Epidermal growth factor attenuatesClostridium difficiletoxin A- and B-induced damage of human colonic mucosa
Autor: | Gerhard Hamilton, Roland Sedivy, G Bischof, Etienne Wenzl, Ignazio Castagliuolo, W Feil, Tacettin Sogukoglu, Martin Riegler, J. T. Lamont, Charalabos Pothoulakis, B Teleky, E. P. Cosentini |
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Rok vydání: | 1997 |
Předmět: |
Colon
Physiology Bacterial Toxins Clostridium difficile toxin A Genistein Clostridium difficile toxin B Enterotoxin In Vitro Techniques Membrane Potentials Microbiology Enterotoxins Necrosis chemistry.chemical_compound Bacterial Proteins Ileum Epidermal growth factor Physiology (medical) medicine Animals Humans Clostridiaceae Intestinal Mucosa Cells Cultured Epidermal Growth Factor Hepatology biology Clostridioides difficile Gastroenterology Clostridium difficile biology.organism_classification Molecular biology Actins Epithelium Rats medicine.anatomical_structure chemistry |
Zdroj: | American Journal of Physiology-Gastrointestinal and Liver Physiology. 273:G1014-G1022 |
ISSN: | 1522-1547 0193-1857 |
DOI: | 10.1152/ajpgi.1997.273.5.g1014 |
Popis: | 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 (10−6M) 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. |
Databáze: | OpenAIRE |
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