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The Vi capsular polysaccharide enables Salmonella enterica serovar typhi to evade microbe-guided neutrophil chemotaxis.
[typhoid]
Salmonella
enterica
serovar
Typhi
(
S
.
Typhi
)
causes
typhoid
fever
,
a
disseminated
infection
,
while
the
closely
related
pathogen
S
.
enterica
serovar
Typhimurium
(
S
.
Typhimurium
)
is
associated
with
a
localized
gastroenteritis
in
humans
.
Here
we
investigated
whether
both
pathogens
differ
in
the
chemotactic
response
they
induce
in
neutrophils
using
a
single
-cell
experimental
approach
.
Surprisingly
,
neutrophils
extended
chemotactic
pseudopodia
toward
Escherichia
coli
and
S
.
Typhimurium
,
but
not
toward
S
.
Typhi
.
Bacterial-guided
chemotaxis
was
dependent
on
the
presence
of
complement
component
5
a
(
C
5
a
)
and
C
5
a
receptor
(
C
5
aR
)
.
Deletion
of
S
.
Typhi
capsule
biosynthesis
genes
markedly
enhanced
the
chemotactic
response
of
neutrophils
in
vitro
.
Furthermore
,
deletion
of
capsule
biosynthesis
genes
heightened
the
association
of
S
.
Typhi
with
neutrophils
in
vivo
through
a
C
5
aR-dependent
mechanism
.
Collectively
,
these
data
suggest
that
expression
of
the
virulence-associated
(
Vi
)
capsular
polysaccharide
of
S
.
Typhi
obstructs
bacterial-guided
neutrophil
chemotaxis
.