PMID- 30116142 OWN - NLM STAT- MEDLINE DCOM- 20181211 LR - 20181211 IS - 1466-1861 (Electronic) IS - 0962-9351 (Print) IS - 0962-9351 (Linking) VI - 2018 DP - 2018 TI - Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages. PG - 1312626 LID - 10.1155/2018/1312626 [doi] LID - 1312626 AB - 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 B(12) 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 B(12), 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-kappaB (NF-kappaB) 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. FAU - Samblas, Mirian AU - Samblas M AUID- ORCID: 0000-0003-0866-2300 AD - Department of Nutrition, Food Science, and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, Spain. AD - Centro de Investigacion Biomedica en Red de la Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. FAU - Martinez, J Alfredo AU - Martinez JA AUID- ORCID: 0000-0001-5218-6941 AD - Department of Nutrition, Food Science, and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, Spain. AD - Centro de Investigacion Biomedica en Red de la Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. AD - Instituto de Investigacion Sanitaria de Navarra (IdiSNA), Pamplona, Spain. AD - IMDEA Food, Madrid, Spain. FAU - Milagro, Fermin AU - Milagro F AUID- ORCID: 0000-0002-3228-9916 AD - Department of Nutrition, Food Science, and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, Spain. AD - Centro de Investigacion Biomedica en Red de la Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. LA - eng PT - Journal Article DEP - 20180704 PL - United States TA - Mediators Inflamm JT - Mediators of inflammation JID - 9209001 RN - 0 (Lipopolysaccharides) RN - 0 (NF-kappa B) RN - 935E97BOY8 (Folic Acid) RN - N91BDP6H0X (Choline) RN - P6YC3EG204 (Vitamin B 12) SB - IM MH - Cell Survival MH - Choline/pharmacology MH - CpG Islands MH - DNA Methylation MH - Enzyme-Linked Immunosorbent Assay MH - Folic Acid/*pharmacology MH - Humans MH - *Inflammation MH - Lipopolysaccharides MH - Macrophages/*drug effects/metabolism MH - NF-kappa B/metabolism MH - Promoter Regions, Genetic MH - Protein Binding MH - THP-1 Cells/*cytology MH - Vitamin B 12/pharmacology PMC - PMC6079441 EDAT- 2018/08/18 06:00 MHDA- 2018/12/12 06:00 PMCR- 2018/07/04 CRDT- 2018/08/18 06:00 PHST- 2018/01/16 00:00 [received] PHST- 2018/04/19 00:00 [revised] PHST- 2018/05/16 00:00 [accepted] PHST- 2018/08/18 06:00 [entrez] PHST- 2018/08/18 06:00 [pubmed] PHST- 2018/12/12 06:00 [medline] PHST- 2018/07/04 00:00 [pmc-release] AID - 10.1155/2018/1312626 [doi] PST - epublish SO - Mediators Inflamm. 2018 Jul 4;2018:1312626. doi: 10.1155/2018/1312626. eCollection 2018.