title: Host pathogenesis in urinary tract infections.
abstract: Urinary tract infections (UTIs) are the result of an interaction between bacterial virulence and host defense factors that compete to invade or protect the host, respectively. Research over the past 30 years has demonstrated that vaginal colonization with uropathogens precedes most UTIs. Receptivity of the vaginal mucosa for uropathogens is an essential initial step in vaginal mucosa colonization. When vaginal and buccal epithelial cells were collected from patients susceptible to reinfection and compared with such cells obtained from controls resistant to UTIs, the strains that caused cystitis adhered much more avidly to the epithelial cells from susceptible women. These genotypic traits for epithelial cell receptivity may be a major susceptibility factor in UTIs. The presence or absence of blood group determinants on the surface of uroepithelial cells may influence an individual's susceptibility to UTIs. The protective effect in women with the secretor phenotype may be due to fucosylated structures at the cell surface which decrease the availability of putative receptors for Escherichia coli. Susceptibility among women who do not secrete blood group antigens may be due to specific E. coli-binding glycolipids that are absent in women who secrete blood group antigens. Recent studies have shown that the vaginal fluid, which forms an interface between uropathogens and epithelial cells, also influences vaginal colonizations.
authors: Department of Urology, Northwestern University Medical School, Tarry 11-715, 300 East Superior Avenue, Chicago, IL 60611-3009, USA. ajschaeffer@nwu.edu
authors: A J
authors: AJ
authors: Schaeffer
authors: N
authors: N
authors: Rajan
authors: Q
authors: Q
authors: Cao
authors: B E
authors: BE
authors: Anderson
authors: D L
authors: DL
authors: Pruden
authors: J
authors: J
authors: Sensibar
authors: J L
authors: JL
authors: Duncan
mesh_terms: D001422:Bacterial Adhesion; D001789:Blood Group Antigens / Q000032:analysis; D003556:Cystitis / Q000097:blood / Q000382:microbiology; D004198:Disease Susceptibility / Q000097:blood / Q000382:microbiology*; D004847:Epithelial Cells / Q000378:metabolism / Q000382:microbiology; D004926:Escherichia coli / Q000472:pathogenicity*; D005260:Female; D005643:Fucose / Q000097:blood; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006017:Glycolipids / Q000097:blood; D006031:Glycosylation; D006801:Humans; D007071:Immunoglobulin A, Secretory / Q000032:analysis; D009061:Mouth Mucosa / Q000382:microbiology* / Q000502:physiology; D010641:Phenotype; D011956:Receptors, Cell Surface / Q000378:metabolism; D014552:Urinary Tract Infections / Q000097:blood / Q000235:genetics / Q000382:microbiology*; D014621:Vagina / Q000382:microbiology* / Q000502:physiology; D014774:Virulence
chemical_list: D001789:Blood Group Antigens; D006017:Glycolipids; D007071:Immunoglobulin A, Secretory; D011956:Receptors, Cell Surface; D005643:Fucose