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INFLAMMATION AND IMMUNOPHARMACOLOGY
Production in an Intercellular Adhesion Molecule-1- and B7.1-Dependent Manner
Departments of Tumour Biology (T.M., H.K.T., H.I., R.T., N.T.), Pharmacology (H.K.T., M.Y., S.M., M.N.), and Pathology (T.Y., T.A.), Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan
Received August 6, 2002; accepted October 29, 2002.
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Abstract |
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production induced by
LPS in peripheral blood mononuclear cells (PBMCs) was inhibited by the
addition of antibodies against these adhesion molecules, suggesting the
dependence of TNF- production on cell-cell interaction through these
adhesion molecules. Moreover, we found that histamine
(10-7–10-4 M) concentration
dependently inhibited the expression of ICAM-1 and B7.1, but not B7.2 on
monocytes induced by LPS. Histamine also inhibited the responses of
TNF- production induced by LPS. The modulatory effects of histamine on
ICAM-1 and B7.1 expression and TNF- production were all concentration
dependently antagonized by famotidine but not by d-chlorpheniramine
and thioperamide, and were mimicked by selective H2-receptor agonists but not
by H1-, H3-, and H4-receptor agonists, indicating the involvement of
H2-receptors in the histamine action. Dibutyryl cAMP down-regulated ICAM-1 and
B7.1 expression on monocytes stimulated by LPS, suggesting the mediation by
the cyclic adenosine monophosphate-protein kinase A pathway of H2-receptor
activation. These results as a whole indicated that histamine via H2-receptor
inhibited the LPS-induced TNF- production through the regulation of
ICAM-1 and B7.1 expression, leading to the reduction of innate immune response
stimulated by LPS.
),
vascular endothelial cells (Loppnow and
Libby, 1989), and granulocytes
(Schade et al., 1987).
Activated cells in turn release many kinds of inflammatory mediators such as
interleukin (IL)-1
, IL-6, interferon (IFN)-
, TNF-,
macrophage migration inhibitory factor, and chemokines
(Bozza et al., 1999;
Morelli et al., 2001).
TNF- and macrophage migration inhibitory factor seem to be very
important for the development of endotoxin shock
(Beutler et al., 1985;
Roger et al., 2001). The
myelomonocytic differentiation antigen CD14, a principal receptor for a
complex of LPS and LPS-binding protein, lacks a transmembrane domain.
Therefore, the presence of transmembrane signaling molecules has been
suggested and explored. The recently discovered Toll-like receptor (TLR) 4,
together with its accessory protein MD2, transmits LPS-CD14 binding signals
intracellularly, resulting in the activation of several signaling pathways,
the I
B kinase-nuclear factor-B pathway and three mitogen-activated
protein kinase pathways: extracellular signal-regulated kinases 1 and 2, c-Jun
N-terminal kinase, and p38 (Tapping et
al., 2000; Guha et al.,
2001).
Histamine is a well known bioactive amine in the granules of mast cells and
basophils and plays an important role in inflammatory and allergic responses
once these cells are activated by IgE-dependent and -independent stimuli. A
different mode of the presence of histamine has been suggested, which was
induced by LPS and some cytokines. LPS produced the induction of histidine
decarboxylase, a histamine-synthesizing enzyme, in murine tissues
(Endo, 1982), macrophages
(Takamatsu et al., 1996), and
T lymphocytes (Aoi et al.,
1989). This induced histamine has been repeatedly suggested to
have different kinetics from that in stored pools
(Takeuchi et al., 1999) and
may also have an immunomodulatory function. In addition to its inflammatory
effects, histamine has immunomodulatory effects: regulation of cytotoxic
T-cell activity (Khan et al.,
1989), enhancement of natural killer (NK) cell activity
(Hellstrand et al., 1994), and
regulation of cytokine production in peripheral blood mononuclear cells
(PBMCs) (Elenkov et al., 1998;
Takahashi et al., 2002b).
