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Establishment and Characterization of UTI and CAUTI in a Mouse Model
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Cytolethal Distending Toxin Enhances Escherichia coli Urinary Tract Infection.

Santosh Paudel1, Benjamin E Curtis2, Harry L T Mobley1

  • 1Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, USA.

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Cytolethal distending toxin (CDT) is crucial for *Escherichia coli* to cause urinary tract infections (UTI). This toxin promotes bacterial survival and causes inflammation and tissue damage during UTI progression.

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Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Cytolethal distending toxin (CDT) is a key virulence factor in Gram-negative bacteria like *Escherichia coli* (E. coli).
  • E. coli is a primary cause of urinary tract infections (UTIs), and strains producing CDT are found in UTI patients.
  • The precise role of CDT in UTI development and progression has remained unclear.

Purpose of the Study:

  • To investigate the specific function of CDT in the pathogenesis of ascending urinary tract infections (UTIs) caused by *E. coli*.
  • To determine the impact of CDT on bacterial colonization, host immune response, and tissue damage during UTI.

Main Methods:

  • Generation of an *E. coli* mutant strain lacking the *cdtABC* genes.
  • Co-infection of a mouse model of ascending UTI using wild-type and *cdt* mutant *E. coli* strains.
  • Assessment of bacterial load in urine, bladder, and kidneys, alongside histopathological analysis of infected tissues.

Main Results:

  • The *cdt* mutant exhibited a significant colonization defect in urine, bladder, and kidneys compared to wild-type bacteria at 1 day post-inoculation.
  • Single infections with the *cdt* mutant showed reduced kidney colonization, indicating CDT's role in ascending infection.
  • Infection with CDT-producing *E. coli* led to increased inflammation and tissue damage in kidneys and bladders compared to the *cdt* mutant.

Conclusions:

  • CDT plays a critical role in the progression of *E. coli*-mediated urinary tract infections.
  • CDT contributes to bacterial survival and colonization within the urinary tract.
  • CDT exacerbates host inflammatory responses and tissue damage during UTI.