Vitamin D Strongly Influences Colonic Gene Regulation

D-hormone and the immune system

Cantorna MT, Mahon BD.

Department of Nutritional Sciences, Pennsylvania State University, University Park, Pennsylvania 16802, USA. mxc69@psu.edu

D-hormone [1,25(OH)2 D3] is an important immune system regulator that has been shown to inhibit development of autoimmune diseases including experimental inflammatory bowel disease (IBD), rheumatoid arthritis (RA), multiple sclerosis (MS), and type 1 diabetes. Paradoxically, other immune mediated diseases (experimental asthma) and immunity to infectious organisms were not found to be affected by D-hormone treatment. The effectiveness of D-hormone treatment of autoimmune diseases is due to inhibition of the development and function of Th1 cells and the induction of other Th cells including Th2 cells. We report results of microarray analysis of colons from D-hormone treated mice with experimental IBD. Two hundred thirty-nine genes were inhibited and 298 genes were upregulated in the colon by D-hormone treatment of mice with IBD. Of interest was the D-hormone mediated inhibition of 3 tumor necrosis factor-alpha (TNF-alpha, lipopolysaccharide-induced TNF-alpha factor, and TNF receptor) related genes in the colon. It is likely that the effectiveness of D-hormone treatment of experimental autoimmunity is due in part to the inhibition of the TNF family of genes. D-hormone is a selective regulator of the immune system, and the outcome of D-hormone treatment depends on the nature (infectious disease, asthma, autoimmune disease, etc.) of the immune response.

That's a lot of gene controlling going on there. Vitamin D works by influencing certain genes to work properly by flipping them on and off.

Also of interest is the inhibition of three tumor necrosis factors. This has huge implications for cancer development and treatment. I wasn't quite sure what TNFs were until I looked it up in Wikipedia:

Tumor necrosis factor (TNF, cachexin or cachectin and formally known as tumor necrosis factor-alpha) is a cytokine involved in systemic inflammation and is a member of a group of cytokines that all stimulate the acute phase reaction.

TNF causes apoptotic cell death, cellular proliferation, differentiation, inflammation, tumorigenesis, and viral replication.

TNF's primary role is in the regulation of immune cells.

Dysregulation and, in particular, overproduction of TNF have been implicated in a variety of human diseases, as well as cancer.

Now, I know I'm no scientist, but Ds ability to regulate TNF production seems like a beneficial activity, at least at first glance. This could be one of the underlying mechanisms of Ds known, powerful anti-inflammatory activity. It seems reasonable to conclude that someone with a chronic inflammatory disease (like is proposed for autism, IBD, etc.) would benefit from the TNF inhibition, and thus inflammatory reduction induced by activated D hormone.