Role of adherence in pathogenesis of Enterococcus faecalis urinary tract infection and endocarditis

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Abstract

Enterococcus faecalis strains isolated from urinary tract infections (UTIs) and endocarditis were analyzed for their ability to adhere to urinary tract epithelial cells (ECs) and Girardi heart (GH) and human embryonic kidney (HEK) cell cultures. UTI isolates adhered to urinary tract ECs more efficiently than to the cultured cells, at the same time showing the least affinity for GH cells. In contrast, endocarditis isolates adhered to GH cell cultures more readily than to urinary tract ECs. Moreover, although strains isolated from endocarditis adhered to GH cells more efficiently than those derived from UTI, the latter strains adhered to urinary tract cells better than the former. Studies of the ability of GH and HEK cells to internalize E. faecalis showed that for UTI isolates, 9 to 74% of adhered bacteria were internalized, while for endocarditis isolates, the percentage varied from 76 to 82%. All strains were able to associate with human neutrophils; endocarditis strains, however, associated less efficiency than UTI isolates. Growth in serum raised the adherence of all tested strains by at least 1.5- to 3-fold, with the greatest increase being observed in UTI strain adherence to GH cells (8-fold). In contrast, the association of serum-grown cells with polymorphonuclear leukocytes was reduced by two- to fivefold. In both cases, the observed serum-dependent alterations were cancelled by a few subcultures in brain heart infusion broth. These results indicate that adhesive properties are important virulence factors in the pathogenesis of UTI and endocarditis and also suggest that UTI strains showing the highest invasion and adhesive potential invade the kidneys, cause bacteremia, and, after having expressed the serum-dependent surface modification, colonize the heart.

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Guzman, C. A., Pruzzo, C., LiPira, G., & Calegari, L. (1989). Role of adherence in pathogenesis of Enterococcus faecalis urinary tract infection and endocarditis. Infection and Immunity, 57(6), 1834–1838. https://doi.org/10.1128/iai.57.6.1834-1838.1989

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