It was reported that long-term treatment with LPS can induce human
T-lymphocyte proliferation and cytokine production, which was strongly
dependent on direct cell-to-cell contact of responding T lymphocytes with
monocytes (Mattern et al.,
1994). In addition to T-cell receptor-major histocompatibility
complex recognition, the costimulatory signals from adhesion molecules are
required for inducing T-cell response, including lymphocyte
function-associated antigen (LFA)-1, (CD11a/CD18)/intercellular adhesion
molecule (ICAM)-1 (CD54), and CD28/B7 (B7.1, CD80, B7.2, and CD86)
(Gollob et al., 1996;
Greenfield et al., 1998). All
these molecules are important participants in the activation of T cells,
lowering the concentration of antigen required for stimulation and promoting
more sustained signaling from the T-cell receptor. However, little is known
about the roles of these adhesion molecules on the acute effects of LPS on the
cytokine production.
In the present study, we examined the effect of LPS on the expression of
ICAM-1, B7.1, and B7.2 on human monocytes using fluorescence-activated cell
sorting analysis and their involvement in LPS-stimulated TNF-
production. Second, we investigated the effect of exogenous histamine on the
LPS-induced changes in the expression of ICAM-1, B7.1, and B7.2 and the
production of TNF- to evaluate the role of histamine on innate immune
response induced by LPS.
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Materials and Methods |
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TopAbstractMaterials and MethodsResultsDiscussionReferences |
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, and
IFN- were purchased from R&D Systems (Minneapolis, MN). Mouse IgG2a
against human anti-TNF- Ab was purchased from R&D Systems. IgG2a
class-matched control (CMC) was purchased from Sigma-Aldrich. Histamine was
purchased from Nakalai Tesque (Kyoto, Japan). Dimaprit, 4-methylhistamine, and
2-(2-pyridyl)ethylamine dihydrochloride were kindly donated by Drs. W.A.M.
Duncan and D.-J. Durant (The Research Institute, Smith Kline & French
Laboratories, Welwyn Garden City, Hertfordshire, UK).
R-()-Methylhistamine dihydrochloride [(R)--MH]
was a gift from Dr. J.-C. Schwartz (Unite de Neurobiologie, Centre Paul Broca
de l' Institut National de la Santé et de la Recherche Médicale,
Paris, France). d-Chlorpheniramine maleate, ranitidine, and
famotidine were provided by Yoshitomi Pharmaceutical Co. Ltd. (Tokyo, Japan),
Glaxo Japan (Tokyo, Japan) and Yamanouchi Pharmaceutical Co. Ltd. (Tokyo,
Japan), respectively. Thioperamide hydrochloride was provided by Eisai Co.
Ltd. (Tokyo, Japan). dbcAMP was purchased from Wako Pure Chemicals (Tokyo,
Japan). For flow cytometric analysis, fluorescein isothiocyanate
(FITC)-conjugated mouse IgG1 mAb against ICAM-1/CD54 (6.5B5) and
phycoerythrin-conjugated anti-CD3, anti-CD14, or anti-CD19 mAb were purchased
from DAKO (Glostrup, Denmark). FITC-conjugated mouse IgG1 mAb against
B7.1/CD80 (MAB104) was purchased from Immunotech (France, Marseille).
FITC-conjugated mouse IgG1 mAb against B7.2/CD86 (2331FUN-1) was purchased
from BD PharMingen (San Diego, CA). FITC-conjugated IgG1 CMC was purchased
from Sigma-Aldrich. Isolation and Culture of PBMCs. Normal human PBMCs were obtained from human volunteers after oral informed consent. Twenty to fifty milliliters of peripheral blood was withdrawn from the vein of the forearm. PBMCs were isolated from buffy coat of 10 healthy volunteers by centrifugation on Ficoll-Paque (Pharmacia AB, Uppsala, Sweden), and then washed three times in RPMI 1640 medium (Nissui Co. Ltd., Tokyo, Japan) supplemented with 10% (v/v) heat-inactivated fetal calf serum, 20 µg/ml kanamycin, and 100 µg/ml streptomycin and penicillin (Sigma-Aldrich). PBMCs were suspended at a final concentration of 5 x 105 cells/ml in RPMI 1640 medium supplemented with 10% (v/v) heat-inactivated fetal calf serum. Endotoxin concentrations of the medium described above were measured by the endospecy (Seikagaku Kogyo, Tokyo, Japan) kit with a lower limit of detection of 0.06 EU/ml.
