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Preliminary evidence that Clostridium perfringens type A enterotoxin is present in a 160,000-Mr complex in mammalian

A P Wnek1, B A McClane

  • 1Department of Microbiology, Biochemistry and Molecular Biology, University of Pittsburgh School of Medicine, Pennsylvania 15261.

Infection and Immunity
|February 1, 1989
PubMed

Insights

Clostridium perfringens enterotoxin (CPE) binds to rabbit intestinal membranes and Vero cells, forming a large complex. This complex involves CPE interacting with host proteins, suggesting conserved receptor sites.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Clostridium perfringens type A produces enterotoxin (CPE), a key virulence factor.
  • Understanding CPE's interaction with host cells is crucial for elucidating its mechanism of action.

Purpose of the Study:

  • To investigate the molecular interactions of 125I-labeled CPE with rabbit intestinal brush border membranes (BBMs) and Vero cells.
  • To identify the host proteins involved in CPE binding and complex formation.

Main Methods:

  • Binding of 125I-CPE to BBMs and Vero cells, followed by solubilization with CHAPS.
  • Analysis of solubilized complexes using gel filtration chromatography (Sepharose 4B) and SDS-PAGE without boiling.
  • Affinity chromatography using immobilized CPE.

Main Results:

  • Specifically bound 125I-CPE formed a complex of approximately 160,000 Mr with both BBMs and Vero cells.
  • SDS-PAGE analysis indicated the complex contains 50,000-Mr and 70,000-Mr proteins in equimolar amounts.
  • CPE (35,000 Mr) likely interacts with these host proteins to form the larger complex.

Conclusions:

  • CPE forms a membrane-dependent complex with host proteins of approximately 160,000 Mr.
  • The receptor or target sites for CPE appear similar in rabbit BBMs and Vero cells.
  • These findings provide insights into CPE binding, insertion, and biological activity.

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