DNA methylation has been suggested as a regulatory mechanism behind some inflammatory processes. The physiological actions of methyl donors, such as
folic acid,
choline, and
vitamin B12 on
inflammation-related disease have been associated with the synthesis of the universal methyl donor S-adenosyl
methionine (SAM). The aim of this study was to evaluate the effects of
folic acid,
choline,
vitamin B12, and a combination of all on preventing the
lipopolysaccharide- (LPS-) induced inflammatory response in human THP-1 monocyte/macrophage cells.
Folic acid and the mixture of methyl donors reduced
interleukin 1 beta (IL1B) and tumour
necrosis factor (TNF) expression as well as
protein secretion by these cells.
Folic acid and
choline decreased C-C motif
chemokine ligand 2 (CCL2)
mRNA levels. In addition to this, the methyl donor mixture reduced Cluster of differentiation 40 (CD40) expression, but increased
serpin family E member 1 (SERPINE1) expression. All methyl donors increased methylation levels in CpGs located in IL1B, SERPINE1, and
interleukin 18 (
IL18) genes. However, TNF methylation was not modified.
After treatment with
folic acid and the methyl donor mixture, ChIP analysis showed no change in the binding affinity of nuclear factor-κB (NF-κB) to IL1B and TNF promoter regions after the treatment with
folic acid and the methyl donor mixture. The findings of this study suggest that
folic acid might contribute to the control of chronic
inflammation in inflammatory-related disease.