Dietary 25-Hydroxyvitamin D(3) Supplementation Alleviates Porcine Epidemic Diarrhea Virus Infection by Improving Intestinal Structure and Immune Response in Weaned Pigs

SIMPLE SUMMARY: Porcine epidemic diarrhea is one of the major problems in current swine husbandry worldwide, and effective measures for prevention and treatment are scarce. We found that high dose 25-hydroxyvitamin D(3) supplementation could ease intestinal injury and inhibit intestinal immune response induced by porcine epidemic diarrhea virus (PEDV), suggesting that feeding a high dose of 25-hydroxyvitamin D(3) could be used as an approach against PEDV infection. ABSTRACT: We conducted this experiment to determine if feeding 25-hydroxyvitamin D(3) (25(OH)D(3)) to weaned pigs would alleviate porcine epidemic diarrhea virus (PEDV) infection and immune response. Forty-two weaned pigs were allotted to 1 of 6 dietary 25(OH)D(3) treatments (5.5, 5.5, 43.0, 80.5, 118.0, 155.5 μg 25(OH)D(3)/kg diet) for 26 days. On day 22 of the trial, all the treatments were orally administrated with PEDV except for one of the 5.5 μg 25(OH)D(3)/kg treatments, which was challenged with the same volume of sterile saline and served as control. Another 5.5 μg 25(OH)D(3)/kg group for PEDV challenge was named CON-PEDV. Average daily gain (p < 0.05) was reduced by PEDV infection. PEDV administration also induced severe diarrhea (p < 0.05), reduction of villous height and the ratio of villous height to crypt depth, and increase of crypt depth and serum diamine oxidase activity (p < 0.05). Serum IgM and complement component 4 levels were increased by PEDV challenge. However, 155.5 μg 25(OH)D(3)/kg supplementation alleviated intestinal damage (p < 0.05) compared with CON-PEDV. Furthermore, 155.5 μg 25(OH)D(3)/kg supplementation downregulated the mRNA abundance of inflammatory cytokines and interferon signal pathway-related genes (p < 0.05) compared with CON-PEDV. These results suggested that dietary supplementation of 155.5 μg 25(OH)D(3)/kg could alleviate intestinal damage and protect against PEDV-induced inflammatory status.