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[Modulation of P-fimbriation by ciprofloxacin in uropathogenic Escherichia coli]

I Abalia1, E Rodríguez, A Umaran

  • 1Departamento de Enfermería I, Facultad de Medicina, Universidad del País Vasco (UPV/EHU), Leioa.

Enfermedades Infecciosas Y Microbiologia Clinica
|May 1, 1997
PubMed
Abstract

Insights

Subinhibitory ciprofloxacin reduces P fimbriae expression in uropathogenic Escherichia coli by inhibiting protein synthesis, not through genetic mutation. This impacts bacterial adhesion in urinary tract infections.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Uropathogenic Escherichia coli (UPEC) are a major cause of urinary tract infections (UTIs).
  • P fimbriae are crucial virulence factors for UPEC, mediating adhesion to host tissues.
  • Ciprofloxacin is a widely used antibiotic for treating UTIs, but subinhibitory concentrations can have complex effects on bacterial physiology.

Purpose of the Study:

  • To investigate the impact of subinhibitory ciprofloxacin concentrations on P fimbriae expression in UPEC.
  • To elucidate the mechanism by which ciprofloxacin affects fimbrial protein synthesis and bacterial adherence.

Main Methods:

  • Quantitative analysis of fimbriation using electron microscopy before and after ciprofloxacin treatment.
  • Electrophoretic separation of fimbrial proteins and outer membrane proteins (OMPs) to assess qualitative changes.

Main Results:

  • No qualitative alterations in OMPs or fimbrial proteins were observed after ciprofloxacin exposure.
  • Electron microscopy revealed a general decrease in the percentage of fimbriated bacterial cells.

Conclusions:

  • Subinhibitory ciprofloxacin likely inhibits fimbrial protein synthesis as a secondary effect of cellular repair mechanisms, rather than inducing specific mutations.
  • This mechanism may reduce bacterial virulence by decreasing P fimbriae expression, potentially impacting UTI pathogenesis.

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