Flow Cytometric Analysis. PBMCs (1 x 106 cells/ml) were cultured at 37°C in a 5% CO2/air mixture under different conditions as indicated. The culture cells (5 x 105 cells/sample) were washed once with washing buffer (phosphate-buffered saline supplemented with 2.5% normal horse serum, 0.1% NaN3, and 0.01 M HEPES, pH 7.3). Then, the cells were incubated with 1 µg of FITC-conjugated anti-CD54 Ab, anti-CD80 Ab, anti-CD86 Ab, anti-CD40 Ab, anti-CD58 Ab, and CMC, or phycoerythrin-conjugated Abs (anti-CD3 Ab, anti-CD14 Ab, and anti-CD19) for 20 min at 4°C. After washing, the cells were fixed with 2% paraformaldehyde and analyzed with a FACS Calibur (BD Biosciences, San Jose, CA), and data were processed using the CELL QUEST program (BD Biosciences). The data were expressed as the relative fluorescent intensities against CMC. The results are represented as the means ± S.E.M. of five donors.
Cytokine Assays. PBMCs (1 x 106 cells/ml) were
incubated under the same conditions as described under Flow Cytometric
Analysis. The cells were incubated with LPS for 24 h. When the effects of
histamine or Abs against adhesion molecules were examined, these were added to
the media simultaneously with LPS at the start of the culture. After culture,
the cell suspensions were transferred into Eppendorf tubes and centrifuged.
The cell-free supernatant fractions were assayed for IL-18, IL-12 (p70),
TNF-, and IFN- protein. The cytokines were measured using ELISA
with the multiple Abs sandwich principle (Quantikine; R&D Systems). The
detection limits of the ELISA for IL-18, IL-12, TNF-, and IFN-
were 10 pg/ml. The results were expressed as the mean ± S.E.M. of five
donors.
Statistical Analysis. The statistical significances were evaluated using analysis of variance, followed by the Student's two-tailed t test. A probability value less than 0.05 was considered to be significant.
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Results |
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Effect of LPS on Expression of ICAM-1. The timecourse (2–48 h) changes in the expression of ICAM-1, B7.1, and B7.2 on monocytes induced by LPS (1000 pg/ml) (Fig. 3, A–C) and the dose-response relationship for the effect of LPS (Fig. 3, D–F) were determined in detail. As shown in Fig. 3, A to C, LPS time dependently up-regulated ICAM-1, B7.1, and B7.2 expression on monocytes. The expression of all three antigens was increased to significant levels 18 h after the start of the stimulation with LPS (1000 pg/ml) and reached an almost maximum level at 24 h. The effect of LPS on the changes in the expression of ICAM-1, B7.1, and B7.2 was concentration-dependent (1–1000 pg/ml) when the effect was determined 24 h after the start of incubation. A spontaneous increase in the expressions of ICAM-1 and B7.2, but not B7.1 on monocytes was observed in untreated PBMCs. The effect of LPS on ICAM-1 expression was significant at 100 pg/ml and above, whereas that on B7.1 and B7.2 was significant at 10 pg/ml and above.
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Inhibitory Effect of Histamine on LPS-Induced ICAM-1 and B7.1 Expressions on Human Monocytes. The effect of histamine (10-7–10-4 M) on LPS (1000 pg/ml)-induced expression of ICAM-1, B7.1, and B7.2 was determined at 24 h after the start of incubation (Fig. 4). Histamine prevented LPS-induced ICAM-1 and B7.1 expression on monocytes in a concentration-dependent manner (Fig. 4). The maximal inhibition of histamine on ICAM-1 and B7.1 expression was 60%. However, in the same concentration range, histamine had no effect on LPS-induced B7.2 expression at all. IC50 values for the inhibitory effect of histamine on the expression of ICAM-1 or B7.1 induced by LPS were estimated to be both 1.0 µM.
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Effects of Histamine Receptor Antagonists and Selective Histamine
Receptor Agonists on LPS-Induced ICAM-1 and B7.1 Expressions. To determine
the histamine receptor subtypes involved in the effects of histamine on
LPS-induced ICAM-1 and B7.1 expression, one of four classes of receptor
antagonists, d-chlorpheniramine (H1-receptor antagonist), famotidine
(H2-receptor antagonist), or thioperamide (H3- and H4-receptor antagonist),
was added to the culture medium at the concentration of
10-6 Mor10-4 M in the presence
(10-4 M) or the absence of histamine. These antagonists
alone had no effect on the LPS-induced ICAM-1 and B7 expression without
histamine (Fig. 5, A and C).
