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

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Author

Summary, in English

Mucosal pathogens differ from normal flora constituents in that they provoke a host response that upsets mucosal integrity. We investigated whether the elaboration of discrete adherence factors is sufficient to break the inertia of the mucosal barrier. PapG-mediated adherence was selected as an example, because P fimbrial expression characterizes uropathogenic Escherichia coli and because adherence starts the attack on the mucosal barrier. Patients were inoculated intravesically with transformed nonvirulent E. coli strains expressing functional P fimbriae (E. coli pap(+)) or mutant fimbriae lacking the adhesin (E. coli DeltapapG). E. coli pap(+) was shown to activate the innate host response, and adherent gfp(+) bacteria were observed on excreted uroepithelial cells. E. coli DeltapapG failed to trigger a response and was nonadhesive. We conclude that PapG-mediated adherence breaks mucosal inertia in the human urinary tract by triggering innate immunity and propose that this activation step differentiates asymptomatic carriage from infection.

Publishing year

2004

Language

English

Pages

1734-1742

Publication/Series

Journal of Infectious Diseases

Volume

189

Issue

9

Document type

Journal article

Publisher

Oxford University Press

Topic

  • Infectious Medicine

Status

Published

Research group

  • Clinical Microbiology, Malmö
  • Urology

ISBN/ISSN/Other

  • ISSN: 1537-6613