Vitamin a Deficiency Increases Inflammatory Responses

Abstract

The authors studied the influence of vitamin A deficiency on immediate and delayed type hypersensitivity as well as granulocyte-mediated inflammatory reactions in vitamin A depleted and control rats. The number of circulating leucocytes was 43% higher in the vitamin A deficient than in the control animals. The leucocytosis was a result of a general increase of white blood cells and was not due to an increase in one particular type. The ratio between CD4+ and CD8+ T cells was unchanged. The vitamin A deficient rats had a four times higher T-cell proliferative response and a two times higher interferon-gamma production in vitro than the control animals. In accordance, the DTH reaction was consistently higher in the vitamin A deficient rats. The granulocyte dependent inflammation, induced by olive oil injection, was also strongly enhanced in the vitamin A deficient rats compared with the controls. In addition, the spontaneous release of nitric oxide from the peritoneal phagocytes was five times higher in the vitamin A deficient animals. The number of peritoneal mast cells was about one and a half times higher in the vitamin A deficient than in the control animals. The density of IgE-receptors on the mast cells, the IgE receptor occupancy and the histamine release from the mast cells did not differ between the groups, however. The vitamin A deficient immunized rats displayed a consistently stronger immediate skin reaction after intracutaneous antigen injection than the immunized control rats, despite lower IgE antibody levels. The skin reaction after intracutaneous injection of histamine was also significantly greater in the deficient animals. Despite the stronger reaction to antigen and histamine, the passive cutaneous anaphylaxis reaction was lower in the vitamin A deficient rats. In conclusion the study shows that vitamin A deficiency aggravates the clinical manifestations of inflammatory reactions. Thus, vitamin A deficiency might lead to a higher risk of acquiring irreversible tissue damage and disabling destruction.

Vitamin A as an anti-inflammatory agent

“…Both tumour necrosis factor α and NO were higher in our study in the VAD group; these inflammatory markers increased when insufficient amounts of VA were available. These findings are in agreement with those of previous studies that have demonstrated an anti-inflammatory effect of VA and an increase in the inflammatory process during VAD (Sharma et al 1990;Wiedermann et al 1996). Our data are also consistent with those from a human study documenting an increased risk for chronic obstructive lung disease with decreased VA intake and an inverse relationship between plasma retinol status and the extent of airway obstruction assessed by forced expiratory volume (Morabia et al 1990).…”

A CYP26B1 Polymorphism Enhances Retinoic Acid Catabolism and May Aggravate Atherosclerosis

“…Retinoids are major regulators of both inflammation and cholesterol flux (9), and increased systemic and local retinoid levels promote antiinflammatory immunity, including differentiation of regulatory T cells, and reduce inflammation (8,40). Levels of atRA are tightly regulated by enzymes in the CYP26 family (41), and our finding of CYP26B1 expression inside human atherosclerotic lesions implies that atRA levels are regulated locally in the vessel wall.…”

Effect of vitamin A deficiency on the immune response in obesity

“…In animal models, vitamin A deficiency shifts from a Th2 response to a Th1 response, decreasing antibody production and Ig maturation (21) . This increase in the inflammatory response is due to a higher production of IFN-g by T lymphocytes (101,102) . In addition to its effect on the T-cells response, vitamin A deficiency also diminishes the activity of neutrophils, macrophages and natural killer cells (1,3,103) .…”