Objective: 

Sodium caprate is discussed as a pharmaceutically applied absorption enhancer in intestinal epithelia. We have analyzed effects of caprate in the human intestinal epithelial cell line HT-29/B6.

Methods: 

Confluent monolayers of HT-29/B6 cells were mounted in Ussing-type chambers, and transepithelial resistance and apparent permeability for 10 kDa FITC-dextran (FD10) were measured. Two-path impedance spectroscopy was employed to differentiate between transcellular (R^trans) and paracellular resistance (R^para). Tight junction proteins as well as cytoskeletal markers and signaling were analyzed by Western blotting and confocal laser-scanning microscopy.

Results: 

Sodium caprate (10 mM) resulted in an about tenfold increase in FD10 permeability and a strong and reversible decrease of transepithelial resistance. The latter is based on a threefold drop in R^para while R^trans was unchanged. Confocal-laser scanning microscopy revealed a reduction of claudin-5 in bicellular tight junctions (bTJ) and a disappearance of tricellulin from tricellular tight junctions (tTJ) within 30 min.

Conclusion: 

Sodium caprate induces a specific opening of the paracellular pathway by opening of tight junctions in bicellular and tricellular epithelial cell contacts. The decrease of R^para is caused by claudin displacement from the bTJ, whereas the increase in FD10 permeability is caused by tricellulin displacement from the tTJ. Therefore, sodium caprate is a valuable compound for pharmacological approaches focusing on selective drug targeting.