Famotidine concentration dependently antagonized the effects of histamine on
ICAM-1 and B7.1 expression (Fig. 5, A and
C). In contrast, the same concentrations of
d-chlorpheniramine and thioperamide had no antagonizing effect.
Another H2-receptor antagonist, ranitidine, also exerted a similar effect to
famotidine (data not shown). Consistent with the effect of H2-antagonists on
histamine action, selective H2-receptor agonists dimaprit and
4-methylhistamine (Black et al.,
1972; Parsons et al.,
1977) mimicked the effects of histamine on ICAM-1 and B7.1
responses induced by LPS (Fig. 5, B and
D). On the contrary, both selective H1-receptor agonist
2-(2-pyridyl) ethylamine (Durant et al.,
1975; Levi et al.,
1976) and H3/H4-receptor agonist
R-()-methylhistamine
(Arrang et al., 1987;
Nakamura et al., 2001) had no
effect on LPS-induced ICAM-1 and B7.1 expression
(Fig. 5, B and D).
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Effect of Dibutyryl cAMP on LPS-Induced ICAM-1, B7.1, and B7.2 Expression on Human Monocytes. To explore the mechanism by which histamine inhibited the LPS-elicited expression of ICAM-1 and B7.1, the effect of a cAMP analog, dbcAMP (10-7–10-4 M) on the LPS (1000 pg/ml)-induced expression of ICAM-1 and B7.1 on monocytes was examined (Fig. 6). dbcAMP concentration dependently inhibited LPS-induced ICAM-1 and B7.1 expression, but did not exhibit any effect on B7.2 expression. IC50 values for the inhibitory effect of dbcAMP on the expression of ICAM-1 or B7.1 induced by LPS were estimated to be both 2 µM. Thus, the effect of dbcAMP mimicked that of histamine.
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Dose-Response Relationship for Effect of Histamine on LPS-Induced
TNF- Production in PBMCs. The effect of histamine
(10-7–10-4 M) on LPS (1000
pg/ml)-induced production of TNF- was determined at 24 h after the
start of culture (Fig. 7A).
Histamine inhibited LPS-induced TNF- production in PBMCs in a
concentration-dependent manner (Fig.
7A). At 10-4 M, histamine completely
abolished the LPS-induced production of TNF-. The IC50 value
for the inhibitory effect of histamine on TNF- production was estimated
to be 500 nM. As in the case of the regulation of the expression of adhesion
molecules, we determined the receptor subtypes involved in histamine action.
PBMCs were stimulated with histamine (10-4 M) in the
presence of antagonists (10-6 or
10-4 M), d-chlorpheniramine (H1), famotidine
(H2), or thioperamide (H3 or H4). Among the antagonists used, famotidine
concentration dependently antagonized the inhibitory effect of histamine on
TNF- production (Fig.
7B). Another H2-receptor antagonist, ranitidine, also exerted a
substantially similar effect to famotidine (data not shown). Selective
H2-receptor agonists dimaprit and 4-methylhistamine mimicked the effects of
histamine on TNF- production induced by LPS; however, H1-selective
agonist 2-pyridyl-ethylamine (2-PEA) and H3/H4-agonist
R-()-methylhistamine had no effect
(Fig. 7C). DbcAMP also
concentration dependently inhibited LPS-induced TNF- production
(Fig. 7D). At
10-4 M, the inhibition by dbcAMP was complete. These
results strongly suggested that the effect of histamine on TNF-
production induced by LPS was mediated by the stimulation of typical
H2-receptors.
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Inhibition of LPS-Induced TNF- Production in PBMCs by
Anti-ICAM-1Ab, Anti-LFA-1 Ab, Anti-B7.1 Ab, or Anti-B7.2 Ab. We
investigated the effect of the addition of anti-ICAM-1, anti-LFA-1, anti-B7.1,
or anti-B7.2 Ab on LPS (1000 pg/ml)-induced TNF- production to evaluate
the possible involvement of ICAM-1, B7.1, or B7.2 in the response
(Fig. 8). These Abs themselves
had no effect on TNF- production (data not shown).
