Inoculation of weaned pigs with E. coli reduces depots of vitamin E

Summary

This study was designed to investigate the effect of vitamin E supplementation on vitamin E depots and immune responses in weaned pigs after an E. coli inoculation. The design was a 2×2 factorial with vitamin E supplementation (150 mg/kg RRR-α-tocopheryl acetate versus a control diet containing 60 mg all-rac-α-tocopheryl acetate) and E. coli 0 149 inoculation (inoculation of 1×108 CFU on day 2 and 3 after weaning versus inoculation of vehicle). The pigs were housed individually during the experiment which lasted for 10 days from weaning at 7 weeks of age. Blood was sampled on day 1 (day of weaning) and 9 of the experiment, and serum was analyzed for α-tocopherol concentration. On day 10 of the experiment, pigs were killed and samples of liver, heart, muscle, adipose tissue and intestinal epithelium were obtained, and immune cells (alveolar macrophages) were harvested, and analyzed for α-tocopherol concentration. Immune cells were furthermore analyzed for PGE2 synthesis after in vitro stimulation. The concentration of IgA and IgM was analyzed in samples obtained from the bile, and in mucosal and intestinal content from three sites of the intestine. The results showed that E. coli inoculation reduced the concentration of liver α-tocopherol with 30–37%, increased the concentration of IgA in bile, and reduced the concentration of IgM in intestinal content of pigs. The vitamin E supplementation increased the concentration of α-tocopherol in serum, organs and tissue samples except the adipose tissue. The stereoisomer composition of α-tocopherol in serum, liver and immune cells was highly influenced by the dietary provision of natural vitamin E. In conclusion, dietary natural vitamin E supplementation increased the
α-tocopherol depots of the pigs, and notably the RRR-form of α-tocopherol, but had no influence on the measured immune responses. Irrespective of dietary supplementation with vitamin E, short-term inoculation of pigs with E. coli led to a decreased liver α-tocopherol status.