ORIGINAL RESEARCH article
Front. Cell Dev. Biol.
Sec. Cell Adhesion and Migration
This article is part of the Research TopicRegulation of Permeability of Tight JunctionsView all 6 articles
Helicobacter pylori CagA disrupts pancreatic epithelial barrier integrity
Provisionally accepted
- 1Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies, National Polytechnic Institute of Mexico (CINVESTAV), México City, Mexico
- 2Department of Cellular and Tissular Biology, Faculty of Medicine, Universidad Nacional Autonoma de Mexico, Mexico City, Mexico
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The oncoprotein CagA is the major virulence factor of Helicobacter pylori and plays a central role in the development of gastric disorders. H. pylori CagA+ infection has been implicated with an increased risk of developing extragastric diseases such as pancreatic cancer; however, the mechanisms remain unclear. In this study, BxPC-3 pancreatic epithelial cells were infected with H. pylori bacterial strains CagA+ (26695 and PMSS1) or CagA- (Tx30a). Infection with CagA+ strains resulted in a significant disruption of epithelial barrier integrity, as demonstrated by transepithelial electrical resistance assays. Western blot and immunofluorescence analyses revealed altered expression and cytoplasmic relocalization of key apical junctional complex proteins. Meanwhile, claudin-4 and occludin increased, ZO-1 remained unchanged, and E-cadherin and β-catenin decreased. Likewise, cytoskeletal rearrangements were observed, particularly the loss of the actin apical ring and the mislocalization of actin-binding proteins, such as cortactin and vinculin, at the cell borders. The loss of barrier integrity and cytoskeletal alterations were associated with morphological This is a provisional file, not the final typeset article changes and increased cell motility, as demonstrated by wound healing assays. In addition, infection was accompanied by an increase in IL-8 secretion. These findings suggest that CagA alters the pancreatic epithelial cells' functions. Therefore, CagA represents an undescribed risk factor in the pathogenesis of H. pylori-associated pancreatic illness.
Keywords: BXPC-3 cells, apical junctional complex, tight junction, Actin Cytoskeleton, Migration, IL-8
Received: 19 Aug 2025; Accepted: 27 Oct 2025.
Copyright: © 2025 Romero-Fabela, Silva, Chacon, Rendon-Huerta and Betanzos. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Abigail Betanzos, abetanzos@cinvestav.mx
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