Host-specificity of uropathogenic Escherichia coli depends on differences in binding specificity to Gal alpha

N Strömberg1, B I Marklund, B Lund

  • 1Department of Cariology, Faculty of Odontology, University of Gothenburg, Sweden.

The EMBO Journal
|June 1, 1990
PubMed

Insights

This study reveals how uropathogenic Escherichia coli adhesins bind to host cells. Variations in adhesin receptor specificity explain differences in binding to human and dog cells, suggesting a mechanism for host adaptation.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Urology

Background:

  • Uropathogenic Escherichia coli (UPEC) utilizes adhesins to colonize the urinary tract.
  • G adhesins are crucial virulence factors in UPEC, mediating bacterial attachment to host cells.
  • Understanding adhesin-receptor interactions is key to deciphering host specificity and developing targeted therapies.

Purpose of the Study:

  • To characterize the glycolipid and eukaryotic cell binding specificities of four G adhesins from UPEC.
  • To investigate the role of receptor binding variations in UPEC host specificity (human vs. dog).
  • To correlate adhesin binding patterns with the presence of specific glycolipid isoreceptors on host cells.

Main Methods:

  • Cloning and expression of four G adhesin variants from UPEC.
  • Binding assays using purified glycolipids and eukaryotic cell lines (human T24, canine MDCK II).
  • Hemagglutination assays to confirm receptor-binding specificities.
  • Analysis of predicted amino acid sequences for receptor-binding domains.

Main Results:

  • PapG adhesins (PapGAD110, PapGIA2, PapGJ96) exhibited similar binding to Gal alpha 1-4Gal-containing glycolipids, while PrsG adhesin (PrsGJ96) showed distinct patterns.
  • PapG adhesins bound human uroepithelial cells but not canine cells, whereas PrsG adhesins showed the opposite preference.
  • Binding patterns correlated with the presence of specific glycolipid isoreceptors, with steric hindrance potentially affecting PapG binding to canine cells.

Conclusions:

  • G adhesin receptor specificity varies, influencing binding to different host cell types.
  • Differences in glycolipid isoreceptor composition and presentation on host cells contribute to UPEC host specificity.
  • Adhesin variation is a key evolutionary mechanism for UPEC adaptation to different hosts, driven by host receptor topography.

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