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Am J Physiol Cell Physiol (June 30, 2004). doi:10.1152/ajpcell.00007.2004
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Submitted on January 6, 2004
Accepted on June 28, 2004

Ochratoxin A Increases Permeability Through Tight Junctions by Removal of Specific Claudin Isoforms

John McLaughlin1, Philip J Padfield1, Julian P Burt2, and Catherine A O'Neill1*

1 Gastrointestinal Sciences, University of Manchester, Manchester, Greater Manchester, United Kingdom
2 School of Informatics, University of Wales, Bangor, Bangor, Gwynedd, United Kingdom

* To whom correspondence should be addressed. E-mail: coneill{at}fs1.ho.man.ac.uk.

On interaction with the intestine, the mycotoxin Ochratoxin A is know to cause rapid inflammation, diarrhoea and increased bacterial translocation. All these effects are consistent with a decrease in epithelial barrier function. However, this has not been shown directly. We determined that ochratoxin A is able to reduce the barrier properties of the model intestinal cell line Caco-2. Over 24 hours, Ochratoxin A reduces the transepithelial resistance of Caco-2 monolayers growing on transwell filters by approximately 40%. At the same time, the permeability of the monolayer is increased with respect to 4, and 10KDa FITC dextrans, but not to 20 or 40kDa dextrans. Immunoblotting and immuofluorescence reveal that the decrease in barrier properties is concomitant with disappearance of claudins 3 and 4, but not claudin 1 from Caco-2 cell membranes. These results suggest that Ochratoxin A is able to modulate the barrier function of Caco-2 cells by removal of specific claudin isoforms.




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