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INFLAMMATION AND IMMUNOPHARMACOLOGY
Departments of Pharmacology (H.K.T., S.M., M.N.), Tumour Biology (H.K.T., H.I., R.T., D.X., N.T.), and Pathology (M.S., T.Y.), Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan
Received July 2, 2003; accepted September 15, 2003.
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Abstract |
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in PBMC in the presence and absence of IL-18, whereas PGE1 induced IL-10 production. In conclusion, IP receptor and EP2/EP4 receptor play an important role in the action of PGE1 on the expression of adhesion molecules on monocytes and cytokine production.
; Ranger et al., 1996; Camacho et al., 2001). IL-18, a Th1 cytokine, plays a key role in regulating IFN- production (Okamura et al., 1995). IL-18 augments T -cell activation in conjunction with cell-cell interaction through adhesion molecules (Takahashi et al., 2002a,b) and therefore is capable of influencing the development of innate immune responses. It has been reported that IL-18-induced adhesion molecule expression was mediated through nuclear factor-
B (NF-B) and phosphatidylinositol (PI) 3-kinase in monocytes and T-cells (Matsumoto et al., 1997; Kojima et al., 1999).
PGE1 is one of the prostanoids synthesized from linoleic acid in vivo and differs from the products of the arachidonate cascade. The major function of PGE1 has been known as vasodilatation and antiplatelet aggregation. The prostaglandin family plays important roles in the regulation of immune responses through various receptors. Receptor binding experiments to determine the affinity of prostaglandins for eight types of receptors (DP, IP, TP, FP, EP1, EP2, EP3, EP4) expressed in cultured Chinese hamster ovary (CHO) cells clearly showed that PGE1 had high affinity for IP receptor in addition to EP1, EP2, EP3, and EP4 receptors, whereas PGE2 had a high affinity for FP, EP1, EP2, EP3, and EP4 receptors (Narumiya et al., 1999). The EP2 and EP4 receptors are coupled to Gs and mediate the increase in cAMP (Narumiya et al., 1999). The IP receptor has also been found to stimulate adenylate cyclase; however, expression studies revealed that it may couple with multiple signaling pathways including PI response and Ca2+ mobilization (Namba et al., 1994). In fact, PGI2, an IP receptor agonist, has been demonstrated to induce the elevation of free Ca2+ concentration in several cultured cell lines (Watanabe et al., 1991). Despite the clear difference in the receptor activation profile of PGE1 and PGE2, there is little information about the action characteristics of PGE1 on particular immune responses. Previously, we reported that PGE2 inhibited IL-18-induced expression of ICAM-1 and B7.2 on human monocytes through the stimulation of EP2 and EP4 receptors (Takahashi et al., 2002a). These effects of PGE2 on adhesion molecules in turn modulated the production of IL-12, tumor necrosis factor (TNF)-
, and IFN- in PBMC (Takahashi et al., 2002a); however, little is known about the pharmacological action of PGE1 on adhesion molecule expression on monocytes and the differences between the effects of PGE1 and PGE2 on the cell-cell interaction and cytokine production profiles.
In the present study, we examined the effect of PGE1 on the expression of ICAM-1, B7.1, B7.2, CD40, and CD40L as well as the production of IL-12, IFN-, and IL-10 in human PBMC in the presence or absence of IL-18 to clarify a functional role of PGE1 and the differences between PGE1 and PGE2 using prostaglandin receptor subtype-selective agonists. Interestingly, we found that PGE1 had a distinct action profile compared with that of PGE2. We also found that the stimulation of IP receptor had a unique effect on adhesion molecule expression and cytokine production.
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Materials and Methods |
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Isolation of PBMC. Normal human PBMC were obtained from human volunteers with their oral informed consent. Samples of 50 ml of peripheral blood were withdrawn from a forearm vein. PBMC were isolated from the buffy coat of 10 healthy volunteers by centrifugation on Ficoll-Paque (Pharmacia AB, Uppsala, Sweden) then washed three times in RPMI 1640 medium (Nissui Pharmaceutical 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). PBMC were suspended at a final concentration of 1 x 106 cells/ml in RPMI 1640 medium supplemented with 10% (v/v) heat-inactivated fetal calf serum.
