Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Community-Acquired Pneumonia and LPS-Induced Macrophages

Abstract EN

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.