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We also examined by CGH the distribution of the eight RDIs that are shown
to be involved in the pathogenesis of
E. coli
meningitis among representative
E. coli
K1 strains (
Xie et al., 2006a,b
). RDI 16 harbors the K1 capsule biosyn-
thesis gene cluster and, as expected, is present in all of these
E. coli
K1 strains.
The other pathogenic RDIs are found to exist in strains belonging to group 1 and
phylogenetic group B2. For example, RDI 1, 7, 13, 20, and 22 are widely dis-
tributed among this group of
E. coli
K1 strains. Previous studies using PCR, dot
blot, and Southern blot suggest that PAI III
536
-like, PAI II
J96
-like, and GimA-
like ectochromosomal DNA domains (ECDNA) are prevalent among O18:K1
strains, the most common serogroup in meningitis-causing
E. coli
(
Bonacorsi
et al., 2003
). Based on their virulence signatures, those ECDNAs correspond to
RDI 4, 21, and 22, respectively (
Xie et al., 2006a,b
). The distribution of these
three islands among O18:K1 strains based on CGH is consistent with previous
findings (
Bonacorsi et al., 2003
;
Xie et al., 2006a,b
). Our CGH analysis also
revealed that type VI secretion system (T6SS)-like gene clusters, including the
icmF
-like component,
clpV
,
dotU
, and
hcp2
, are present in the RDI 1 (
Xie et al.,
2006a,b
). Of interest, the T6SS clusters have two
hcp-
like genes located next to
each other in the chromosome of strain RS218, and we showed that the two Hcp
family proteins have different roles in meningitis-causing
E. coli
K1 infection
and coordinately contribute to the pathogenicity of
E. coli
K1 interaction with
HBMEC, e.g.
E. coli
binding to and invasion of HBMEC as well as release of
IL-6 and IL-8 from HBMEC (
Zhou et al., 2012
).
In addition, microbial DNA microarrays offer new opportunities for
exploring microbial gene expression profiling during microbial-host interac-
tions. For example, using
E. coli
DNA microarray analysis with microarray-
grade bacterial RNA isolated from
E. coli
K1 interacting with HBMEC, we
showed that the expression of the type 1 fimbriae and flagella genes are sig-
nificantly greater for
E. coli
associated with HBMEC compared to
E. coli
not associated with HBMEC (
Teng et al., 2005
;
Parthasarathy et al., 2007
;
Xie et al., 2008
). We subsequently showed that type 1 fimbriae and flagel-
lin play an important role in
E. coli
K1 binding to and invasion of HBMEC
(
Teng et al., 2005
;
Parthasarathy et al., 2007
), indicating that microbial DNA
microarray analysis has a potential for elucidating microbial-host interac-
tions that contribute to the pathogenesis of
E. coli
meningitis (
Kim et al.,
2005
;
Korczak et al., 2005
).
PREVENTION OF
E. COLI
PENETRATION INTO THE
BRAIN BY TARGETING THE MICROBIAL-HOST FACTORS
CONTRIBUTING TO
E. COLI
INVASION OF HBMEC
MONOLAYER
We have shown that meningitis-causing
E. coli
K1 penetration into the brain
requires
E. coli
binding to and invasion of HBMEC, involving specific micro-
bial-host interactions (so-called ligand-receptor interactions) and host cell sig-
naling molecules (
Kim, 2008, 2010, 2012
). For example, CNF1-mediated
E. coli
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