Writing in the March 1, 2012, issue of The Journal of Immunology, researchers at National Jewish Health in Denver report their discovery of a molecular pathway through which vitamin D inhibits inflammation.
Assistant professor of pediatrics Elena Goleva and her associates cultured human white blood cells with varying amounts of vitamin D or no vitamin D before exposing them to lipopolysaccharide, a pro-inflammatory compound. They found that cells incubated without vitamin D or with a reduced concentration of 15 nanograms per milliliter produced high amounts of the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a), both of which are involved in the inflammatory response. However, white blood cells that received concentrations of 30 nanograms per milliliter or more of vitamin D, which is a level considered by some researchers to be sufficient when measured in the bloodstream, had a decreased inflammatory response, with 50 nanograms per milliliter vitamin D resulting in the greatest reduction. Among other findings, the team observed that vitamin D treatment upregulated the expression of mitogen-activated protein kinase (MAPK) phosphatase-1, which interferes with inflammation. “This study goes beyond previous associations of vitamin D with various health outcomes,” stated Dr Goleva. “It outlines a clear chain of cellular events, from the binding of DNA, through a specific signaling pathway, to the reduction of proteins known to trigger inflammation. Patients with chronic inflammatory diseases, such as asthma, arthritis and prostate cancer, who are vitamin D deficient, may benefit from vitamin D supplementation to get their serum vitamin D levels above 30 nanograms/milliliter.”
“The fact that we showed a dose-dependent and varying response to levels commonly found in humans also adds weight to the argument for vitamin D’s role in immune and inflammatory conditions,” she added.