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A tributyrin-monolaurin complex protects piglets against PEDV infection via viral inhibition, lipid metabolism restoration, and microbiota modulation
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DOI：10.1016/j.aninu.2026.04.006.png)
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Abstract
En 中文
Porcine epidemic diarrhea virus (PEDV) is a major pathogen causing severe diarrhea and intestinal damage in piglets. Monolaurin (GML) and tributyrin (TB) are well-documented functional lipids with intestinal health benefits, but their combined efficacy against PEDV infection remains unclear. The present study first investigated the anti-PEDV effect of GML, TB, and their mixtures using PEDV-infected Vero cells. Then, the effects of a microencapsulated TB-GML complex (PE) were evaluated in PEDV-infected piglets, focusing on its protective mechanisms. Vero cells were simultaneously treated with PEDV and graded concentrations of GML (20-40 μmol/L), TB (0.25-0.50 mmol/L), or their combinations to determine for synergistic antiviral effects. In vivo, a total of 30 piglets (2.49 ± 0.38 kg), 7-d-old, were randomly assigned to three groups: negative control (NC), PEDV, and PE + PEDV. After a 3-d adaptation period, piglets in the PE + PEDV group received an oral dose of PE at 100 mg/kg body weight for 7 consecutive days. On d 8, piglets in the PEDV and PE + PEDV groups were orally inoculated with 1 × 106 50% tissue culture infective dose (TCID50) of PEDV per piglet. The experiment lasted for 11 d. The results showed that 40 μmol/L GML alone, or 0.25 mmol/L TB combined with 20-40 μmol/L GML, suppressed virus replication (P = 0.023). The PE administration improved villus morphology and increased expression of genes involved in water and ion transport in the jejunum, including AQP10, KCNJ13, NHE2, and NHE3 (P < 0.05). Additionally, PE reduced serum interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) levels, and downregulated jejunal relative mRNA expression of inflammation-related genes, mainly IL-8, IL-1β, and CXCL2 (P < 0.05). The PE reversed the enhanced antioxidant stress response in the jejunum by reducing total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and myeloperoxidase (MPO) activities (P < 0.05). The PE inhibited PEDV replication, downregulated relative mRNA expression of IFN-β and its downstream genes, and reduced protein abundance of PEDV-N (P < 0.05). Transcriptomic and quantitative real-time PCR (RT-qPCR) analyses revealed that PE restored lipid metabolic homeostasis by balancing lipogenesis, lipid transport, and fatty acid β-oxidation. Moreover, PE increased the abundance of Proteobacteria, Bacteroidota, Bacteroides, and Halomonas, while decreasing the abundance of Firmicutes and Lactobacillus. In conclusion, PE mitigated inflammation, enhanced antioxidant and antiviral capacities, while alleviating disruptions in water and ion transport, lipid metabolism, and gut microbiota.
Keywords:
Tributyrin
Monolaurin
Porcine epidemic diarrhea virus
Piglet
Lipid metabolism
Gut microbiota
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