Synergy between type 1 fimbriae expression and C3 opsonisation increases internalisation of <it>E. coli </it>by human tubular epithelial cells

<p>Abstract</p> <p>Background</p> <p>Bacterial infection of the urinary tract is a common clinical problem with <it>E. coli </it>being the most common urinary pathogen. Bacterial uptake into epithelial cells is increasingly recognised as an important feature of infection. Bacterial virulence factors, especially fimbrial adhesins, have been conclusively shown to promote host cell invasion. Our recent study reported that C3 opsonisation markedly increases the ability of <it>E. coli </it>strain J96 to internalise into human proximal tubular epithelial cells via CD46, a complement regulatory protein expressed on host cell membrane. In this study, we further assessed whether C3-dependent internalisation by human tubular epithelial cells is a general feature of uropathogenic <it>E. coli </it>and investigated features of the bacterial phenotype that may account for any heterogeneity.</p> <p>Results</p> <p>In 31 clinical isolates of <it>E. coli </it>tested, C3-dependent internalisation was evident in 10 isolates. Type 1 fimbriae mediated-binding is essential for C3-dependent internalisation as shown by phenotypic association, type 1 fimbrial blockade with soluble ligand (mannose) and by assessment of a type 1 fimbrial mutant.</p> <p>Conclusion</p> <p>we propose that efficient internalisation of uropathogenic <it>E. coli </it>by the human urinary tract depends on co-operation between type 1 fimbriae-mediated adhesion and C3 receptor -ligand interaction.</p>

Abstract licence: CC BY-NC-ND

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