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Macrophage is the determinant of resistance to and outcome of non-lethal Babesia microti infection in mice.
[severe combined immunodeficiency]
In
the
present
study
,
we
examined
the
contributions
of
macrophages
to
the
outcome
of
infection
with
Babesia
microti
,
the
etiological
agent
of
human
and
rodent
babesiosis
,
in
BALB
/
c
mice
.
Mice
were
treated
with
clodronate
liposome
at
different
time
courses
of
B
.
microti
infection
in
order
to
deplete
the
macrophages
.
Notably
,
a
depletion
of
host
macrophages
at
the
early
and
acute
phases
of
infection
caused
a
significant
elevation
of
parasitemia
associated
with
remarkable
mortality
in
the
mice
.
The
depletion
of
macrophages
at
the
resolving
and
latent
phases
of
infection
resulted
in
an
immediate
and
temporal
exacerbation
of
parasitemia
coupled
with
mortality
in
mice
.
Reconstituting
clodronate
liposome-treated
mice
at
the
acute
phase
of
infection
with
macrophages
from
naïve
mice
resulted
in
a
slight
reduction
in
parasitemia
with
improved
survival
,
as
compared
to
mice
that
received
the
drug
alone
.
These
results
indicate
that
macrophages
play
a
crucial
role
in
the
control
of
and
resistance
to
B
.
microti
infection
in
mice
.
Moreover
,
analyses
of
host
immune
responses
revealed
that
macrophage-depleted
mice
diminished
their
production
of
Th
1
cell-cytokines
,
including
gamma
interferon
(
IFN-γ
)
and
tumor
necrosis
factor
alpha
(
TNF
-α
)
.
Furthermore
,
depletion
of
macrophage
at
different
time
courses
exaggerated
the
pathogenesis
of
the
infection
in
deficient
IFN-γ
(
-
)
/
(
-
)
and
severe
combined
immunodeficiency
(
SCID
)
mice
.
Collectively
,
our
data
provides
important
clues
about
the
role
of
macrophages
in
the
resistance
and
control
of
B
.
microti
and
implies
that
the
severity
of
the
infection
in
immunocompromised
patients
might
be
due
to
impairment
of
the
macrophages
'
function
.
