ArticleBMC microbiology2026
Multi-omics analysis reveals that glyceryl monooleate mitigates PEDV-induced intestinal injury in piglets.
Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Correction: Multi-omics analysis reveals that glycerylmonooleate mitigates PEDV-induced intestinal injury in piglets.BMC microbiology · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
This study investigated the protective effects of glyceryl monooleate (GM) against porcine epidemic diarrhea virus (PEDV)-induced intestinal injury in neonatal piglets. In vitro assays revealed that GM inhibited PEDV replication. Twenty-four seven-day-old piglets were assigned to four groups: control, GM, PEDV, and PEDV + GM. Piglets received 100 mg/kg GM from days 4–10 and were challenged with 10⁶ TCID50 PEDV on day 8. Samples collected on day 11 were analyzed for intestinal morphology, oxidative stress, inflammation, and microbiota composition. PEDV infection significantly impaired growth performance and disrupted intestinal integrity, as shown by reduced villus height, increased crypt depth, and decreased plasma D-xylose levels (P < 0.05). It also induced oxidative stress, elevated plasma malondialdehyde (MDA), hydrogen peroxide (H2O2), and myeloperoxidase (MPO) levels, and activated inflammatory responses through the TNF-α signaling pathway, increasing interferon regulatory factor 7 (IRF7), myxovirus resistance protein 1 (MX1), interferon-stimulated gene 15 (ISG15), and tumor necrosis factor-α (TNF-α) expression (P < 0.05). Gut microbiota analysis revealed an increased abundance of Fusobacterium, Collinsella, and Campylobacter, and a reduction in Bacteroidetes and Allelobacterium (P < 0.05). GM supplementation alleviated PEDV-induced intestinal injury by improving villus height, reducing crypt depth, and enhancing antioxidant capacity through increased catalase (CAT) and total superoxide dismutase (T-SOD) activities (P < 0.05). It also suppressed viral replication and inflammatory signaling, downregulating TNF-α–related genes and cytokines (IRF7, MX1, ISG15, 2’-5’-oligoadenylate synthetase like (OASL), TNF-α, and CXCligand2 (CXCL2) expression, and plasma interleukin-1β (IL-1β) and TNF-α concentrations), and restored microbial balance by reducing pathogenic bacteria such as Escherichia coli and Shigella (P < 0.05). Collectively, these results indicate that GM protects against PEDV-induced intestinal damage by inhibiting viral replication, enhancing antioxidant defenses, modulating inflammatory pathways, and maintaining gut microbial homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.