Different signals induce mast cell inflammatory activity: inhibitory effect of Vitamin E

Abstract

Vitamin supplementation in disease reduces morbidity and mortality in humans by promoting the activation of different genes which influence several pathways. The purpose of this article is to clarify the role of vitamin E in mast cell inflammation. Vitamin E is a fat soluble antioxidant which protects from low-density lipoprotein (LDL) oxidation. Vitamin E promotes a barrier function and anti-inflammatory responses by binding the regulatory domain of protein kinase Cα (pkcα) (a regulator and antagonist of heart failure) and decreases the activation of NF-қb, a proinflammatory transcription factor, causing the generation of cytokines/chemokines and mast cell activation. Mast cells participate in innate and acquired immunity and inflammation. Several factors, including cytokines and chemokines, regulate the development and migration of activated mast cells. Mast cells generate and release inflammatory compounds in asthma and allergic diseases and have a detrimental effect on the vessel wall, which can be inhibited by vitamin E. Vitamin E inhibits histamine release generated in activated mast cells, increases calcium Ca2+ uptake and prevents the oxidation of unsaturated fatty acids. Vitamin E is relatively non-toxic, however, administered at very high doses may suppress normal hematological response as well as causing other adverse effects. Therefore, vitamin E may be beneficial in the prevention of diseases mediated by mast cells and can have special value in the treatment of asthma and allergic diseases; however, the exact mechanism by which vitamin E acts is still unclear, thus warranting future research