Preparation of Isolated Monocytes. PBMC were prepared as described under Isolation of PBMC. Separation of monocytes from PBMC was conducted by counterflow centrifugal elutriation using the SRR6Y elutriation system and a rotor equipped with a 4.5-ml chamber (Hitachi Koki Co., Ltd, Tokyo, Japan). PBMC resuspended at 5 to 10 x 107 cells in 10 ml of PBS supplemented with 1% (v/v) fetal calf serum were injected at an initial flow rate of 10 ml/min at 4°C with a rotor speed of 2000 rpm. The flow rate was gradually increased, and the cell fractions were collected serially as follows: fraction 1 (fr. 1), 200 ml at 10 ml/min; fr. 2, 200 ml at 12 ml/min; fr. 3, 200 ml at 14 ml/min; fr. 4, 200 ml at 16 ml/min; and fr. 5, 200 ml at 18 ml/min. The cell population of each fraction was determined by flow cytometry with FITC-conjugated anti-CD14 Ab (monocytes), PE-conjugated anti-CD3 Ab (T-cells) and PE-conjugated anti-CD19 Ab (B-cells). Fraction 2 contained 65% T-cells and 20% B-cells but less than 5% monocytes. Both fr. 3 and 4 contained 85% monocytes but less than 5% T- and B-cells. These two fractions were used as the monocyte-rich fractions. The other fractions contained less than 5% monocytes and T- and B-cells.
Flow Cytometric Analysis. PBMC and isolated monocytes (1 x 106 cells/ml) were incubated with IL-18, PGE1, and IP and EP receptor agonists for 24 h at 37°C in a 5% CO2/air mixture under different conditions. The cells (5 x 105 cells/sample) were washed once with washing buffer (PBS supplemented with 2.5% normal horse serum, 0.1% NaN3, and 0.01 M HEPES, pH 7.3). The changes in expression of human leukocyte antigens (ICAM-1, B7.1, B7.2, CD40, and CD40L) on monocytes were examined by double-labeling flow cytometry using a combination of anti-CD14 Ab with anti-ICAM-1 Ab, anti-B7.1 Ab, anti-B7.2 Ab, anti-CD40 Ab, or anti-CD40L Ab. Then, the cells were incubated with 1 µg of FITC-conjugated anti-ICAM-1 Ab, anti-B7.1 Ab, anti-B7.2 Ab, anti-CD40 Ab or anti-CD40L Ab or CMC, and PE-conjugated anti-CD14 Ab for 20 min at 4°C. After washing, the cells were fixed with 2% paraformaldehyde and analyzed with FACSCalibur (BD Biosciences, San Jose, CA), and data were processed using the CELL QUEST program (BD Biosciences). The data are expressed as the relative fluorescence intensities against CMC. The results are the means ± S.E.M. of five donors.
Cytokine Assay. PBMC (1 x 106 cells/ml) were incubated with PGE1, PGE2, and IP and EP receptor agonists in the presence or absence of IL-18 for 24 h at 37°C in a humidified atmosphere of 5% CO2 in air. After culture, the cell-free supernatant fractions were assayed for IL-12 (p70), IFN-, and IL-10 protein as described previously (Takahashi et al., 2002a,b).
Statistical Analysis. The statistical significance of differences was evaluated by analysis of variance followed by Tukey's test. P < 0.05 was considered statistically significant.
