|DURICK, KATHY - UNIV OF NORTH DAKOTA
|TOMITA, MICHIYO - UNIV OF NORTH DAKOTA
|SANTORO, THOMAS - UNIV OF NORTH DAKOTA
|BRADLEY, DAVID - UNIV OF NORTH DAKOTA
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2004
Publication Date: 3/7/2005
Citation: Durick, K.A., Tomita, M., Hunt, C., Bradley, D. 2005. Evidence that boron down-regulates inflammation through the NF-KB pathway [abstract]. The Federation of American Societies for Experimental Biology Journal. 19(5):A1705.
Technical Abstract: We have previously demonstrated that dietary boron supplementation was able to prevent the onset of, and ameliorate ongoing, collagen-induced arthritis, as well as significantly reduce the incidence of experimental autoimmune encephalomyelitis, suggesting that boron has anti-inflammatory properties. However, little is known about the mechanism of boron in immunoregulation despite evidence that boric acid or substituted boric acid compounds competitively inhibit the in vitro activities of NAD+, NADP- and FAD-requiring oxidoreductase enzymes and serine proteases, enzymes with many important regulatory functions in inflammation. We provide evidence here that boron is able to prevent the activation of pro-inflammatory cytokine and transcription factor genes in vitro. A murine macrophage line, J774-A1, was grown in the presence and absence of supplemental boron for a minimum of 5 days then stimulated with LPS before quantification of the activation of pro-inflammation-related genes by RT-PCR.Compared to the LPS-activated boron controls, the LPS-stimulated J774 cells grown in 10 or 100 mmol supplemental boron displayed decreased levels of TNF-alpha (a), IL-1ß, MIP-1a, and iNOS expression. Each of these factors is under NF-kappa (k) B control. The transcription rate of SOD (not under NF-kB regulation) did not change with boron supplementation of the media. These data suggest that boron may down-regulate the inflammation process at a site upstream of cytokine gene activation in the NF-kB regulated pathway.