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et al., 2006
). These findings suggest that decreased binding of the
ompA
dele-
tion mutant may be related to its lower expression of type 1 fimbriae. The
ompA
deletion mutant was significantly less efficient in its penetration into the brain
in vivo compared to the parent
E. coli
K1 strain (
Wang and Kim, 2002
). Addi-
tional studies are needed to determine whether these in vitro and in vivo defects
of the
ompA
deletion mutant are in part related to its decreased expression of
type 1 fimbriae and to also understand how the deletion of
ompA
affects type
1 fimbria expression.
NlpI
NlpI is shown to be an important factor of Crohn's disease-associated
E.
coli
strain LF82 (083:H1) to interact with intestinal epithelial cells (
Barnich
et al., 2004
). Deletion of
nlpI
in
E. coli
strain LF82 decreased expression of
type 1 fimbriae and flagella (
Barnich et al., 2004
). We showed that NlpI is
an outer membrane-anchored protein and contributes to meningitis-causing
E. coli
K1 binding to and invasion of HBMEC (
Teng et al., 2010
). Unlike
strain LF82, deletion of
nlpI
in meningitis-causing
E. coli,
however, did not
affect the expression of type 1 fimbriae, flagella and OmpA, indicating that
the contribution of NlpI to HBMEC binding and invasion is independent of
those bacterial factors in meningitis-causing
E. coli
. This concept is shown by
the demonstration that mutants deleted of type 1 fimbriae, OmpA and NlpI
exhibited significantly decreased HBMEC binding and invasion compared
to mutants deleted of individual factors or a combination of the two factors
(
Teng et al., 2010
). These findings suggest that type 1 fimbriae, OmpA and
NlpI are likely to contribute to HBMEC binding and invasion independent of
each other. It remains, however, incompletely understood how and why sev-
eral bacterial factors of meningitis-causing
E. coli
are involved in HBMEC
binding.
E. coli
structures contributing to invasion of HBMEC
Previous studies using
TnphoA
mutagenesis, signature-tagged mutagenesis and
differential fluorescence induction with screening of a
gfp
fusion library identi-
fied several
E. coli
determinants contributing to invasion of HBMEC, which
include Ibe (named after
i
invasion of
b
rain
e
ndothelial cell) proteins and cyto-
toxic necrotizing factor 1 (CNF1) (
Huang et al., 1995, 1999
;
Wang et al., 1999
;
Badger et al., 2000a,b
;
Hoffman et al., 2000
;
Khan et al., 2002
). Isogenic dele-
tion mutants were significantly less invasive in HBMEC and less able to pen-
etrate into the brain in vivo (
Table 10.2
) and their invasive defects were restored
to the levels of the parent strain by complementation with respective wild-type
genes.
Ibe proteins
Ibe A, B, and C proteins were identified via
TnphoA
mutagenesis of meningitis-
causing
E. coli
K1 strain RS218 and screening of the mutants for loss of invasion
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