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Effects of IP and EP Receptor Agonists on ICAM-1, B7.1, B7.2, CD40, and CD40L Expression on Human Monocytes. To determine which PGE1 receptor subtypes (IP, EP1, EP2, EP3, EP4) are involved in the effects of PGE1 on ICAM-1, B7.1, B7.2, CD40, and CD40L expression, we examined the effects of EP receptor agonists (0–10–6 M) on ICAM-1, B7.1, B7.2, CD40, and CD40L expression on monocytes in the presence and absence of IL-18 (100 ng/ml) after a 24-h incubation of PBMC (Fig. 2). ONO-DI-004 (EP1 receptor agonist) (Suzawa et al., 2000; Kitagawa et al., 2001) and ONO-AE-248 (EP3 receptor agonist) (Suzawa et al., 2000; Kitagawa et al., 2001), in the concentration range from 10–9 to 10–6 M, had no effect on the expression of these five adhesion molecules regardless of the presence of IL-18 (data not shown). ONO-AE1-259-01 (EP2 receptor agonist) and ONO-AE1-329 (EP4 receptor agonist) (Suzawa et al., 2000; Kitagawa et al., 2001) also had no effect on the expression of these five adhesion molecules in the absence of IL-18 (Fig. 2, A–C). ONO-AE1-259-01 and ONO-AE1-329 inhibited ICAM-1, B7.2, and CD40 expression on monocytes in the presence of IL-18 (Fig. 2, D–F) but had no effect on the expression of B7.1 and CD40L (data not shown). IC50 value for the inhibitory effect of ONO-AE1-259-01 on the expression of ICAM-1 was estimated to be 100 nM (Fig. 2). Moreover, we found that ONO-1301 (IP receptor agonist) (Hayashi et al., 1997; Imawaka and Sugiyama, 1998) strongly prevented the expression of ICAM-1, B7.2, and CD40 in the presence and absence of IL-18 (Fig. 2) but had no effect on the expression of B7.1 and CD40L (data not shown). IC50 value for the inhibitory effect of ONO-1301 on the expression of ICAM-1 was estimated to be 3 nM (Fig. 2).
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Effect of PGE1, IP, EP2, and EP4 Agonist on ICAM-1 Expression on Isolated Monocytes. The effects of PGE1, IP, EP2, and EP4 agonist (10–6 M) on the expression of ICAM-1 on isolated monocytes were examined (Fig. 3). ONO-1301 as well as PGE1 prevented the expression of ICAM-1 in the presence and absence of IL-18 (100 ng/ml). Although EP2 and EP4 agonists inhibited the expression of ICAM-1 in the presence of IL-18, these two agonists did not do so in the absence of IL-18.
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Effect of ONO-1301 and 11-Deoxy-PGE1 on ICAM-1, B7.2, and CD40 Expression on Human Monocytes. We examined the effects of ONO-1301 and 11-D-PGE1 (EP2/EP4 receptor agonist) on IL-18-induced ICAM-1, B7.2, and CD40 expression (Fig. 4). In the presence (10–8 M) and absence of ONO-1301, 11-D-PGE1 (0–10–6 M) concentration-dependently suppressed the expression of ICAM-1, B7.2, and CD40. At the concentration (10–6 M) of ONO-1301, 11-D-PGE1 had no effect on the expression of these adhesion molecules (Fig. 4A). On the other hand, ONO-1301 (0–10–6 M) inhibited the expression of ICAM-1, B7.2, and CD40 in the presence (10–8 and 10–6 M) and absence of 11-D-PGE1 (Fig. 4B).
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Dose-Response Relationship of the Effects of PGE1 and PGE2 on Cytokine Responses in PBMC. The effect of PGE1 and PGE2 (0–10–6M) on the production of IL-12, IFN-, and IL-10 in PBMC treated with and without IL-18 was determined by ELISA after 24 h of culture (Fig. 5). In the absence of IL-18 stimulus, PGE1 prevented the spontaneous production of IFN- and IL-10 in a concentration-dependent manner, but had no effect on the production of IL-12. PGE2 induced the production of IFN- without IL-12 production but inhibited the production of IL-10. The same concentration of PGE1 and PGE2 inhibited IL-12 and IFN- production in IL-18-stimulated PBMC, but induced IL-10 production. The IC50 value for the inhibitory effect of PGE1 on the production of IL-12 induced by IL-18 was estimated to be 5 nM.
