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

Abstract

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-kappaB (NF-kappaB) 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-kappaB (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.

Activation of retinoic acid receptor‐α favours regulatory T cell induction at the expense of IL‐17‐secreting T helper cell differentiation

“…Vitamin A and its derivatives are capable of ameliorating various models of autoimmunity, including inflammatory bowel disease, rheumatoid arthritis, type 1 diabetes, and experimental encephalomyelitis [6][7][8][9]. Deficiency of vitamin A leads to exacerbation in experimental colitis [10]. Supplementation of vitamin A results in decreased prevalence of diarrhoea in children [11], and retinoids are used in the therapy of rosacea and psoriasis [12].…”

Protective effect of retinoid against endotoxin-induced mastitis in rats

“…Vitamin A deficiency (VAD) heightens inflammatory responses, as manifested by an increase in the number of circulating leukocytes, enhanced T-cell proliferation and release of nitric oxide from peritoneal phagocytes [11]. In 2002, Reifen demonstrated that colitis was amplified by VAD and ameliorated by retinoid supplementation [12].…”

All-transRetinoic Acid Inhibits Type 1 Diabetes by T Regulatory (Treg)-Dependent Suppression of Interferon-γ–Producing T-cells Without Affecting Th17 Cells

“…Both vitamin A and ATRA have important immune modulatory functions. For example, vitamin A deficiency can lead to exacerbation of experimental autoimmune colitis (10), as well as an excess of Th1 and a reduction of Th2 cell responses in animals with parasite infection (11). Supplementation of vitamin A to animals results in a decrease in serum pro-inflammatory cytokines, including tumor necrosis factor-␣ and IFN-␥, and an increase in the immunosuppressive cytokine IL-10 (12,13).…”