*Inhalation of Ascorbic Acid Modulates Sinonasal Immune System DOI: http://dx.doi.org/10.5772/intechopen.110891*

ability, and both natural killer cell function and lymphocyte blastogenic responses to T- and B-cell mitogens were returned to normal concentrations after ascorbic acid administration. Although the human researches are supported the effect of ascorbic acid to lymphocyte, it is clear that more human experimental researches are required to validate these researches [14, 22].

Recent study in wild-type and Gulo knockout mice showed that parenteral supplementation of 0.2 g/kg ascorbic acid increased proliferation of regulatory T-cells (Tregs) and suppressed the negative immunoregulation of Tregs (by suppressing the expression of specific transcription factors, antigens, and cytokines) observed in severe infection. The mechanisms depend on the gene regulatory impacts of ascorbic acid. For instance, recent study has involved ascorbic acid in epigenetic modulation via its function as a cofactor for the iron-containing dioxygenases which hydroxylate methylated DNA and histones [14]. The Ten-eleven Translocation (TET) enzymes hydroxylate methylcytosine residues, which may act as epigenetic marks in their own right, and also facilitate removal of the methylated residues, a pivotal step in epigenetic modulation. Preliminary data shows that ascorbic acid can modulate T-cell maturation through epigenetic pathway including the TETs and histone demethylation. It is believed that ascorbic acid function as gene modulatory functions and cell signaling, through modulation of transcription factors and epigenetic marks, have important parts in its immune-regulating functions [14, 15].
