Multi-omics profiling reveals Poria cocos polysaccharides mitigate PEDV-induced intestinal injury by modulating lipid metabolism in piglets.

BACKGROUND

Porcine epidemic diarrhea virus (PEDV) infection poses a significant challenge to the swine industry, with limited effective control measures available. Poria cocos polysaccharides (PCP) is the primary active ingredient of Poria cocos, and has been demonstrated to show beneficial effects on intestinal damage in previous studies. However, its mechanism has not been fully understood. In the present study, 18 seven-day-old piglets were divided into 3 groups: Control group, PEDV group, and PCP + PEDV group. After three days of adaptation, piglets in the PCP + PEDV group were orally administered 10 mg/kg body weight/d PCP from d 4 to 10. On d 8, piglets were orally administered with PEDV at the dose of 10 TCID/piglet. This study aimed to investigate the potential effects of PCP on PEDV-induced intestinal injury and explored the underlying mechanisms.

RESULTS

The results showed that PCP administration effectively alleviated diarrhea, reduced PEDV replication in the small intestine and colon of piglets, and significantly improved intestinal mucosal morphology. Specifically, PCP increased the villus height in both the jejunum and ileum and increased the villus height to crypt depth ratio in the ileum (P < 0.05). Improved intestinal function was further evidenced by elevated plasma D-xylose levels and decreased diamine oxidase activity (P < 0.05). Transcriptomic and proteomic analyses revealed that lipid metabolism is a key pathway regulated by PCP during PEDV infection. Notably, PCP significantly upregulated sphingolipid metabolism-related genes, including ectonucleotide pyrophosphatase/phosphodiesterase family member 7 and N-acylsphingosine amidohydrolase 2. Metabolomic analysis revealed that PCP primarily modulated the levels of plasmanylphosphoethanolamine, lysophosphatidylcholine, and carnitine. Additionally, PCP reversed the expression of key genes involved in fatty acid uptake, intracellular lipid transport, and fatty acid synthesis, such as fatty acid binding protein 2, fatty acid transport protein 4, apolipoprotein B, apolipoprotein C3, fatty acid synthase, long-chain fatty acyl CoA synthetase 3, lipoprotein lipase and acyl-CoA thioesterases 12 (P < 0.05).

CONCLUSIONS

These findings demonstrate that PCP mitigates PEDV-induced intestinal injury by modulating lipid metabolism and highlight its potential as a dietary supplement for enhancing anti-PEDV defenses and promoting intestinal health in piglets.