Ochratoxin A, citrinin and deoxynivalenol decrease claudin-2 expression in mouse rectum CMT93-II cells

Area of Science:

• Toxicology
• Cell Biology
• Gastroenterology

Background:

• Intestinal epithelial cells are primary targets for ingested mycotoxins.
• Mycotoxins disrupt the intestinal barrier by altering tight junctions and claudin expression.
• Extracellular signal-related kinase (ERK) pathway is implicated in mycotoxin-induced cellular changes.

Purpose of the Study:

• To investigate the effects of ochratoxin A, citrinin, and deoxynivalenol on claudin-2 expression and ERK1/2 phosphorylation in intestinal epithelial cells.
• To determine if claudin-2 regulation by mycotoxins is organ-specific.

Main Methods:

• Utilized CMT93-II intestinal epithelial cells, which express claudin-2.
• Exposed cells to ochratoxin A, citrinin, and deoxynivalenol.
• Assessed claudin-2 expression and ERK1/2 phosphorylation via Western blotting and immunofluorescence.
• Measured transepithelial electrical resistance and fluorescein flux.
• Investigated effects in MDCK II renal cells.

Main Results:

• All tested mycotoxins reduced claudin-2 expression in cell-cell contacts.
• Citrinin and deoxynivalenol reduced phosphorylated ERK1/2, while ochratoxin A did not alter it.
• Mycotoxins increased transepithelial electrical resistance but did not affect fluorescein flux.
• Deoxynivalenol, but not ochratoxin A or citrinin, reduced claudin-2 in renal MDCK II cells.

Conclusions:

• Claudin-2 expression in intestinal cells is modulated by mycotoxins, independent of ERK1/2 pathway activation.
• Mycotoxin-induced effects on claudin-2 exhibit organ-specific regulation.
• Further research is needed to elucidate alternative pathways involved in claudin-2 regulation.