ArticleAnnals of the New York Academy of Sciences2022
Unraveling the intestinal epithelial barrier in cyanotoxin microcystin-treated Caco-2 cell monolayers.
Article in Annals of the New York Academy of Sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Phenolic Fractions from Walnut Milk Residue: Antioxidant Activity and Cytotoxic Potential.Plants (Basel, Switzerland) · 2024Article
- The cytotoxicity of microcystin-LR: ultrastructural and functional damage of cells.Archives of toxicology · 2024Review
- Microcystin-LR-Induced Interaction between M2 Tumor-Associated Macrophage and Colorectal Cancer Cell Promotes Colorectal Cancer Cell Migration through Regulating the Expression of TGF-β1 and CST3.International journal of molecular sciences · 2023Article
- CDT ofToxins · 2023Article
- Human organoids are superior to cell culture models for intestinal barrier research.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Microcystin is a widespread cyanobacterial toxin that affects the intestine to produce diarrheal symptoms after ingestion of freshwater blue-green algae. Our study aimed to characterize the mechanism by which the toxin leads to diarrhea via epithelial barrier dysfunction in a small intestine Caco-2 cell model. Microcystin-treated human Caco-2 epithelial monolayers were functionally and molecularly analyzed for barrier dysfunction. Tight junctions (TJs) and cell damage were analyzed in relation to transepithelial electrical resistance (TER) changes. TER of microcystin-treated Caco-2 cells was reduced by 65% of the initial value after 24 h; concomitantly, permeability for fluorescein increased 2.6-fold. Western blot analysis showed reduced claudin-1 expression, while expression of claudin-3 and -4 remained unchanged. Super-resolution stimulated emission depletion microscopy revealed that TJ integrity was compromised by fraying and splitting of the TJ domain of the epithelial cells. Epithelial apoptosis did not significantly contribute to epithelial barrier dysfunction, while cytoskeletal actomyosin constriction was associated with TJ disintegration and the barrier defect. Our results indicate that microcystin causes intestinal barrier leakiness, which helps to explain the leak flux type of diarrhea as the main pathomechanism after ingestion of cyanobacterial toxin.
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