2 APRIL 2001
Contact: Barbara Hale
University Park, Pa. – Experiments with human cells conducted by Penn State researchers have shed new light on vitamin A's role in the immune response, suggesting that the vitamin's active form may enhance the effectiveness of interferon, one of the body's natural defense chemicals and an immune system regulator.
Dr. Catharine Ross, who holds the Dorothy Foehr Huck Chair in nutrition in Penn State's College of Health and Human Development, led the research effort. "There are quite a few animal studies that show that vitamin A deficiency affects inflammation and the immune system's response," she says. "These new data from experiments with human cells suggest that vitamin A augments natural interferon's regulatory response. Less interferon may be necessary when the active form of vitamin A is adequate."
In autoimmune diseases, the victim's immune system overreacts and attacks the body. For example, in multiple sclerosis, the immune system attacks the brain and spinal cord. In arthritis, the joints are attacked and in inflammatory bowel disease, the gut is the target. Modified forms of interferon are currently being used to treat various autoimmune diseases such as multiple sclerosis, arthritis, inflammatory bowel disease, or chronic inflammation. Ross speculates that the new data suggest that maintaining a person's normal levels of vitamin A may enhance the effectiveness of the form of interferon that is already in use as a medicine.
The research was presented today (April 2) at the Experimental Biology 2001 conference in Orlando, Fla., by Dr. Qiuyan Chen, research associate, who is first author of the Penn State's team's paper. The paper is titled, "Effect of retinoic acid in lipopolysaccharide (LPS) and cytokine induced signal transducers and activators of transcription-1 (STAT-1) activation and expression in human THP-1 monocytic cells." The co-authors are Yifan Ma, a graduate fellow and research assistant, and Dr. Ross.
In the Penn State experiments, human cells, called macrophages, that are the first step in antibody production as well as potent mediators in the inflammatory response, were stimulated under both vitamin A deficient and sufficient conditions.
Dr. Chen says, "The cells were deficient in vitamin A at the outset when we observed their response to inflammatory stimuli. Then, we gave them a normal physiological level of retinoic acid, the form in which vitamin A is active in the body, and observed an enhanced activity of the interferon."
The experiments also showed that the presence of retinoic acid can inhibit other known inflammatory and immune response mediators, including tumor necrosis factor (TNF).
Dr. Ross explains, "We're looking at these basic cellular processes in order to understand the mechanisms of productive immune responses and to try to find ways to control the pathologic responses. While these basic studies are not targeted at specific diseases, they do shed light on the underlying disease processes.
continue to follow their personal physician's advice," she adds. "Vitamin
A is a potent drug as well as a nutrient."
The Penn State team's research is supported in part by a grant from the National Institutes of Health Institute of Diabetes, Digestive and Kidney Disease.
EDITORS: Dr. Ross is at (814) 865-4721 or firstname.lastname@example.org by email.