Vitamin A deficiency increases inflammatory responses.
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.
Wiedermann
U
U
Department of Clinical Immunology, University of Göteborg, Sweden.
Chen
X J
XJ
Enerbäck
L
L
Hanson
L A
LA
Kahu
H
H
Dahlgren
U I
UI
D000818:Animals; D002452:Cell Count; D002455:Cell Division; D002478:Cells, Cultured; D006632:Histamine / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000276:immunology; D007249:Inflammation / Q000276:immunology*; D007371:Interferon-gamma / Q000276:immunology; D007958:Leukocyte Count; D018655:Lymphocyte Count; D008297:Male; D008407:Mast Cells / Q000166:cytology / Q000276:immunology; D009504:Neutrophils / Q000276:immunology*; D009569:Nitric Oxide / Q000276:immunology; D051381:Rats; D017208:Rats, Wistar; D017455:Receptors, IgE; D013154:Spleen / Q000166:cytology / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology; D014801:Vitamin A / Q000097:blood; D014802:Vitamin A Deficiency / Q000276:immunology*
D017455:Receptors, IgE; D014801:Vitamin A; D009569:Nitric Oxide; D007073:Immunoglobulin E; D006632:Histamine; D007371:Interferon-gamma