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P fimbriae
P fimbria was the first UPEC virulence factor characterized ( Eden et al., 1976 ).
The pap ( p yelonephritis a ssociated p ili) operon encoding P fimbriae consists of
11 genes, with the main fimbrial subunit encoded by papA and the tip adhesin
encoded by papG ( Hull et al., 1981 ). The adherence mediated by P fimbriae
is mannose-resistant, unlike that of type 1 fimbriae, and is specific to P blood
group antigen, a glycosphingolipid, in which the key epitope is a digalactoside,
α-D-Gal-(1-4)-β-D-Gal ( Källenius and Möllby, 1979 ). There are three alleles
of papG , each with substrate specificity to a different region of the Gal-Gal
disaccharide-containing glycosphingolipids ( Stromberg et al., 1991 ). P fimbriae
are encoded in the genomes of 54-70% of UPEC isolates as compared to 20-
25% of fecal E. coli strains, with the papG allelic distribution being papG 1
(0-1% UPEC, 0-1% fecal), papG 2 (36-46% UPEC, 16-18% fecal), papG 3
(17-23% UPEC, 5-9% fecal) ( Johanson et al., 1993 ; Johnson et al., 1998 ;
Spurbeck et al., 2011 ). P fimbriae enhance the severity of UTI by promoting
adherence strongly to vascular endothelium, the muscular layer, and weakly to
bladder epithelial surfaces ( Virkola et al., 1988 ), as well as increasing mucosal
inflammation. Although there is a positive correlation between severity of infec-
tion and presence of P fimbriae ( Spurbeck et al., 2011 ; Vigil et al., 2011b ), and
antibodies to P fimbriae are present in the serum of infected individuals ( de
Ree and van den Bosch, 1987 ), there is no defect in colonization of the mouse
model of ascending UTI in the P fimbria isogenic mutant ( Mobley et al., 1993 ).
However, in a pyelonephritis model in cynomolgus monkeys wild-type E. coli
DS17 colonized the urinary tract longer and caused a loss of kidney function,
whereas E. coli DS17-8 (Δ papG ) was cleared earlier and did not cause as exten-
sive kidney damage ( Roberts et al., 1994 ). While P fimbriae are thought to play
only a subtle role in uropathogenesis, the presence of the pap operon is clearly
a marker of highly virulent strains.
F1C fimbriae
In a recent study, the prevalence of F1C fimbriae was not significantly different
between UPEC (16%) and fecal E. coli strains (10%) ( Spurbeck et al., 2011 ),
however, other studies have shown that the presence of F1C fimbriae correlates
with pyelonephritis isolates ( Johnson et al., 2005b ). An operon of seven genes,
focAICDFGH , encodes F1C fimbria ( Riegman et al., 1990 ), with FocA repre-
senting the major subunit of the pilus and FocH the tip adhesin. F1C fimbriae
bind receptors present in both the bladder and kidneys ( Virkola et al., 1988 ). F1C
fimbriae mediate adhesion to the endothelium and the muscular layer of the blad-
der, but not to the epithelium ( Virkola et al., 1988 ). In the kidneys, F1C mediates
adherence primarily to the distal tubules and collecting ducts, however, these
fimbriae also bind in the glomeruli and to the vascular endothelium ( Virkola
et al., 1988 ). The receptor structure of F1C fimbriae was determined to be the
GalNAcβ1-4Galβ sequence of glycolipids ( Khan et al., 2000 ). Therefore, F1C
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