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Infection and Immunity, December 1998, p. 5897-5905, Vol. 66, No. 12
Department of Molecular Genetics and
Biochemistry, University of Pittsburgh School of Medicine,
Pittsburgh, Pennsylvania 15261
Received 8 May 1998/Returned for modification 1 July 1998/Accepted 17 September 1998
After binding, Clostridium perfringens enterotoxin
(CPE) initially localizes in a small (~90-kDa) complex in plasma
membranes. This event is followed by formation of a second membrane
complex, referred to as large (160-kDa) complex. Contrary to a previous hypothesis proposing that CPE inserts into intestinal brush border membranes (BBMs) when this toxin is localized in the small complex, this study shows that BBMs do not offer CPE localized in the small complex protection from pronase. However, our experiments indicate that
BBMs do substantially protect CPE from pronase when this toxin is
localized in large complex. Since the onset of CPE-induced permeability alterations closely coincides with large-complex formation, these new results suggest that CPE-induced alterations in
permeability may result from pore formation due to the partial membrane
insertion of CPE when this toxin is present in large complex.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Characterization of Membrane-Associated Clostridium
perfringens Enterotoxin following Pronase Treatment
and
*
Corresponding author. Mailing address: E1240 Biomedical
Science Tower, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261. Phone: (412) 648-9022. Fax: (412) 624-1401. E-mail: bamcc{at}pop.pitt.edu.
Present address: Department of Microbiology and Immunology,
Uniformed Services University of the Health Sciences, Bethesda, MD
20814-4799.
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