Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages

• Published in: Mediators of inflammation Vol. 2018; no. 2018; pp. 1 - 8
• Main Authors: Samblas, Mirian, Milagro, Fermín I., Martínez, J. Alfredo
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01-01-2018; Hindawi; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: Analysis; Biochemistry; CD40 antigen; Cell culture; Cell Survival; Choline; Choline - pharmacology; Control equipment industry; CpG Islands; Cytokines; Deoxyribonucleic acid; Diet; Disease; DNA; DNA Methylation; Enzyme-Linked Immunosorbent Assay; Epigenetics; Folic acid; Folic Acid - pharmacology; Gene expression; Genes; Hepatology; Homeostasis; Humans; Hypertension; Immunology; Inflammation; Inflammatory diseases; Interleukin 1; Interleukin 18; Lipopolysaccharides; Macrophages; Macrophages - drug effects; Macrophages - metabolism; Metabolism; Methionine; Methylation; Mitogens; Monocyte chemoattractant protein 1; Monocytes; mRNA; NF-kappa B - metabolism; NF-κB protein; Nutrition; Promoter Regions, Genetic; Protein Binding; RNA; Rodents; Signal transduction; THP-1 Cells - cytology; Tumor necrosis factor; Tumors; Vitamin B; Vitamin B 12 - pharmacology; Vitamin B12; Canada; United States; Spain; United States > US
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1155/2018/1312626

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.