Vitamin C mitigates oxidative stress and tumor necrosis factor-alpha in severe community-acquired pneumonia and LPS-induced macrophages

Mediators Inflamm. 2014:2014:426740. doi: 10.1155/2014/426740. Epub 2014 Sep 1.

Abstract

Oxidative stress is an important part of host innate immune response to foreign pathogens. However, the impact of vitamin C on oxidative stress and inflammation remains unclear in community-acquired pneumonia (CAP). We aimed to determine the effect of vitamin C on oxidative stress and inflammation. CAP patients were enrolled. Reactive oxygen species (ROS), DNA damage, superoxide dismutases (SOD) activity, tumor necrosis factor-alpha (TNF-α), and IL-6 were analyzed in CAP patients and LPS-stimulated macrophages cells. MH-S cells were transfected with RFP-LC3 plasmids. Autophagy was measured in LPS-stimulated macrophages cells. Severe CAP patients showed significantly increased ROS, DNA damage, TNF-α, and IL-6. SOD was significantly decreased in severe CAP. Vitamin C significantly decreased ROS, DNA damage, TNF-α, and IL-6. Vitamin C inhibited LPS-induced ROS, DNA damage, TNF-α, IL-6, and p38 in macrophages cells. Vitamin C inhibited autophagy in LPS-induced macrophages cells. These findings indicated that severe CAP exhibited significantly increased oxidative stress, DNA damage, and proinflammatory mediator. Vitamin C mitigated oxidative stress and proinflammatory mediator suggesting a possible mechanism for vitamin C in severe CAP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Animals
  • Ascorbic Acid / pharmacology*
  • Blotting, Western
  • Cell Line
  • Cell Survival / drug effects
  • Female
  • Humans
  • In Vitro Techniques
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology*
  • Lung / drug effects
  • Lung / metabolism
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Male
  • Mice
  • Middle Aged
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • Ascorbic Acid