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Updated: Jun 26, 2025

Urinary Tract Infection in a Small Animal Model: Transurethral Catheterization of Male and Female Mice
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Murine Ribonuclease 6 Limits Bacterial Dissemination during Experimental Urinary Tract Infection.

Hanna Cortado1, Macie Kercsmar1, Birong Li1

  • 1Kidney and Urinary Tract Center, The Abigail Wexner Research Institute at Nationwide Children's, Columbus, Ohio, USA.

Journal of Innate Immunity
|May 14, 2024
PubMed
Summary
This summary is machine-generated.

Ribonuclease 6 (RNase6) deficiency increases susceptibility to urinary tract infections (UTIs) by impairing bacterial killing in immune cells. This study shows RNase6 is crucial for host defense against uropathogenic E. coli (UPEC).

Keywords:
Antimicrobial peptideAntimicrobial proteinBacterial infectionCystitisHost defenseMacrophageMonocytePyelonephritisUrinary tract infection

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Establishment and Characterization of UTI and CAUTI in a Mouse Model

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Area of Science:

  • Immunology
  • Microbiology
  • Genetics

Background:

  • The ribonuclease (RNase) A superfamily includes cationic antimicrobial proteins effective against uropathogenic bacteria.
  • Ribonuclease 6 (RNase6), a leukocyte-derived peptide, exhibits potent microbicidal activity against uropathogenic Escherichia coli (UPEC).
  • Uropathogenic E. coli (UPEC) is the primary cause of bacterial urinary tract infections (UTIs).

Purpose of the Study:

  • To investigate the role of endogenous RNase 6 in limiting host susceptibility to UTIs.
  • To generate and analyze RNase6-deficient mice to understand its impact on UTI pathogenesis.

Main Methods:

  • Generation of a Rnase6-EGFP knock-in allele in mice.
  • Identification of cellular sources of RNase6.
  • Assessment of antimicrobial activity and UTI susceptibility in RNase6-deficient mice.

Main Results:

  • Monocytes and macrophages were identified as the primary cellular sources of RNase6 in the urinary tract.
  • RNase6 deficiency led to increased UPEC burden in the upper urinary tract during experimental UTI.
  • UPEC exhibited enhanced intracellular survival within RNase6-deficient macrophages.

Conclusions:

  • RNase6 plays a critical role in preventing pyelonephritis by promoting intracellular UPEC killing.
  • Monocytes and macrophages are key cellular components in RNase6-mediated UTI defense.
  • Endogenous antimicrobial RNase A proteins contribute significantly to host defense against UTIs.