Enteral Vitamin E Supplementation Inhibits the Cytokine Response to Endotoxin

Abstract

Our data demonstrate that a short-term, high-dose enteral supplementation of vitamin E can modulate the monocyte and macrophage response to endotoxin. These data, along with other animal studies showing a protective effect of vitamin E treatment in sepsis and ischemia-reperfusion injury, suggest a potential role for vitamin E supplementation in patients at risk of the systemic inflammatory response syndrome.

Vitamin E and omega-3 fatty acids independently attenuate plasma concentrations of proinflammatory cytokines and prostaglandin E2 in Escherichia coli lipopolysaccharide-challenged growing–finishing pigs1

“…Conversion of the 18-carbon n-6 fatty acid arachidonic acid into PGE 2 is facilitated by transcription of cyclooxygenase-2 (COX-2) on signaling mechanisms through proinflammatory cytokines such as TNF-α or IL-1β (Rivest, 2010;Kalinski, 2012). In a study using LPS-stimulated rats, 100 mg of Vit E supplementation depressed TNF-α production in peritoneal macrophages and the degree of TNF-α suppression was correlated to serum Vit E levels (Bulger et al, 1997). A mouse study also demonstrated that 500 mg Vit E supplementation reduced age-related ex vivo production of PGE 2 in a spleen homogenate (Meydani et al, 1986;Wu et al, 1998).…”

Randomized, Prospective Trial of Antioxidant Supplementation in Critically Ill Surgical Patients

“…Additionally, extensive in vitro data support the relationship between oxidative stress and the induction of genes integral to the systemic inflammatory response, including TNF-␣, IL-1, IL-8, and ICAM-1, putatively mediated through activation of the nuclear transcription factor NF-B. 2,31,32 Several in vivo studies document a clear benefit to antioxidant supplementation in animal models of endotoxemia, ARDS, and reperfusion injury 4,5,[33][34][35][36][37] and have confirmed that there is a relationship between oxidative stress and NF-B activation in vivo. 4 The importance of oxidative stress in the early phases of critical illness is underscored by the relative antioxidant depletion reported in many observational studies of this population.…”

Vitamin E-Coated Dialyzer Membranes Downregulate Expression of Monocyte Adhesion and Co-Stimulatory Molecules

“…In vitro and in vivo this vitamin is able to modify monocyte cytokine production [12,13] . The randomized controlled trial SPACE suggested a potential benefi t of vitamin E on the incidence of cardiovascular events in hemodialysis patients [14] .…”