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.
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Contact: Barbara Hale
bah@psu.edu
814-865-9481
Penn State
1-Apr-2001