In

asymptomatic carriers, the mucosa remains inert,

despite the presence of large bacterial numbers in the
lumen. Conversely, in acute pyelonephritis, both local
and systemic inflammatory response pathways are
activated.

P fimbriae and
type 1 fimbriae use different receptors and different TLR4 signalling pathways. P fimbriae bind to
the Gala1-4Galb receptor
epitope in the globoseries of glycosphingolipids (GSLs) and activate epithelial cells through TLR4 in
an LPS-independent, Ser/Thr
protein kinases-dependent manner and by the release of ceramide. Type 1 fimbriae bind mannose
residues (aMan) on glycoproteins
and also activate epithelial cells through TLR4, but with the involvement of a tyrosine protein
kinase and LPS.

In epidemiological studies, P fimbriae have shown

the strongest association with acute disease severity,
with at least 90% of acute pyelonephritis but less then
20% of ABU strains expressing this phenotype

This is in contrast to type 1 fimbriae which

can be expressed by more than 90% of commensal and
uropathogenic E. Coli

P fimbriated
bacteria trigger a significant host response in the murine
urinary tract (Linder et al., 1988, 1991). The response is
primarily innate rather than specific, and involves the
activation of chemokines and the recruitment of
neutrophils

P fimbriae promote
bacterial persistence and enhance the mucosal host
response, while type 1 fimbriae do not appear to
influence the establishment of bacteriuria or trigger a
mucosal host response in the human urinary tract in this
way.