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Nutritional Immunology

Vitamin A Deficiency Exacerbates Inflammation in a Rat Model of Colitis through Activation of Nuclear Factor-B and Collagen Formation

R. Reifen¹, T. Nur, K. Ghebermeskel^*, G. Zaiger, R. Urizky and M. Pines

School of Nutritional Sciences, The Hebrew University of Jerusalem, Rehovot, Israel; ^* The Institute of Brain Chemistry and Human Nutrition, The University of North London, London, UK; and The Volcani Center, Agricultural Research Organization, Bet Dagan, Israel

¹To whom correspondence should be addressed. E-mail: reifen{at}agri.huji.ac.il.

Inflammatory bowel disease is characterized by oxidative stress, inflammation and tissue damage. Vitamin A is an antioxidant, a regulator of epithelial proliferation and differentiation and vital for optimal immune function. To investigate the effect of vitamin A on the course of colitis, it was induced by administration of trinitrobenzene sulfonic acid (TNBS) into the colons of rats fed for 7 wk vitamin A–deficient (VAD), sufficient (VAS) or supplemented (VASUP) diet, or VAS pair-fed (PF) to the VAD rats. Inflammation and fibrosis were examined by hematoxin and eosin, and Sirius red staining. Activation of nuclear factor-B (NF-B) and oxidative stress were determined by electrophoretic mobility shift and plasma malondialdehyde (MDA) and RBC Cu/Zn-superoxide dismutase activity, respectively. Vitamin A deficiency in the noncolitic rats impaired food consumption and weight gain (P < 0.05) and increased plasma MDA, (P = 0.01) activity of NF-B (P < 0.05) and deposition of collagen in the colon. Our data suggest that vitamin A deficiency induces colonic inflammation. Colitis is amplified by deficiency and ameliorated by supplementation of the vitamin. These findings have implications for the management of inflammatory bowel disease.

KEY WORDS: • vitamin A • colitis • nuclear factor-B • fibrosis • oxidative stress

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