Acetylsalicylic acid supplementation improves protein utilization efficiency while vitamin E supplementation reduces markers of the inflammatory response in weaned pigs challenged with enterotoxigenic .

Background: This experiment was conducted to test the hypothesis that vitamin E (Vit E) and acetylsalicylic acid (ASA), a cyclooxygenase-2 (COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E (PGE) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of .

Methods: The experiment was conducted in a research facility with 192 individually-housed male weaner pigs (Landrace × Large White) weighing 6.6 ± 0.04 kg (mean ± SEM). The pigs were experimentally infected with an enterotoxigenic strain of and were allocated to a 2 × 3 factorial design with the respective factors being without and with 125 ppm ASA and three levels of Vit E supplementation (50, 100 or 200 IU/kg diet, -α-tocopheryl acetate).

Results: Acetylsalicylic acid supplementation improved average daily gain ( 0.05) and tended to improve feed:gain ratio ( 0.10) during the first 14 d after weaning. Acetylsalicylic acid supplementation also improved ( < 0.001) amino acid utilization efficiency (as assessed by plasma urea level) and tended to decrease ( < 0.10) PGE production in the liver without affecting small intestinal histology and tight junction protein mRNA expression in the jejunal epithelium. Vitamin E supplementation greater than 100 IU/kg diet sustained both the plasma Vit E concentration ( < 0.001) and plasma haptoglobin content ( < 0.001) after weaning. However, there was no additive effects of the combined supplementation of ASA and Vit E on performance, intestinal barrier function and inflammatory responses of weaned pigs.

Conclusions: Although ASA and vitamin E improved amino acid utilization efficiency and reduced acute inflammatory responses, ASA and vitamin E did not additively reduce production of PGE and inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of .