Nature Communications· 2026Q1
Small extracellular vesicle-mediated epithelial–macrophage crosstalk contributes to macrophage dysfunction during PEDV infection
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- 2026year
Short summary
Porcine epidemic diarrhea virus (PEDV) hijacks epithelial small extracellular vesicles (sEVs) to deliver miR-190a and TS2083 to macrophages, impairing their migration and phagocytosis.
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Key points
- PEDV infection leads to epithelial cells releasing sEVs enriched in immunoregulatory noncoding RNAs.
- miR-190a within sEVs targets TMOD3, disrupting macrophage migration.
- TS2083 within sEVs promotes annexin A2 degradation, suppressing macrophage phagocytosis.
- Serum sEVs from infected piglets exhibit similar RNA profiles and impair macrophage function.
AI-generated from the title and abstract; the full text is not read.
Abstract
Abstract Mucosal immune defense depends on coordinated communication between epithelial and immune cells, yet pathogens can disrupt this crosstalk through diverse mechanisms. Here we show that porcine epidemic diarrhea virus (PEDV), an enteric alphacoronavirus, reshapes epithelial small extracellular vesicle (sEV) signaling to impair macrophage function. Despite detection by the intestinal innate immune system, PEDV promotes the release of epithelial sEVs enriched in immunoregulatory noncoding RNAs. Among this cargo, miR-190a targets the actin-regulating protein TMOD3 and disrupts F-actin remodeling, reducing macrophage migration. In parallel, the long noncoding RNA TS2083 promotes annexin A2 degradation, impairing phagocytic cup formation and suppressing phagocytosis. Moreover, serum sEVs from PEDV-infected piglets are enriched in both RNAs and impair isolated alveolar macrophage migration and phagocytosis, suggesting distal macrophage modulation. Collectively, these findings implicate sEV-mediated macrophage reprogramming in PEDV-mediated immune evasion and highlight sEV-associated RNAs as potential biomarkers of PEDV infection and therapeutic targets for restoring macrophage-mediated mucosal immunity.
The authors' abstract, as published at the source. Nature Communications, 2026 · DOI ↗
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Field: Animal Science and Zoology
Animal Science and ZoologyAgricultural and Biological Sciences