A dynamic interface
Junction and cytoskeletal remodeling, immune-cell carriage, mucus proteins, goblet-cell secretion, and neural control can each change the path of infection.
03 / 04
Barrier
Barrier
biology
Tracing how epithelia, mucus, immune cells, and neural signals block—or enable—pathogen movement.
Evidence map03
Porcine mucosa in context
Neonatal piglets, nasal and intestinal tissues, polarized IPEC-J2 cells, porcine mucus, and PEDV/TGEV tracing and challenge models dominate the evidence.
Follow the route
Histology, polarized infection, junction assays, pathway inhibition, animal challenge, cell-transfer tracing, mucus fractionation, spike hydrolysis, and secretion perturbation.
Three intervention surfaces
The work points toward preserving the barrier, blocking host-mediated transport routes, and developing endogenous mucus factors as antiviral leads.
Independent editorial synthesis · reviewed 7 September 2026
ORCID 0000-0002-2349-0028 · NJAU College of Veterinary Medicine
Representative evidence
Six papers selected for conceptual importance and temporal coverage. They are examples, not a substitute for the complete reconciled bibliography.
Diversity of tight junctions (TJs) between gastrointestinal epithelial cells and their function in maintaining the mucosal barrier
This review supplies the epithelial-junction framework; it should not be presented as a new experimental discovery.
Official bibliography role: Correspondence AuthorQinghua Yu, Qian Yang Open source record · DOI 10.1016/j.cellbi.2008.09.007 ↗
Transmissible gastroenteritis virus and porcine epidemic diarrhoea virus infection induces dramatic changes in the tight junctions and microfilaments of polarized IPEC-J2 cells
TGEV and PEDV remodeled junctions and microfilaments in polarized porcine cells, with coinfection more disruptive; a cell layer is not a complete intestinal barrier.
Verified paper role: Correspondence AuthorShanshan Zhao, Junkai Gao, Liqi Zhu, Qian Yang Open source record · DOI 10.1016/j.virusres.2014.08.014 ↗
An alternative pathway of enteric PEDV dissemination from nasal cavity to intestinal mucosa in swine
Cell tracing demonstrated a controlled nasal-to-intestinal PEDV route via dendritic and T cells, complementing rather than replacing the fecal–oral route.
Official bibliography role: Correspondence AuthorYuchen Li, Qingxin Wu, Lulu Huang, Chen Yuan, Jialu Wang, Qian Yang Open source record · DOI 10.1038/s41467-018-06056-w ↗
PEDV infection in neonatal piglets through the nasal cavity is mediated by subepithelial CD3(+) T cells
In neonatal piglets, subepithelial CD3+ T cells provided an alternative carrier population where nasal dendritic cells were sparse.
Official bibliography role: Correspondence AuthorChen Yuan, Yuxin Jin, Yuchen Li, En Zhang, Penghao Zhang, Qian Yang Open source record · DOI 10.1186/s13567-020-00883-w ↗
Calpain-1: a Novel Antiviral Host Factor Identified in Porcine Small Intestinal Mucus
Mucus-derived calpain-1 bound and hydrolyzed a PEDV spike region and protected piglets in the reported challenge.
Official bibliography role: Correspondence AuthorYuchen Li, Xiuyu Wang, En Zhang, Ruiling Liu, Chengjie Yang, Ying Duan, Yuqi Jiang, Qian Yang Open source record · DOI 10.1128/mbio.00358-22 ↗
Goblet cells dictate viral tropism and pathogenesis in nasal and intestinal mucosae
Mucus secretion blocked viral entry, while neural induction of goblet-cell antigen passages moved bacteria across intact epithelium and amplified inflammation.
Official bibliography role: Participating authorsWenqian Wang, Wenwen Chao, Hui Zeng, Rongfeng Tang, Ruiling Liu, Chengcheng Wang, Xuan Wu, Jiaxin Qi, Yunlei Cao, Yuchen Li, Qian Yang Open source record · DOI 10.1073/pnas.2514150122 ↗
Read as a program,
not a priority claim.
These overlapping themes are an editorial synthesis of the publication record. They do not claim sole scientific ownership, clinical validation, regulatory approval, or independent replication. Titles and bibliographic facts come from the reconciled record; explanatory summaries are constrained to the cited evidence.
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