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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| Language: | English |
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Wiley
2018-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/1312626 |
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| author | Mirian Samblas J. Alfredo Martínez Fermín Milagro |
| author_facet | Mirian Samblas J. Alfredo Martínez Fermín Milagro |
| author_sort | Mirian Samblas |
| collection | DOAJ |
| 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. |
| format | Article |
| id | doaj-art-f882e953b91c4e31ad86e7693c78e754 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-f882e953b91c4e31ad86e7693c78e7542025-08-20T02:22:34ZengWileyMediators 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 |
| spellingShingle | Mirian Samblas J. Alfredo Martínez Fermín Milagro Folic Acid Improves the Inflammatory Response in LPS-Activated THP-1 Macrophages Mediators of Inflammation |
| title | 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_short | 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 |
| url | http://dx.doi.org/10.1155/2018/1312626 |
| work_keys_str_mv | AT miriansamblas folicacidimprovestheinflammatoryresponseinlpsactivatedthp1macrophages AT jalfredomartinez folicacidimprovestheinflammatoryresponseinlpsactivatedthp1macrophages AT ferminmilagro folicacidimprovestheinflammatoryresponseinlpsactivatedthp1macrophages |