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Göran Bergsten, Martin Samuelsson, Börn Wult, Irene Leijonhufvud, Hans Fischer, Catharina Svanborg, PapG-Dependent Adherence Breaks Mucosal Inertia and Triggers the Innate Host Response, The Journal of Infectious Diseases, Volume 189, Issue 9, 1 May 2004, Pages 1734–1742, https://doi.org/10.1086/383278
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Abstract
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 ΔpapG). E. coli pap+ was shown to activate the innate host response, and adherent gfp+ bacteria were observed on excreted uroepithelial cells. E. coli ΔpapG 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.