Figure 8 shows that all four
Abs inhibited LPS-induced TNF- production in a concentration-dependent
manner. The maximal effects obtained with anti-ICAM-1, anti-LFA-1, anti-B7.1,
or anti-B7.2 Ab were 60, 29, 33, and 38%, respectively. Although the
combination of anti-ICAM-1 Ab, anti-B7.1 Ab, and anti-B7.2 Ab produced about
90% inhibition of the cytokine responses induced by LPS, the combination of
anti-ICAM-1 Ab and anti-B7.1 Ab also produced about 85% inhibition
(Fig. 8). The class-matched
non-relevant Ab at the concentration of 100 µg/ml had no effect on
LPS-induced cytokine response.
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Involvement of Endogenous TNF- on LPS-Induced Changes in
ICAM-1, B7.1, and B7.2 Expression on Monocytes. To examine whether the
endogenously produced TNF- was involved in the effect of LPS on ICAM-1,
B7.1, and B7.2 expression, we added different concentrations (1–1000
ng/ml) of anti-TNF- Ab to the culture with LPS (1000 pg/ml). We found
that anti-TNF- Ab blocked only the expression of ICAM-1
(Fig. 9). The CMCs (IgG2a) of
anti-TNF- had no effect on the expression of these adhesion molecules
(Fig. 9).
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Discussion |
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TopAbstractMaterials and MethodsResultsDiscussionReferences |
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;
Zou et al., 2000), we
confirmed the time-dependent up-regulation of the expression of ICAM-1, B7.1,
and B7.2 induced by LPS (Fig.
3). The inhibition of TNF- production by anti-ICAM-1 Ab and
anti-LFA-1 Ab clearly indicated the involvement of ICAM-1/LFA-1 interaction in
LPS-induced production of TNF- (Fig.
8). This finding was similar to a previous result that
IL-18-induced production of IL-12, TNF-, and IFN- in human PBMCs
was dependent on the interaction between ICAM-1 and LFA-1 on monocytes and
T/NK cells (Yoshida et al.,
2001; Takahashi et al.,
2002a). Thus, the interaction of ICAM-1/LFA-1 plays important
roles in inducing TNF- production in LPS-stimulated human PBMCs as in
the case of IL-18-stimulated TNF- production. Moreover, anti-B7.1 Ab
and anti-B7.2 Ab also inhibited the production of TNF- induced by LPS
(Fig. 8), suggesting the
involvement of B7/CD28 interaction in LPS action.
The activation of NF-B in monocytes/macrophages has been repeatedly
demonstrated to mediate LPS-CD14-TLR4 signaling for increased transcription of
TNF- (Ardeshna et al.,
2000). Moreover, the promotor/enhancer regions of ICAM-1, B7.1,
and B7.2 genes contains binding sites for NF-B
(van de Stolpe and van der Saag,
1996; Roebuck and Finnegan,
1999; Lim et al.,
2002). Therefore, it might be possible that both ICAM-1 and B7
expression as well as TNF- production in monocytes is stimulated by the
same signaling pathway, NF-B activation. In this case, endogenously
produced TNF- in turn stimulated ICAM-1 expression in an autocrine
manner because anti-TNF- Ab inhibited the LPS-induced ICAM-1 expression
on monocytes to some extent in the present study
(Fig. 9). Moreover, it might be
possible that an intracellular signaling through ICAM-1 associated with LFA-1
plays a permissive role in TNF- production in addition to
TLR4-NF-B activation. The relationship between LPS-induced expression of
costimulatory adhesion molecules and the production of TNF- in PBMCs
might be more complex if the production of TNF- occurs in T/NK cells in
addition to monocytes. LPS-induced proliferative response in T cells provided
another example of cell-to-cell interaction between monocytes and T cells
initiated by LPS (Mattern et al.,
1994); however, the underlying mechanism has not been explored.
Further studies are necessary to clarify this matter. Recent studies
demonstrated that TLR2 was essential for the responses to peptidoglycans and
lipopeptide, whereas TLR4 was essential for the responses to lipoteichoic acid
as well as to LPS (Takeuchi et al.,
2000). Because it has been known that commercial available
preparations of LPS contain additional TLR2-stimulating bacterial
contaminations (Tapping et al.,
2000), our data might be affected by TLR2-dependent pathway.
