Abstract
Cranberry consumption has shown prophylactic effects against urinary tract infections (UTI), although the mechanisms involved are not completely understood. In this paper, cranberry phenolic compounds and their potential microbial-derived metabolites (such as simple phenols and benzoic, phenylacetic and phenylpropionic acids) were tested for their capacity to inhibit the adherence of uropathogenic Escherichia coli (UPEC) ATCC®53503™ to T24 epithelial bladder cells. Catechol, benzoic acid, vanillic acid, phenylacetic acid and 3,4-dihydroxyphenylacetic acid showed anti-adhesive activity against UPEC in a concentration-dependent manner from 100–500 µM, whereas procyanidin A2, widely reported as an inhibitor of UPEC adherence on uroepithelium, was only statistically significant (p < 0.05) at 500 µM (51.3% inhibition). The results proved for the first time the anti-adhesive activity of some cranberry-derived phenolic metabolites against UPEC in vitro, suggesting that their presence in the urine could reduce bacterial colonization and progression of UTI.
Highlights
Uropathogenic Escherichia coli (UPEC) is responsible for 70%–90% of urinary tract infections (UTI)
In order to optimize the method for evaluating the adherence of UPEC American Type Culture Collection (ATCC)®53503TM to T24 epithelial cells, different initial inocula of E. coli (103, 105 and 108 CFU·mL−1) were tested, and it was concluded that the value of 108 CFU·mL−1 (1000:1 ratio of bacteria cells per epithelial cell) led to higher bacteria adherence rates (10%–14% of the total number of bacteria added initially)
Inhibition of adherence of UPEC ATCC®53503TM to T24 uroepithelial cells was established by incubating constant numbers of uroepithelial cells and bacteria preincubated with phenolic compounds (Table 1)
Summary
Uropathogenic Escherichia coli (UPEC) is responsible for 70%–90% of urinary tract infections (UTI). Strains of uropathogenic E. coli have structures called fimbriae that support adhesins, by means of which they join to the receptors of the uroepithelial cells. The type P-fimbriae encoded by the papG gene are more prevalent among strains that cause invasive and persistent UTI [1,2]. The recurrence of such infections despite antibiotic treatment, as well as the morbidity associated with them, has prompted the exploration and assessment of therapeutic alternatives to the standard antibiotic treatment [3]. An optimized anti-adhesive entity should interact more or less with adhesins of the pathogen, leading to a significant inhibition of the docking process between pro- and eukaryotic cells and further minimization of the invasion or infection of the epithelial cells [4,5]
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