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Inhibition of IL-18-Induced Cytokine Responses in PBMC by IP and EP Receptor Agonists. We examined the effect of IP, EP1, EP2, EP3, and EP4 receptor agonist on the production of IL-12, IFN-, and IL-10 in PBMC in the presence and absence of IL-18 (Fig. 6). Whereas ONO-AE1-259-01 and ONO-AE1-329 induced the production of IFN- in the absence of IL-18, ONO-1301 inhibited it. ONO-1301, ONO-AE1-259-01, and ONO-AE1-329 inhibited IL-10 production but did not affect IL-12 production. In IL-18-treated PBMC, ONO-1301, ONO-AE1-259-01, and ONO-AE1-329 prevented the production of IL-12 and IFN- but induced IL-10 production. ONO-DI-004 and ONO-AE-248 had no effect on the expression of these cytokines regardless of the presence of IL-18 (data not shown).
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Effect of ONO-1301 and 11-Deoxy-PGE1 on Cytokine Responses in PBMC. The effect of ONO-1301 and 11-D-PGE1 on IL-18-induced IL-12, IFN-, and IL-10 production was investigated (Fig. 7). In the presence (10–8 M) and absence of ONO-1301, 11-D-PGE1 (0–10–6 M) concentration-dependently inhibited IL-12 and IFN- production but induced IL-10 production. At the concentration (10–6 M) of ONO-1301, 11-D-PGE1 did not affect the production of IL-12, IFN-, and IL-10 (Fig. 7A). In the presence (10–8 and 10–6 M) and absence of 11-D-PGE1, ONO-1301 (0–10–6 M) inhibited IL-12 and IFN- production (Fig. 7B).
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Discussion |
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-induced ICAM-1 and vascular cell adhesion molecule-1 expression, leading to the inhibition of interaction between leukocytes and endothelial cells (Weiss et al., 1995; Natori et al., 1997; Iwata et al., 1999). However, little is known about the effect of PGE1 on the cell-cell interaction between monocytes and T/natural killer cells. In the present study, we found that PGE1 concentration-dependently inhibited the spontaneous expression of ICAM-1, B7.2, and CD40 on monocytes 24 h after the start of incubation (Fig. 1A). PGE1 also prevented the expression of ICAM-1, B7.2, and CD40 in the presence of IL-18 (Fig. 1B). Previously, we found that PGE2 inhibited the IL-18-induced expression of ICAM-1 and B7.2, but had no effect on the expression of ICAM-1, B7.1, and B7.2 in the absence of IL-18 (Takahashi et al., 2002a). The effects of PGE1 on the spontaneous expression of the three adhesion molecules were in contrast to those of PGE2.
It was reported that PGE1 binds to EP2 and EP4 receptor (Fan and Chapkin, 1998), whereas earlier studies suggested the existence of distinct receptors for PGE1 from those for PGE2 (Datta-Ray et al., 1983; Kanba et al., 1991). The IP receptor-selective agonist ONO-1301, whose affinity for IP receptor was expressed in CHO cells, was reported to be almost the same as that of PGE1 (Narumiya et al., 1999). In the present study, we found that ONO-1301 (IP receptor agonist) suppressed the expression of ICAM-1, B7.2, and CD40 in the absence of IL-18; however, EP receptor agonists had no effect on these adhesion molecules' expression (Fig. 2). ONO-1301, ONO-AE1-259-01 (EP2 receptor agonist), and ONO-AE1-329 (EP4 receptor agonist) inhibited IL-18-induced ICAM-1, B7.2, and CD40 expression (Fig. 2), but ONO-DI-004 (EP1 receptor agonist) and ONO-AE-248 (EP3 receptor agonist) had no effect on the expression of adhesion molecules (data not shown). The affinity of PGE1 for IP receptor is higher than that for EP2 and EP4 receptor (Narumiya et al., 1999). The inhibitory effect of ONO-1301 (10–6 M) on the expression of ICAM-1 showed a significant difference from that of ONO-AE1-259-01 (10–6 M) and ONO-AE1-329 (10–6 M) (Tukey's test). As shown in Fig. 4, increasing concentrations of 11-D-PGE1 had no additive inhibitory effect on the expression of adhesion molecules in the presence of ONO-1301 (10–6 M), whereas ONO-1301 additively inhibited the expression of ICAM-1, B7.2, and CD40 in the presence of 11-D-PGE1 (10–6 M). Therefore, the stimulation of IP receptor might be involved in the effect of PGE1 both in the presence and absence of IL-18, and the stimulation of EP2 and EP4 receptor might be involved in the effect of PGE1 in the presence of IL-18 as in the case of PGE2 (Takahashi et al., 2002a) (Fig. 2). Although the expression of IP receptor on human monocytes was observed (Li et al., 1997), it remained unclear whether the direct stimulation of IP receptors on monocytes caused the change in adhesion molecules expression on monocytes in PBMC preparation. In the present study, we found for the first time that the stimulation of IP receptor on isolated monocytes suppressed the expression of ICAM-1 (Fig. 3).
