Vitamin A deficiency predisposes to Staphylococcus aureus infection.
Wiedermann U; Tarkowski A; Bremell T; Hanson LA; Kahu H; Dahlgren UI
Infect Immun 1996 Jan;64(1):209-14
We have investigated the consequences
of vitamin A deficiency in a rat model of T-cell-dependent and superantigen-mediated
Staphylococcus aureus arthritis. After intravenous inoculation of enterotoxin
A-producing staphylococci, the vitamin-A-deficient rats showed a decreased
weight gain compared with the paired fed controls despite equal food consumption.
The control rats developed arthritis in the first few days after bacterial
inoculation, with a peak frequency at day 5, and then gradually recovered;
however, the frequency of arthritis 18 days after bacterial inoculation
was 86% among the vitamin A-deficient rats and 44% among the control rats.
During this period, 3 of 10 deficient rats and 1 of 10 control rats died.
Further in vitro analysis revealed that T-cell responses to S. aureus
were significantly higher in the vitamin A-deficient rats than in the
control animals. In contrast, B-cell reactivity, measured as immunoglobulin
levels, autoantibody levels, and specific antibacterial antibody levels
in serum, did not differ between the groups. Interestingly, the innate
host defense mechanisms against S. aureus were also profoundly affected
by vitamin A deficiency. Thus, despite a larger number of circulating
phagocytic cells in the vitamin-A-deficient group, the capacity to phagocytize
and exert intracellular killing of S. aureus was significantly decreased
in comparison with the control rats. Furthermore, serum from the vitamin
A-deficient rats inoculated with Staphylococcus aureus displayed decreased
complement lysis activity. Our results suggest 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, and decreased complement activity.