Host defense within the urinary tract. I. Bacterial adhesion initiates an uroepithelial defense mechanism

Abstract

Uroepithelial defense has ben suggested to contribute to the local host resistance against ascending urinary tract infection. The cellular mechanism, however, is not known. In this study, bacterial growth was measured under the direct and indirect influence of uroepithelial cells. To study if a specific ligand-receptor interaction is required for uroepithelial cell (UEC) activation, isogenic Escherichia coli mutants expressing either mannose-sensitive, mannose-resistant (p), or mannose resistant (s) pili were tested for their capacity to induce the UEC defense mechanism. The antibacterial effect of UEC was abolished either by performing coculture in chambers with a fluid-permeable membrane which separates UEC from bacteria or by inhibiting membrane contact using the antiadherence factor pentosane polysulfate. No difference between the various types of pili could be shown. All E. coli strains adhered comparably to the UEC and were subsequently suppressed in their growth. Even a "naked" mutant without expression of common pili showed a similar behavior. In conclusion, bacterial growth suppression depends on direct contact between the UEC and bacteria, but is independent of common pili expressed on E. coli.

Pathogenicity Islands in BacterialPathogenesis

“…However, internalization causes exfoliation of the superficial bladder cells harboring internalized bacteria into the urine. Before clearance, intracellular bacteria start to replicate and induce host cytokine responses, leading to the symptoms of UTI (221,246,305).…”

Non-antibacterial alternative measures for urinary tract infection in children. Part 1. Suppression of the microbial initiation of the inflammation

“…В контексте взаимоотношений «инфекция-уро-телий» нельзя не упомянуть об антибактериаль-ном эффекте эпителиальных клеток мочи здоро-вых детей по отношению к уропатогенным E. coli, который реализуется только при прямом контакте с бактериями и нивелируется антиадгезивными со-единениями [34]. При рецидивирующих инфекциях мочевой системы, включая пиелонефрит, подоб-ный эффект эпителия мочи в значительной степени снижается и частично восстанавливается in vitro препаратами, повышающими внутриклеточный аде-нозинмонофосфат, возможно, за счет стимуляции «респираторного взрыва».…”

Mild dehydration: a risk factor of urinary tract infection?

“…One most effective bladder defence mechanism lies in the bladder mucosa itself. Independent from urine flow, contact with the bladder mucosa inhibited the growth of adhering and nonadhering pathogenic E. coli strains (Schlager et al, 1993;Mannhardt et al, 1996). Harrison et al (1988) evaluated the contributions of different host defence mechanisms to bacterial clearance in rats infected with E. coli.…”