The effects of exogenous PGE1 and PGE2 on cytokine production in human PBMC stimulated with concanavalin A or LPS were reported (Dooper et al., 2002). The production of TNF-, IFN-, and, to a lesser extent, IL-10 was inhibited by PGE1 and PGE2 in concanavalin A-stimulated PBMC concomitant with unaffected IL-2 levels (Dooper et al., 2002). In LPS-stimulated PBMC, TNF- production was inhibited by PGE1 and PGE2, whereas IL-6 remained unaffected and IL-10 production was increased (Dooper et al., 2002). In the previous (Takahashi et al., 2002a) and the present study (Fig. 5), both PGE1 and PGE2 inhibited IL-18-induced IL-12 and IFN- production but induced IL-10 production. In IL-18-treated PBMC, ONO-1301, ONO-AE1-259-01, and ONO-AE1-329 suppressed the production of IL-12 and IFN- (Fig. 6), whereas ONO-DI-004 and ONO-AE-248 did not (data not shown). Therefore, the stimulation of IP, EP2, and EP4 receptor might contribute to the inhibition of IL-18-elicited cytokine production. In the experiment on the effect of ONO-1301 and 11-D-PGE1 (Fig. 7), ONO-1301 showed a dominant effect on IL-18-elicited cytokine production as well as on adhesion molecules. Anti-ICAM-1 and anti-B7.2 antibodies inhibited IL-18-induced IL-12 and IFN- production but induced IL-10 production (Takahashi et al., 2002a). In addition, anti-CD40 antibody had no effect on these cytokines' production (data not shown), suggesting that PGE1 might inhibit IL-18-initiated cytokine production through regulating the expression of ICAM-1, B7.2, and CD40 as suggested for PGE2 action (Takahashi et al., 2002a) (Fig. 5).
It is known that IP receptor shows a high affinity for PGE1 but not for PGE2 (Narumiya et al., 1999). The biological effects of IP receptor stimulation include anti-thrombosis (Murata et al., 1997) and vasodilator actions, which have been targeted therapeutically to treat pulmonary hypertension (Tuder et al., 1999; Hoeper et al., 2000). The expression of IP-receptor mRNA has been shown in various mouse organs, including neurons, megakaryocytes, and the smooth muscles of arteries (Oida et al., 1995). However, the function of IP receptor in monocytes remains unknown. The IP receptor is coupled to Gs and Gq proteins, leading to not only a rise in cAMP levels but also PI responses in CHO cells (Namba et al., 1994). The elevation of cAMP inhibits NF-B activation in the human monocytic cell line THP-1 (Delgado and Ganea, 2001). Dibutyryl cAMP, a membrane-permeable cAMP analog, inhibited the expression of ICAM-1 and B7.2 on IL-18-treated monocytes; however, it had no effect on the expression of ICAM-1 and B7 in the absence of IL-18 (Takahashi et al., 2002a). Thus, there might be IP-receptor signaling other than the regulation of activation of NF-B by cAMP in the absence of IL-18.
