Vitamin C is an essential nutrient that influences several aspects of the immune system, particularly barrier integrity and leukocyte function [45]. The fact that vitamin C is actively accumulated into the epidermal and dermal cells and into leukocytes, via sodium-dependent transporter, suggests that the vitamin plays a crucial role within the skin and the leukocytes [46]. Vitamin C is a potent water-soluble antioxidant and plays an important role in maintaining redox homeostasis within cells and in protecting host cells against the actions of reactive oxygen species (ROS) [45], released by phagocytes in order to lead to the deactivation of viruses and the killing of bacteria. Thus, acid ascorbic as scavenger of ROS may both protect crucial cell structural components and modulate the pro-inflammatory signaling pathway activated by the oxidative burst [46,47]. Vitamin C influences innate immunity also by regulating several aspects of neutrophil function [48], particularly the chemotactic ability, as shown in several in vitro and in vivo animal studies [49,50]. Severe septic syndromes are associated with impaired neutrophil chemotactic ability [51], and studies conducted in children and neonates may suggest that it could be due also by a severe infection-induced status of vitamin C deficiency [52,53]. Furthermore, studies have shown that, in patients with recurrent infections or affected by genetic conditions such as Chediak–Higashi syndrome (CHS), supplementation with vitamin C improved significantly the antibacterial activity of neutrophils [54,55]. Ascorbic acid may also influence the apoptotic process of neutrophils, thus promoting resolution of inflammation and reducing extensive tissue damage [46]. Lastly, promising in vitro and preclinical data suggest that vitamin C supplementation could play a role on more recently discovered functions of neutrophils, such as the formation of neutrophil extracellular traps (NETs), resulting by the release of toxic intracellular components following the necrotic death of neutrophils [56]. Ascorbic acid may attenuate tissue damage reducing the formation of NETs [48].