Open Access
Clostridium perfringens epsilon toxin rapidly decreases membrane barrier permeability of polarized MDCK cells
Author(s) -
Petit Laetitia,
Gibert Maryse,
Gourch Abdelkader,
Bens Marcelle,
Vandewalle Alain,
Popoff Michel R.
Publication year - 2003
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1046/j.1462-5822.2003.00262.x
Subject(s) - paracellular transport , clostridium perfringens , toxin , tight junction , biology , microbiology and biotechnology , lysis , propidium iodide , biophysics , cell membrane , permeability (electromagnetism) , cell , membrane , biochemistry , bacteria , programmed cell death , apoptosis , genetics
Summary Epsilon toxin is produced by Clostridium perfringens types B and D which are responsible for fatal intestinal diseases in animals. The main biological activity of epsilon toxin is the production of oedema in various organs. We have previously found that epsilon toxin forms a large membrane complex in MDCK cells which is not internalized into cell, and induces cell volume enlargement and loss of cell viability (Petit, L., Gibert, M., Gillet, D., Laurent‐Winter, C., Boquet, P., Popoff, M. R. (1997) J Bacteriol 179, 6480–6487). Here, we show that epsilon toxin is very potent to decrease the trans ‐epithelial electrical resistance of polarized MDCK cells grown on filters without altering the organization of the junctional complexes. The dose‐dependent decrease in trans ‐epithelial electrical resistance, more marked when the toxin was applied to the apical side than to the basal side of MDCK cells, was associated with a moderate increase of the paracellular permeability to low‐molecular‐weight compounds but not to macromolecules. Epsilon toxin probably acts by forming large membrane pores which permit the flux of ions and other molecules such as the entry of propidium iodide and finally to the loss of cell viability.