is the official journal of the American College of Chest Physicians. It has. Chest .... PIE syndrome. Following steroid therapy, pleural fluid disappeared,.
Interleukin-5 levels of pleural fluid and serum samples in a patient with PIE syndrome. R Matsumoto, M Ando, H Kohrogi, S Araki and K Takatsu Chest 1992;102;1296-1297 DOI 10.1378/chest.102.4.1296 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/102/4/1296
Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1992by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692
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needed,
we
possible,
should
should
think
that
be
make
valve
tried,
valve
reconstruction,
even
iflater
replacement
on
whenever
valve
An
unavoidable.
ciency.
J
Am
Cardiol
J.
2 Eskilsson
JP, 1973;
Tricuspid
SE Traumatic
tricuspid
insufficiency
caused
by
Ann
trauma.
Thorac
Surg
1991;
course
ofsevere
valve
insufficiency
anteroseptal myocardial infarction, coronary tricular septal defect as a result of blunt chest 1989;
with
fistula,
and
yen-
injury.
Z Kardiol
insufficiency:
a clinical
8 Stephenson
LW,
Mac
nonpenetrating
Vaugh
rupture
and
incompetence
H III,
HJ.
Traumatic
1982;
trauma.
Cardiol
1970;
10 Brandenburg Traumatic valve.
J
Cardiol
1966;
Justice J, Olsen patients with suspected 1990; 50:530-33 ML.
Trauma 13
RC,
by 77:
ofblunt
chest A,
Piwnica
tricuspide. vase
monitoring
injury.
Thorac
of myocardial
Ann
contusion:
trauma.
tricuspid
A,
MB,
Miller
FA.
1986; 26:510-20
J,
reconstructive
Soyer
R,
operation
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evalu-
Cardiovasc
Cardiol
1972;
W, K#{246}rferR. Traumatic Surg
1978;
incompetence.
J
Cardio-
19:557-61
Hirotsugu
Kishi *Fmm
Ando, (Drs.
Kohrogi,
Takatsu, the First
of Pleural Fluid in a Patient
M.D., Ph.D.; Masayuki M.D.; Shukuro Araki, Ph.D. Department
ofinternal
Medicine
M.D. , FC.C.P;
(Drs.
IL-5
that
be
determined
humans,
serum
infection
IL-5.
can
and
have
eosino-
parasite
of
others
IL-5
we
samples
examined
and
pleural
syndrome. AND
were
normal
with
obtained
and
centrifuged
cells
at - 20#{176}C until
with
fluid
was
five
other
from
showed
PIE
The and
pleural
debris.
syndrome
obtained
from
patients
no eosinophilia
effusion.
remove
a patient
Pleural
syndrome who
to
from
volunteers.
PIE
METHODS
Fluid.c
carcinomatous pleurisy eral blood or pleural
in their fluid
These
test
a
with periph-
samples
were
samples
were
use.
Reagents human
with
IL-2,
human
from Genzyme
TB13,
react
IL-i,
Recombinant
more,
human
IL-5
IL-S,5
IL-S.
IL-3,
IL-6
was
and
M-CSF
Mass).
Further-
antibody
as previously
were
and
(Boston,
monoclonal
psorified
TGF-3
C-CSF
IL-4,
Corporation
an anti-mouse
Assay
For the method
to Detect
assay
coated
mM
NaCl,
which
can
described.6
Matsumoto,
IL-5 IL-5,
to detect
with pH
TB13
7.4)
with at
Human
of human
established
were
(5 g/ml)
overnight
PBS
room
we
mouse
slightly
modified
IL-5.3
Briefly,
in PBS
(10
containing
2 percent
temperature.
After
Labs,
polyclonal
rabbit
incubated
again
and
peroxidase-coupled
Richmond,
room
Cal)
was
temperature.
propionic
acid
percent
H202
added
reactions
percent
rIL-S binant
were 320
Figure
nm)
the
by adding
IL-3,
The
lnterteukin-6
test samples at 4#{176}C. Then,
were after
IgG
percent
(10 mM,
10 h at room
(Bio-Rad incubation
3-(4-hydroxy
pH
7.0)
I 0.03
temperature.
