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

In English

Författare

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.

Publiceringsår

2004

Språk

Engelska

Sidor

1734-1742

Publikation/Tidskrift/Serie

Journal of Infectious Diseases

Volym

189

Issue

9

Dokumenttyp

Artikel i tidskrift

Förlag

Oxford University Press

Ämne

  • Infectious Medicine

Status

Published

Forskningsgrupp

  • Clinical Microbiology, Malmö
  • Urology

ISBN/ISSN/Övrigt

  • ISSN: 1537-6613