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Mouse liver contains a Pseudomonas aeruginosa exotoxin A-binding protein

J J Forristal1, M R Thompson, R E Morris

  • 1Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Ohio 45267.

Infection and Immunity
|September 1, 1991
PubMed

Insights

Pseudomonas aeruginosa exotoxin A (PE) binds to a 350 kDa glycoprotein found on mouse cell membranes. This protein may act as a receptor, facilitating toxin entry and causing cell death.

Area of Science:

  • Microbiology
  • Toxicology
  • Cell Biology

Background:

  • Pseudomonas aeruginosa is an opportunistic pathogen that produces exotoxin A (PE), a key virulence factor.
  • PE inhibits protein synthesis by depleting elongation factor 2, primarily in the liver of burned mice.
  • Cellular sensitivity to PE may be mediated by specific cell surface receptors.

Purpose of the Study:

  • To investigate the presence and characteristics of PE-binding proteins in mouse tissues.
  • To isolate and compare the PE-binding protein from mouse liver with that from mouse fibroblasts.
  • To determine if these binding proteins function as receptors for PE.

Main Methods:

  • Extraction of detergent-soluble proteins from various mouse tissues.
  • Affinity purification of PE-binding proteins.
  • Molecular characterization including molecular mass determination and protease digestion profiling.
  • Comparison of binding proteins from liver and LM fibroblasts.

Main Results:

  • PE-binding proteins were identified in liver, kidney, lung, spleen, and heart extracts.
  • A ~350 kDa glycoprotein that binds PE with high avidity was isolated from mouse liver.
  • This protein shares similarities with, but has distinct glycosylation patterns from, the PE-binding protein in LM fibroblasts.
  • The binding moiety is associated with the plasma membrane.

Conclusions:

  • A ~350 kDa glycoprotein in mouse liver specifically binds exotoxin A.
  • This glycoprotein is glycosylated and located on the plasma membrane, suggesting it functions as a PE receptor.
  • Differences in glycosylation between tissue sources indicate potential variations in receptor structure or processing.
  • The identified protein is a strong candidate for mediating PE internalization and subsequent cell death.

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