VITAMIN-A-DEFICIENCY PREDISPOSES TO STAPHYLOCOCCUS-AUREUS INFECTION

We have investigated the consequences of vitamin A deficiency in a rat model of T-cell-dependent and superantigen-mediated Staphylococcus au reus arthritis, After intravenous inoculation of enterotoxin A-produci ng staphylococci, the vitamin A-deficient rats showed a decreased weig ht gain compared with the paired fed controls despite equal food consu mption, The control rats developed arthritis in the first few days aft er bacterial inoculation, with a peak frequency at day 5, and then gra dually recovered; however, the frequency of arthritis in the deficient rats increased continuously during the experimental period, The preva lence of arthritis 18 days after bacterial inoculation was 86% among t he vitamin A-deficient rats and 44% among the control rats, During thi s period, 3 of 10 deficient rats and 1 of 10 control rats died, Furthe r in vitro analysis revealed that T-cell responses to S, aureus were s ignificantly higher in the vitamin A-deficient rats than in the contro l animals, In contrast, B-cell reactivity, measured as immunoglobulin levels, autoantibody levels, and specific antibacterial antibody level s in serum, did not differ between the groups, Interestingly, the inna te host defense mechanisms against S, aureus were also profoundly affe cted by vitamin A deficiency, Thus, despite a larger number of circula ting phagocytic cells in the vitamin A-deficient group, the capacity t o phagocytize and exert intracellular killing of S, aureus was signifi cantly decreased in comparison with the control rats, Furthermore, ser um from the vitamin A-deficient rats inoculated with Staphylococcus au reus displayed decreased complement lysis activity, Our results sugges t that the increased susceptibility to S, aureus infection observed in the vitamin A-deficient rats is due to a concerted action of antigen- specific T-cell hyperactivity, impaired function of the phagocytes, an d decreased complement activity.