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Am J Physiol Gastrointest Liver Physiol 273: G1014-G1022, 1997;
0193-1857/97 $5.00
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Vol. 273, Issue 5, G1014-G1022, November 1997

Epidermal growth factor attenuates Clostridium difficile toxin A- and B-induced damage of human colonic mucosa

Martin Riegler1, Roland Sedivy2, Tacettin Sogukoglu1, Ignazio Castagliuolo3, Charalabos Pothoulakis3, Enrico Cosentini1, Georg Bischof1, Gerhard Hamilton1, Bela Teleky1, Wolfgang Feil4, J. Thomas Lamont3, and E. Wenzl1

1 University Clinic of Surgery and 2 Institute of Clinical Pathology, University of Vienna, A-1090 Vienna; 4 Department of Surgery, Danube Hospital, A-1220 Vienna, Austria; and 3 Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215

Epidermal growth factor (EGF) exhibits a cytoprotective effect on gastrointestinal epithelia via a receptor-mediated mechanism. We investigated the effect of EGF on Clostridium difficile toxin A (TxA)- and toxin B (TxB)-induced damage of human colon. Ussing-chambered colonic mucosa was exposed serosally to EGF before and during luminal exposure to TxA and TxB. Resistance was calculated from potential difference and short-circuit current. Epithelial damage was assessed by light microscopy and alteration of F-actin by fluoresceinated phalloidin. Luminal exposure of colonic strips to TxA and TxB caused a time- and dose-dependent decrease in electrical resistance, necrosis and dehiscence of colonocytes, and disruption and condensation of enterocyte F-actin. These effects were inhibited by prior, but not simultaneous, serosal application of EGF (20 nM). Administration of the tyrosine kinase inhibitor genistein (10-6 M) inhibited the protective effects of EGF. We conclude that EGF protects against TxA and TxB probably by stabilizing the cytoskeleton, the main target of these toxins.

enterotoxins; genistein; human colonic epithelium


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