The effects of histamine on the production of TNF- as well as the
expression of ICAM-1 and B7.1 were mimicked by selective H2-receptor agonists
dimaprit and 4-methylhistamine and antagonized by H2-antagonists famotidine
and ranitidine (Figs. 5 and
7), indicating the mediation of
histamine effects by H2-receptors. Recently discovered H4-receptor was found
in database that has homology to H3-receptors. In contrast to the exclusive
expression of H3-receptors in the brain, H4-receptors were demonstrated to be
expressed in peripheral tissues, including leukocytes
(Oda et al., 2000;
Nakamura et al., 2001). In the
present study, R-()-methylhistamine and thioperamide, which
were reported to be H4-agonist and antagonist as well as H3-agonist and
antagonist (Oda et al., 2000),
had no effects (Figs. 5 and
7). Therefore, H1-, H3-, and
H4-receptors were concluded not to be involved in histamine action. Because
dbcAMP mimicked the effects of histamine on the expression of adhesion
molecules and TNF- production (Figs.
6 and
7) and H2-receptor has been
demonstrated to couple with adenylate cyclase
(Del Valle and Gantz, 1997), it
is likely that H2-receptor-stimulated cAMP mediated the histamine response. It
has also been reported that cAMP inhibits the activation of NF-B
(Parry and Mackman, 1997).
Therefore, these results as a whole implied that the effect of histamine might
be through inhibiting signal transduction via NF-B in monocytes.
LPS-induced B7.2 expression was not inhibited by either dbcAMP or histamine,
strongly indicating that B7.2 expression was not regulated by a sole
cAMP-dependent pathway under the present conditions. The fact that histamine
was able to inhibit TNF- production completely without influencing B7.2
was consistent with the result that the inhibitory effect of combination of
anti-ICAM-1 Ab and anti-B7.1 Ab on TNF- production was almost the same
(85%) as that obtained by anti-ICAM-1 Ab, anti-B7.1 Ab, and anti-B7.2 Ab (90%)
(Fig. 8).
In the previous study (Takahashi et
al., 2002b), we observed similar modulatory effects of histamine
on the IL-18-activated cytokine network in PBMCs through the regulation of
ICAM-1 expression on monocytes. These findings as a whole indicate that
histamine exerts profound effects on the innate immune response through the
regulation of the expression levels of adhesion molecules resulting in a
strong modulation of the cytokine production profile
(Takahashi et al., 2002a). A
very interesting aspect concerning the LPS-induced response and the histamine
effect is the fact that systemic injection of LPS can induce histidine
decarboxylase activity in several tissues, including immune tissues
(Endo, 1982). The kinetics of
the histamine produced was different from storage types of histamine in the
granules of mast cells and basophils
(Endo, 1982). The newly formed
histamine seemed to have a rapid turnover and has been suggested to be
produced in monocytes/macrophages' T lymphocytes and vascular endothelial
cells (Aoi et al., 1989;
Takamatsu et al., 1996).
Therefore, in vivo LPS-induced production of histamine may take place close to
the primary action site of LPS, monocytes/macrophages. If histamine then acts
on monocytes, it produces inhibitory effects on the LPS-induced response of
monocytes as demonstrated in the present study. Thus, inducible histamine may
play a role of negative regulator on LPS-induced response.
In conclusion, we found adhesion molecule-dependent effects of LPS on
TNF- production. Histamine exerted profound effects on the expression
of ICAM-1 and B7.1 on monocytes via H2-receptors, leading to a reduction of
TNF- production. These modulatory effects of histamine on LPS-induced
TNF- production as well as IL-18-induced cytokine production through
the regulation of expression of adhesion molecules play a negative regulatory
role in the innate immune response.
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Acknowledgements |
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Footnotes |
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ABBREVIATIONS: LPS, lipopolysaccharide; IL, interleukin; IFN,
interferon; TNF, tumor necrosis factor; TLR, Toll-like receptor; NK, natural
killer; PBMC, peripheral blood mononuclear cell; LFA, lymphocyte
function-associated antigen; ICAM, intercellular adhesion molecule; CMC,
class-matched control; dbcAMP, dibutyryl cAMP; FITC, fluorescein
isothiocyanate; mAb, monoclonal antibody; Ab, antibody; ELISA, enzyme-linked
immunosorbent assay; 2-PEA, 2-(2-pyridyl) ethylamine; R-()-MH,
R-()-methylhistamine.
Address correspondence to: Dr. Masahiro Nishibori, Department of Pharmacology, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. E-mail: mbori{at}md.okayama-u.ac.jp
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