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PapG-dependent adherence breaks mucosal inertia and triggers the innate host response

Goran Bergsten1, Martin Samuelsson, Bjorn Wullt

  • 1Department of Microbiology, Institute of Laboratory Medicine, Lund University, Lund, Sweden.

The Journal of Infectious Diseases
|April 30, 2004
PubMed

Insights

PapG-mediated adherence by uropathogenic Escherichia coli breaks mucosal inertia by triggering innate immunity. This adherence is key to differentiating asymptomatic carriage from infection in the urinary tract.

Area of Science:

  • Microbiology
  • Immunology
  • Urology

Background:

  • Mucosal pathogens disrupt host defenses, unlike commensal flora.
  • Adherence factors are critical for initiating pathogen invasion.
  • Uropathogenic Escherichia coli (UPEC) utilizes P fimbriae, including PapG adhesin, for urinary tract colonization.

Purpose of the Study:

  • To determine if PapG-mediated adherence alone can overcome the mucosal barrier.
  • To investigate the role of P fimbriae in initiating host responses.
  • To differentiate between asymptomatic colonization and active infection.

Main Methods:

  • Intravesical inoculation of human subjects with engineered E. coli strains.
  • Strains included nonvirulent E. coli expressing functional P fimbriae (E. coli pap(+)) or lacking the PapG adhesin (E. coli Delta papG).
  • Observation of bacterial adherence and host response using microscopy and uroepithelial cell analysis.

Main Results:

  • E. coli pap(+) adhered to uroepithelial cells and triggered an innate host immune response.
  • E. coli Delta papG showed no adherence and did not elicit a host response.
  • PapG-mediated adherence was sufficient to break mucosal inertia.

Conclusions:

  • PapG-mediated adherence is a critical factor in initiating urinary tract infections.
  • The activation of innate immunity by adherence differentiates infection from asymptomatic carriage.
  • Targeting PapG-mediated adherence could be a strategy to prevent UPEC infections.

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