T lymphocyte associated antigen- (CTLA-) 4, membrane associated transforming growth factor-β (TGF-βm+), and the secretion of inhibitory cytokines [including TGF-β and interleukin- (IL-) 10], as well as CD4+ T cells-mediated cellular immunosuppression which was improved by parenteral Vit C in WT and Gulo-/- septic mice. These results suggested that parenteral Vit C has the ability to improve the outcome of sepsis and sepsis-induced MODS and is associated with improvement in cellular immunosuppression.

Publication types

  • Retracted Publication

MeSH terms

  • Animals
  • Ascorbic Acid / therapeutic use*
  • CD4-Positive T-Lymphocytes / metabolism
  • CTLA-4 Antigen / metabolism
  • Forkhead Transcription Factors / metabolism
  • Immunosuppression Therapy
  • Interleukin-10 / metabolism
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • L-Gulonolactone Oxidase / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Multiple Organ Failure / drug therapy*
  • Multiple Organ Failure / immunology
  • Multiple Organ Failure / metabolism
  • Sepsis / drug therapy*
  • Sepsis / immunology
  • Sepsis / metabolism
  • Transforming Growth Factor beta / metabolism

Substances

  • CTLA-4 Antigen
  • Forkhead Transcription Factors
  • Interleukin-2 Receptor alpha Subunit
  • Transforming Growth Factor beta
  • Interleukin-10
  • L-Gulonolactone Oxidase
  • Ascorbic Acid