CLDN1 and infection: Infection of epithelial cell monolayers with EHEC O157:H7 promoted claudin-1 and ZO-1 redistribution and further down-regulation of ZO-1 expression, while toxins released upon the infection of epithelial cells with ETEC K88 and Salmonella typhimurium SL1344 resulted in disruption of the complexes that maintain adhesion between intestinal epithelial cells (88, 89).