NaOH
containing
1.5
measured
at
nm
spectrometer of this
fluorescence
Levels
Ig
was curve
IL-6,
antibodies
0.25N
fluorescence
IL-4,
PBS
IL-S
0.5
buffer
incubated
a standard
2 pg/mI). IL-2,
and
for
with
by an hour’s
washing,
on a fluorescence
1 shows
(sensitivity: IL-i,
stopped
and
NaN3,
(excitation chi).
was
albumin
wells
anti-rabbit
followed
in phosphate
140 were
at 4#{176}C.
goat
added,
After
phenyl) The
anti-human overnight
plates sites
serum the
again,
ELISA
phosphate, binding
bovine
washing
were added
mM
washing
0.05 percent Tween 20 (PBS-Tween), to the wells and incubated overnight
the
polystylen
at 4#{176}C. Nonspecific
applied
containing
at
and
Kohrogi and Araki) and Institute for Medical Immunology Matsumoto and Takatsu), Kumamoto University Medical School, Kumamoto, Japan. Reprint requests: Dr Matswnoto, 1st Department of Internal Medicine, Kumamoto University Medical School, 1-1-1 Honjo, Kumamoto 860, Japan 1296
ten
Horseradish
Ando, M.D.;
PIE
and Pleural
samples
from
2 h
R!,*7ji Matsumoto,
or
in the
eosinophil and
expressing
allergy of
MATERIALS
blocked
lnterleukin-5 Levels and Serum Samples with PIE Syndrome*
We
Surg
25:555-59
mitral
shows
suggest
in mice3
with
factor,
production
of IL-5
Samples
ELISA
Esp
102:1296-97)
humans.2
reports
concentration
patient
araalyzed. P,
y permanente: la insuficiencia
de
a
in
acid
mice
with
method
were obtained Blondeau
for correction
J Thorac
insufficiency.
La anuloplastia selectiva,regulable original para del tratamiento
Rev
the
ofa
stored
Surg
Objective
Dauptain
transgenic
patients
concentration
patient
of
a review
J Trauma
in
These
in some
Recombinant
Deloche
and
teenica
Bircks
RL. Selective
cardiac
that
eosinophilia.’
Serum
L, Giuliani ER. of the tricuspid
61:1-5
15 De Vega NG.
16
blunt
P. Farnell
A, et al. A new
of mitral
una
WR, Prager
1992;
ribonucleic
activity
observed
Serum
insufficiency.
18:911-15
spectrum
Mucha
Carpentier
1971;
Campeau tendineae
is
especially
valvular
caused 1979;
1985; 25:620-27
Frazee
ation 14
The
tricuspid
results
syndrome
of IL-5,
a T-cell-replacing
an ELISA
and
McGoon DC, of the chordae
11 ReifJ,
12 Tenzer
CS. Traumatic
messenger
colony-stimulating
the
26:200-04
RO, rupture
Am
nterleukin-5,’
fluid
Tricuspid
mRNA
Because
71:50-3
KastorJA.
PIE
production
may be due to an enhanced
768-72
J
I
philia
tricuspid
of the ventricular septum J Thorac Cardiovasc Surg
9 Liu SM, Sako Y, Alexander Am
eosinophilia;
with H , Hauch study. Z Kardiol
the
(Che8t
severe
L, Pearson AC. Delayed rupture of tricuspid following blunt chest trauma. Am Heart J 1990; V, Oelert
in
of increased
recently
78:343-47
6 Hilton T, Mezei papillary muscle 119:1410-12 7 Voss H , Petersen
eosinophilia
and serum
These
immunosorbent assay; IHES idiopathic hypereosinophilic syndrome; 1L interleukin; PBS phosphate-buffered saline; PIE pulmonary infiltration with
51:320-22
tricuspid
improved
undetectable.
of a
therapy,
ELISAenzyme-linked
4 Dodd DA, Johns JA, Graham TP Jr. Transient severe mitral and tricuspid regurgitation following blunt chest trauma. Am Heart J 1987; 114:652-54 5 Renner U, Busch UW, Sebening H, Bibra H von, Bauer R. Asymptomatic
(53 pg/mI) steroid
eosinophilia
the lung.
