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

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 m...

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Main Authors: Mirian Samblas, J. Alfredo Martínez, Fermín Milagro
Format: Article
Language:English
Published: Hindawi Limited 2018-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2018/1312626
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spelling doaj-f882e953b91c4e31ad86e7693c78e7542020-11-25T01:41:02ZengHindawi LimitedMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/13126261312626Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 MacrophagesMirian Samblas0J. Alfredo Martínez1Fermín Milagro2Department of Nutrition, Food Science, and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, SpainDepartment of Nutrition, Food Science, and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, SpainDepartment of Nutrition, Food Science, and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, SpainDNA 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.http://dx.doi.org/10.1155/2018/1312626
collection DOAJ
language English
format Article
sources DOAJ
author Mirian Samblas
J. Alfredo Martínez
Fermín Milagro
spellingShingle Mirian Samblas
J. Alfredo Martínez
Fermín Milagro
Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages
Mediators of Inflammation
author_facet Mirian Samblas
J. Alfredo Martínez
Fermín Milagro
author_sort Mirian Samblas
title Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages
title_short Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages
title_full Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages
title_fullStr Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages
title_full_unstemmed Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages
title_sort folic acid improves the inflammatory response in lps-activated thp-1 macrophages
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2018-01-01
description 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.
url http://dx.doi.org/10.1155/2018/1312626
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