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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.

Total levels of IgM and secretory IgM as well as specific antibodies to poliovirus type I antigen, Escherichia coli O antigens, and beta-lactoglobulin were measured in unstimulated and stimulated saliva as well as nasal secretion using an enzyme-linked immunosorbent assay (ELISA). The levels of these antibodies in IgA-deficient adults with and without frequent respiratory infections and children under immunosuppressive therapy for malignant disease were compared to those in normal adults and infants 1-7 months of age. The IgA-deficient adults had significantly higher IgM levels (P less than 0.002) than the normal adults as well as higher levels of IgM antibodies to poliovirus type I (P less than 0.05) and E. coli O antigen (P less than 0.002). There was a less pronounced IgM anti-beta-lactoglobulin compensation. Secretory component (SC)-carrying antibodies against all three antigens were lower than in normal adults. The infants studied had levels of IgM in secretions close to those of the normal adults and significantly lower than those of the IgA-deficient adults (P less than 0.001) but with a higher proportion of SC-carrying IgM. The increase in total IgM and specific bacterial and viral IgM antibodies in saliva above that of the normal adults was significant (P less than 0.001-0.005) for those IgA-deficient individuals without, but not for those with, frequent infections. There was, however, no significant difference between the levels in the two groups of IgA-deficient adults.(ABSTRACT TRUNCATED AT 250 WORDS)

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