nonpenetrating
chest trauma. Acta Med Scand 1985; 218:347-52 3 Noera G, Sanguinetti M, Pensa P. Biagi B, Cremonesi A, Lodi R, et al. Tricuspid valve incompetence caused by nonpenetrating thoracic
that
in the pleural
samples
Following
became
consequence
32:723-26
serum
syndrome.
concentration
suggested
insuffi-
PIE
was detected
IL-5
in the
fluid disappeared,
IL-5
Nolan
of
and
with
pleural RF, Schrank
ng/ml)
patient
REFERENCES
1 Marvin
production
increased
fluid (7.2
deterioration
G-CSF,
of Pleural
Downloaded from chestjournal.chestpubs.org at COMMAX GROUP on July 10, 2011 © 1992 American College of Chest Physicians
405
(F-3000, ELISA of 2 ng/ml GM-CSF
assay
Hitausing
of recomor
Fluid (Matsumoto
TGF-3
et a!)
Recently, 400
the
Samoszuk
cytoplasm
ophilia
E
in
Hodgkin’s
production.
300
C
ease,
C)
C.) C
of
which
assay
we
C) U)
or
parasites,
0) 0
hyperproduction immune
U-
100
I
I
I
Standard 1. A standard
FIGURE
IL-S
ELISA
was
IL-5
curve
100 at 405
asthma
since
stridor.
During
ofIL-S
high
phils
three in
chest
Also,
with
asthma
with
the
steroid
with human
was
allergy
the
and
number
normal range. As shown in Table 1 , we detected before steroid therapy (53 pg/mI) and
on the
that
but
not
in the
senim
pleural
fluid
showed
no eosinophilia
of other
finding
that
IL-5
factor
sample
was
induced
the
and
IL-5 in
after
serum
pleural
fluid
the
therapy
with
carcinomatous
peripheral
blood
IL-5
has
in the
is important
in humans
Concentration
in
back
to
Pleural
FEUI4S*
Samples serum
(n
=
CJ,
biology
of eosinophil
sample (7.2
effects
ng/
nor
in the
pleurisy
who
or plenaral
as well
serum
(before
Patient’s
serum
(after
Patient’s
pleural
Other
patient’s
steroid
therapy)
53 pg/mI
therapy)
fluid pleural
and
ND steroid
ND 7.2
fluids
(n
=
5)
=
not detected.
lung
With
the
and
and
steroid
We
therapy,
conclude
of PIE
IL-5
have
effusion serum
and
undetectable.
IL-5
might
pleural
normalized
pathogenesis
ng/mI ND
HD,
Young
1G.
differentiation
mouse
and
A, Takaki
M , et
disIL-5
that
IL-
syndrome.
Molecular
factor
B cells.
5, Koyama
a] . Transgenic
differentiation
and
cellular
(interluekin-5)
Immunol
factor
LA,
gene
J
Strath
transgenic
M,
mice
N, Katoh
mice
production.
Dent
and
Rev 1988;
its
102:29-
5, Matsumoto
expressing (IL-5)
Exp
develop
Med
Mellor
1991;
AL,
expressing
a
B
R, Migita
cell
growth
and
eosinophilia
and
auto-
173:429-37
Sanderson
CJ.
interleukin
J
5.
Eosinophils
Exp
in
Med
1990;
172:1425-31 S
Mita
et
S,
Hosoya
al.
Y, Kubota
Rapid
interleukin-S
I,
methods (IL-5)
for using
column.
Harada
N,
Kikuchi
Y, et al.
Takahashi
the
T,
Production
anti-murine
characterization
human IL-5
Natl
1989;
M,
Kinashi
Acad
T,
recombinant
antibody-coupled
Method
of murine
Proc
T, Takahashi
Honjo
of
of a monoclonal
factor
II.
T,
Matsumoto
B-cell
growth
Nishihara
purification
J Immunol
the molecular
125:233-41 T,
antibody
T-cell-replacing USA 1987;
Sci
Ohara
J,
useful
in
factor! 84:4581-
55
7 Samoszuk RNA
M , Nansen
philia. 8 Owen D,
L.
in Reed-Sternberg Blood WF, Sheffer
eosinophils *ND
the
blood
eosinophilia.
the
The
50
defined.’
Concentration
10)
Patient’s
to
to the peripheral
Campbell
on human
3 Tominaga
effusion.
