The Journal of nutrition · 2025
Niacin Inhibits Viral Replication and Alleviates the Intestinal Injury in Piglets Infected with Porcine Epidemic Diarrhea Virus by Regulating the Host Immune Responses.
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Wu Mengjun, Zhang Zhiwei, Wang Yujie, Zhang Qian, Li Peng, Song Zhuan, Wang Lei, Zhao Di, Wu Tao, Yi Dan, Hou Yongqing
Аннотация
BACKGROUND: Porcine epidemic diarrhea virus (PEDV) poses a significant threat to the global pig industry. Niacin (NA) may play an important role in improving intestinal health in piglets.
OBJECTIVE: The present study aimed to investigate the effects of NA supplementation on growth performance and intestinal health in young piglets infected with PEDV.
METHODS: Forty 7-d-old healthy piglets were randomly assigned to 4 groups: control, NA, PEDV, and PEDV+NA. After 3 d of adaptation, piglets in the NA and PEDV+NA groups were orally administered NA at 30 mg/kg body weight from day 4 to 11. On day 9, piglets in the PEDV and PEDV+NA groups were orally inoculated with PEDV at a dose of 104.5 TCID50. On day 12, tissue samples were collected following euthanasia and exsanguination. Intestinal injury was confirmed by the determination of intestinal villus height (VH), crypt depth (CD), as well as plasma diamine oxidase (DAO) and D-xylose concentration. qPCR was performed to evaluate the viral load. Western blot analysis was employed to investigate the intestinal immune response. Data were analyzed by 2-way analysis of variance, with PEDV and NA as factors.
RESULTS: NA administration improved average daily gain and mitigated intestinal injury in PEDV-infected piglets, as indicated by reduced CD and increased VH/CD ratios in the duodenum, jejunum, and colon, along with decreased plasma DAO levels (P < 0.05). NA significantly inhibited the expression of PEDV M and N genes in both the jejunum and ileum (P < 0.01). Moreover, NA reduced the protein abundance of interferon-stimulated genes, including interferon-stimulated gene 15 (ISG15), 2'-5'-oligoadenylate synthetase-like protein (OASL), and myxovirus resistance 1 (MX1), in the intestines of PEDV-infected piglets (P < 0.05).
CONCLUSIONS: The results suggest that NA could inhibit viral replication and alleviate the intestinal injury in PEDV-infected piglets by regulating host immune responses.
OBJECTIVE: The present study aimed to investigate the effects of NA supplementation on growth performance and intestinal health in young piglets infected with PEDV.
METHODS: Forty 7-d-old healthy piglets were randomly assigned to 4 groups: control, NA, PEDV, and PEDV+NA. After 3 d of adaptation, piglets in the NA and PEDV+NA groups were orally administered NA at 30 mg/kg body weight from day 4 to 11. On day 9, piglets in the PEDV and PEDV+NA groups were orally inoculated with PEDV at a dose of 104.5 TCID50. On day 12, tissue samples were collected following euthanasia and exsanguination. Intestinal injury was confirmed by the determination of intestinal villus height (VH), crypt depth (CD), as well as plasma diamine oxidase (DAO) and D-xylose concentration. qPCR was performed to evaluate the viral load. Western blot analysis was employed to investigate the intestinal immune response. Data were analyzed by 2-way analysis of variance, with PEDV and NA as factors.
RESULTS: NA administration improved average daily gain and mitigated intestinal injury in PEDV-infected piglets, as indicated by reduced CD and increased VH/CD ratios in the duodenum, jejunum, and colon, along with decreased plasma DAO levels (P < 0.05). NA significantly inhibited the expression of PEDV M and N genes in both the jejunum and ileum (P < 0.01). Moreover, NA reduced the protein abundance of interferon-stimulated genes, including interferon-stimulated gene 15 (ISG15), 2'-5'-oligoadenylate synthetase-like protein (OASL), and myxovirus resistance 1 (MX1), in the intestines of PEDV-infected piglets (P < 0.05).
CONCLUSIONS: The results suggest that NA could inhibit viral replication and alleviate the intestinal injury in PEDV-infected piglets by regulating host immune responses.