On the other hand, PGE1 suppressed the production of IFN- even in the absence of IL-18, whereas under the same condition PGE2 stimulated the production of IFN- (Fig. 5). ONO-1301 also inhibited the spontaneous production of IFN-, whereas ONO-AE1-259-01 and ONO-AE1-329 induced the production of IFN- (Fig. 6), suggesting that the effect of PGE1 on the production of IFN- in the absence of IL-18 might depend on the stimulation of IP receptor. PGE1 is reported to stimulate cAMP production more effectively than PGE2 (Knudson et al., 1986; Salvatori et al., 1992). Dibutyryl cAMP induced the production of IFN- in the absence of IL-18 (data not shown). These results suggested that the regulation of production of IFN- by PGE1 might be in a cAMP-independent manner. Because anti-ICAM-1, anti-B7.2, and anti-CD40 antibodies had no effect on production of cytokines in the absence of IL-18 (data not shown), it is unclear whether the inhibitory effect of ONO-1301 or PGE1 on IFN- production in the absence of IL-18 depends on the suppression of ICAM-1, B7.2, and CD40 expression.
IL-18 has been considered a mediator of inflammatory disease such as allorejection after organ transplantation, rheumatoid arthritis, or hepatitis (Saha et al., 1999; Affleck et al., 2001; Yumoto et al., 2002). Using a mouse model, recent studies reported that PGE1 reduced ischemia-reperfusion injury following lung transplantation (de Perrot et al., 2001), collagen induced arthritis (Moriuchi-Murakami et al., 2000), and LPS-induced liver injury (Mokuno et al., 1999). In addition to the fact that PGE1 possesses anti-inflammatory properties and the ability to modulate vascular reactivity, PGE1 might have some beneficial therapeutic effects on IL-18-initiated diseases. In conclusion, PGE1 is a potent inhibitor of ICAM-1, B7.2, and CD40 expression as well as IFN- production in the presence and absence of IL-18 through the stimulation of IP and EP2/EP4 receptor. These results implicate that the changes by PGE1 might result in the diminution of IFN--dependent events irrespective of the presence of IL-18 and that the immunomodulatory effects of PGE1 and PGE2 might be distinct in cytokine production. We have compared the effect of autacoids such as PGE2, histamine, and epinephrine (Takahashi et al., 2002a,b, 2003; Nishibori et al., 2003) on the expression of adhesion molecules. PGE1 was shown to be more powerful than PGE2 in exerting anti-inflammatory effects in a rat adjuvant arthritis model (Zurier et al., 1977) and mouse lupus model (Zurier, 1982). Taking the present findings along with these results, PGE1 might have distinct biological activities from PGE2 as well as histamine and epinephrine. Since the role of endogenous PGE1 in immune response is not well understood, further effects of PGE1 on immune response should be examined.
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Acknowledgements |
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Footnotes |
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B, nuclear factor-B; PI, phosphatidylinositol; PGE1, prostaglandin E1; ONO-1301, 7,8-dihydro-5-[(E)-[[a-(3-pyridyl)benzylidene]aminooxy]ethyl]-1-naphthyoxy)acetic acid; ONO-DI-004, 17S-2,5-ethano-6-oxo-17,20-dimethyl prostaglandin E1; ONO-AE1-259-01, 11,15-O-dimethyl prostaglandin E2; ONO-AE-248, 16S-9-deoxy-9
-chloro-15-deoxy-16-hydroxy-17,17-trimethylene-19,20-didehydro prostaglandin F2; ONO-AE1-329, 16-(3-methoxymethyl)phenyl-
-tetranor-3,7-dithia prostaglandin E1; CHO; Chinese hamster ovary; TNF, tumor necrosis factor; PBMC, peripheral blood mononuclear cells; 11-D-PGE1, 11-deoxy-PGE1; FITC, fluorescein isothiocyanate; mAb, monoclonal antibody; PE, phycoerythrin; CMC, class-matched control; Ab, antibody; fr., fraction; ELISA, enzyme-linked immunosorbent assay; LPS, lipopolysaccharide. This study was supported in part by a grant for Promotion of Research from Okayama University (No. 21 to M.N.), a grant from Okayama Medical Foundation (to H.K.T.) and grants from Grant-in-Aid for Scientific Research (C) (15590467 to H.K.T. and 15590228 to M.N.).
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.okayamau.ac.jp
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