Samples
IL-S
inflammation.
102:107-135 2 Sanderson
is a T-cell-replacing
Serum
that
K, Tominaga A, Harada N, Mita 5, Matsumoto M, T, et al. T cell-replacing factor (TRF)/interleukin 5 (IL5): molecular and functional properties. Immunol Rev 1988;
colony-stimulating
is not
in the
suggested
Takahashi
6
Normal
limited
in the
detected
was
REFERENCES
antibody
IL-5
eosino-
than
ACKNOWLEDGMENTS: We thank Drs. Y. Hirai, M. Takaoki, T. Kishimoto and T Ishii for providing IL-i, IL-2, IL-6 and TGF-, respectively. We also thank Dr. Y. Hosoya (Olympus Optical Co. Ltd. , Tokyo) for purifying polyclonal rabbit anti-human IL-5 IgG antibodies.
4
eosinophil
Although
became
5
effusion fell
in the
steroid
concentration
With
pleural
of eosinophils
in the
its role
1 -1L-5
been
lung
peripheral
immunoaflinity
Table
of the
have
the
patient, fluid
1 Takatsu
controlled
32-stimulants.
patients
production.
in mice,
from
were
syndrome
activity in humansa made it important to study the relationship in some diseases between pathogenesis of eosinophilia and
might
leakage
center
this there
eosino-
DISCUSSION
The
the
of
precipitating
the PIE
asthma
and
shadow
the
effusion No
Thus,
bronchial
consolidation
was
therapy.
fungi or any parasite
was observed. The
which
revealed cells.
pleural
focus
and
within the
ml),
was
drugs causes
accumulate
In our
in the
fungi,
the
eosinophils
develops.
marked
with
pneumonia
a consolidation
pleural
total
other
shadow
to steroid
effusion
of theophylline
completely,
chest
migrating
showed
of the
diagnosed.
therapy,
probably
production
bronchial
blood,
and
Candida,
administration
had
responsive
pleural
for 90 percent
from
peripheral
but
of the
no drug
disappeared
the
distribution
to Aspergillus,
found.
she
roentenogram
no segmental
accounted
antibodies
suffered
an abnormal
years,
treatment
Examination
who
contained
past
her
with
side.
was obtained
REPORT
woman
eosinophilia
admission,
left
patient’s lung
more
ELISA
which
Since
lung,
blood. That much more IL-5 pleural fluid than in the serum
peripheral
( pg/mi)
eosinophils.
is the
pneumonia
was
an
response,
immune
eosin-
of IL-5 role of IL-5.
an
the pulmonary consolidation appeared, eosinophilia was
school
the
to antibiotic
shadow
which
a
I
2000
nm.
Japanese
marked
On
I
concentration
CASE A 28-year-old
resistant
I
200
is shown.
below
with
I
20
philia
Through
some antigens, of
response
migrating
and
2
elicit
that
enhanced IL-5 role of IL-5 in
picogram-order of the
in
in situ
an
suggested
in vivo for example
a part
mRNA
using
due to a crucial
IHES.
the
clarify
In PIE syndrome,
200
C)
therefore
with
detect
IL-5
cells
and
patients
can
could
detected
disease was et ale reported
Owen
eosinophilia
0
Nansen7
Reed-Sternberg
technique
hybridization
Lt)
and
of
nophilic
1990;
in the syndrome.
of interleukin-5
of Hodgkin’s
messenger
with
disease
eosino-
75:13-16
Rothenberg AL,
Detection cells ME,
5 and
blood
ofpatients
J
Med
Exp
CHEST
J,
Petersen
et oil. Interleukin
with 1989;
I 102
Weller
PF,
Silberstein
phenotypically the
altered
idiopathic
hyperosi-
170:343-48
I 4 I OCTOBER,
Downloaded from chestjournal.chestpubs.org at COMMAX GROUP on July 10, 2011 © 1992 American College of Chest Physicians
1992
1297
Interleukin-5 levels of pleural fluid and serum samples in a patient with PIE syndrome. R Matsumoto, M Ando, H Kohrogi, S Araki and K Takatsu Chest 1992;102; 1296-1297 DOI 10.1378/chest.102.4.1296 This information is current as of July 10, 2011 Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/102/4/1296 Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions.
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