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Salmonella enterica Serovar Typhi conceals the invasion-associated type three secretion system from the innate immune system by gene regulation.
[typhoid]
Delivery
of
microbial
products
into
the
mammalian
cell
cytosol
by
bacterial
secretion
systems
is
a
strong
stimulus
for
triggering
pro-
inflammatory
host
responses
.
Here
we
show
that
Salmonella
enterica
serovar
Typhi
(
S
.
Typhi
)
,
the
causative
agent
of
typhoid
fever
,
tightly
regulates
expression
of
the
invasion-associated
type
III
secretion
system
(
T
3
SS-
1
)
and
thus
fails
to
activate
these
innate
immune
signaling
pathways
.
The
S
.
Typhi
regulatory
protein
TviA
rapidly
repressed
T
3
SS-
1
expression
,
thereby
preventing
RAC
1
-
dependent
,
RIP
2
-
dependent
activation
of
NF-κB
in
epithelial
cells
.
Heterologous
expression
of
TviA
in
S
.
enterica
serovar
Typhimurium
(
S
.
Typhimurium
)
suppressed
T
3
SS-
1
-
dependent
inflammatory
responses
generated
early
after
infection
in
animal
models
of
gastroenteritis
.
These
results
suggest
that
S
.
Typhi
reduces
intestinal
inflammation
by
limiting
the
induction
of
pathogen-induced
processes
through
regulation
of
virulence
gene
expression
.
Diseases
Validation
Diseases presenting
"tightly regulates expression of the invasion-associated type iii secretion system (t3ss-1"
symptom
typhoid
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