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Isolation of Single Intracellular Bacterial Communities Generated from a Murine Model of Urinary Tract Infection for Downstream Single-cell Analysis
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Isolation of Single Intracellular Bacterial Communities Generated from a Murine Model of Urinary Tract Infection for Downstream Single-cell Analysis

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Molecular variations in Klebsiella pneumoniae and Escherichia coli FimH affect function and pathogenesis in the

David A Rosen1, Jerome S Pinkner, Jennifer N Walker

  • 1Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA.

Infection and Immunity
|May 14, 2008
PubMed

Insights

Differences in FimH adhesin function between uropathogenic Escherichia coli and Klebsiella pneumoniae impact urinary tract infection (UTI) pathogenesis. Even minor sequence variations in FimH significantly alter bacterial colonization and virulence.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Type 1 pili, mediated by the FimH adhesin, are crucial for uropathogenic Escherichia coli (UPEC) binding, invasion, and biofilm formation in urinary tract infections (UTIs).
  • Klebsiella pneumoniae also causes UTIs, utilizing Type 1 pili and FimH, but its specific pathogenic mechanisms and FimH functionality remain less understood compared to UPEC.

Purpose of the Study:

  • To molecularly characterize the functional differences between FimH from UPEC isolate UTI89 and Klebsiella pneumoniae isolate TOP52.
  • To investigate how these FimH functional variations influence the pathogenesis of urinary tract infections caused by these distinct bacterial species.

Main Methods:

  • Comparative analysis of FimH adhesin domains, focusing on the mannose binding pocket and surrounding structures.
  • Functional assays including hemagglutination of guinea pig erythrocytes and biofilm formation inhibition studies using mannose derivatives.
  • Infection studies in a murine model of UTI to assess the role of FimH in bacterial colonization, invasion, and inflammatory bladder complex (IBC) formation.

Main Results:

  • K. pneumoniae FimH(52) shares homology with E. coli FimH, including an identical mannose binding pocket, but lacks the ability to agglutinate guinea pig erythrocytes.
  • FimH-dependent biofilm formation in K. pneumoniae is sensitive to heptyl mannose, not methyl mannose, indicating interactions beyond the primary mannose binding site.
  • In a murine UTI model, K. pneumoniae TOP52 required FimH(52) for bladder invasion and IBC formation but not for initial colonization.

Conclusions:

  • Limited sequence variations in FimH between E. coli and K. pneumoniae lead to significant functional differences in binding and biofilm formation.
  • These FimH functional disparities contribute to distinct pathogenic profiles and colonization abilities in the urinary tract.
  • FimH adhesin variations represent a key factor driving differences in UTI pathogenesis between UPEC and K. pneumoniae.

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