the
carotid
incidence ofCPin the atheroscle-
of of
Introduction
investigate
rotic
a
plaques
group
patients
isolated
was first
this
institution.
(CP)
Chlamydia pneuomoniae
attending
bacterium is considered
about 10
a
This
of
years ago.
common cause
bronchitis,
pneumonitis,
Materials andMethods
and chil-
in adultsl
andsinusitis both
pharyngitis,
There was
tend to be
a
total of
men and 16
27
43
infections in the latter
patients,
68
years
dren,2
although
all
mean
of
in
less severe than
the former.
women,
whom
52-84),
Chlamydia pneu-
of
age
(range
moniae
to
a
diverse
group
underwent carotid thromboendarterec-
belong
genetically
trachomatis
bacteria that also includes
for
atheroma-
Risk factors for atherosclerosis
(27
Chlamydia
These
tomy
hemodynamically significant
and
tous stenoses.
psittaci.
microorganisms
Chlamydia
a
intracellular life
are
have
As
included
cycle.
unique, dimorphic,
smoking
patients), hypertension
intracellular
diabetes
(34),
and
cardiac ischemia
they
parasites
depen-
supply
(ATP)
of the
obligate
(15),
(12
to
intracellular environment
adenosine
dent on the
the
The carotid
were
lesions
bilateral in
patients).
metabolite(s)
three
and one had
diffuse atheromatous
triphosphate
patients
within the
and
the
vascular
they replicate
cytoplasm
plaques throughout
In seven
peripheral
several
cells. C.
there was
mild
pneumoniae go through
phases
system.
patients
apparent
First there is
a
to intracellular infection.
leading
to moderate ulceration in association with the
thrombi in the carotid
removed at
containers without
in
extracellular
the
fuses
primitive sporoform existing
The
plaques.
were
plaque speci-
in
that
the
with
metaboli-
a
environment
enters
cell,
pri-
mens
sterile
surgery
placed
to
a
and then
mary liposome,
cally
changes
anyfixatives
and taken to the
released into
active reticular
which is
form,
where
were either
laboratory
they
processed
the intracellular environment.
In commonwith
or stored frozen at -25°C.
DNAwas extracted from all
immediately
manyintracellular
bacteria,
specimens
the
plaque
within
CP can survive and even
replicate
phago-
and
and then we
PCR. Two
(fresh
frozen)
sought
fail to combat their diffu-
which not
cytes,
sion and localization but also assist CP to resist
destruction. These intracellular bacteria cause
only
of CP
of
Pst
the
genome
by using
regions
gene
CP
of
were studied:
in the
(1)
11,
genome
437
a
base
nested PCRfor confir-
pairs, adding
base
229
119
killer cells either
and thus induce
chronic
directly
inflammation,
mation of
SrRNA of
in the
16
gene
activating
(2)
PCR
and;
pairs
or via interleukin
12,
base
then
pairs.
products
sequencing
cell-mediated
activation of
two mechanisms:
(1)
release of
underwent direct automatic
immunityby
(auto-
ABI,
mated DNA
and
3.0
373A
and Sequencer TM
377
macrophages through
Sequencers
T
derived from
Perkin
Gene Codes
(2)
lymphocytes;
lysis
cytokines
Elmer,
Software,
of infected cells
cytotoxic Tcells CD8+.3
AnnArbor,
by
Grayston
USA).
MI,
Corporation,
In the
cific
et a14 identified
1980s
TWAR(ATCC) wereused as
of the CP
con-
spe-
in
atheroscle-
an infective
CP,
trols
positive
genome
of CP
has
(the
antigenic components
sequencing
rotic
thus
DNA
been
normal
and
and
from histo-
plaques,
in
supporting
recently
logically
completed),
field of
the multifactorial
athero-
CPwith
carotid arteries
hypothesis
coronary
of
sclerotic
The association
atherosclerotic disease followed
was used as
a
control.
pathogenesis.
negative
with
seroepide-
with
of
studies and
the
bac-
means
discovery
miologic
Results
was detected in four tissue sam-
in
teria
ofvarious vascular sites
plaques
by
of electron
The CP
microscopy,
immunocytochemistry,
genome
s
the
and
chain reaction
which
Two
examined.
were from womenwith
is
of
two
9.3%
[PRC].5-8
polymerase
ples,
patients
CP was isolated from
were
from men and
69-77
Initially
coronary
organism
anywhere
prevalent
the
almost
but it is nowrevealed that
All were
and smokers or ex-smokers
arteries,
may
age range
years.
hypertensive,
reside in
located
At
CP infestation
plaques
system.
hypercholesterolemic,
the
the
in
vascular
but
of
ischemia
two
showed no evidence
present
myocardial
is that
a
or
role in
marked
There were
hypothesis
plays
respiratory problems.
the
and
of
one of
of
resection
with
aortic
rather
abdominal
progression
plaques
friability
patients
aneurysms,
than in their etiology.9In
volume ofliterature on this
of the
we
whom
this
underwent
light
previous surgical
increasing
decided
lesion.
to
subject
828
v. Auwers
