Folate deficiency enhances the inflammatory response of macrophages

Andreas F Kolb, Linda Petrie

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

B-vitamin deficiency is a risk factor for vascular disease. The mechanism by which the deficiency impacts on disease risk is unclear. We have analysed whether the inflammatory response of mononuclear cells can be modified by cellular folate status in vitro.

We show that the mouse monocyte cell line RAW264.7 grown under folate restriction displays a decrease in intracellular folate levels and a reduced growth rate. The cells also show a 2- to 3-fold increase in expression of the inflammatory mediators, IL1ß, IL6, TNFa and MCP1 at the RNA and protein level (p < 0.01) under conditions of folate deficiency. In contrast the production of the vaso-protective mediator nitric oxide is significantly reduced under these conditions. These metabolic changes are independent of the concentration of homocysteine in the medium and occur in the absence of significant changes in global DNA methylation. Folate deficiency may therefore exacerbate cardiovascular disease by augmenting pro-inflammatory signals in the monocyte-macrophage lineage.
Original languageEnglish
Pages (from-to)164-172
Number of pages9
JournalMolecular Immunology
Volume54
Issue number2
DOIs
Publication statusPublished - Jun 2013

Keywords

  • gene expression
  • DNA methylation
  • nitric oxide

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