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M Nambu

Publications and source records attributed to M Nambu.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effect of dibutyryl cyclic AMP and interferon-gamma on Fc gamma receptor expression on eosinophils.

We studied the effect of dibutyryl cyclic adenosine-3',5'-monophosphate (dbcAMP) and several cytokines on the expression of IgG Fc receptor subclasses (Fc gamma RI, Fc gamma RII, and Fc gamma RIII) and low-affinity IgE Fc receptors (Fc epsilon RII/CD23) on peripheral eosinophils and on eosinophils differentiated in vitro from cord blood mononuclear cells by interleukin 5 (IL-5). These eosinophils expressed Fc gamma RII, and few, if any, Fc gamma RI and Fc gamma RIII as determined by flow cytometry with specific monoclonal antibodies. dbcAMP enhanced the Fc gamma RII expression, but did not induce the Fc gamma RI and Fc gamma RIII expression. Interferon-gamma (IFN-gamma) enhanced Fc gamma RII expression at the same degree as did dbcAMP. IFN-gamma also induced Fc gamma RIII expression on peripheral eosinophils but not on eosinophils grown in the presence of IL-5. Eosinophils grown in the presence of IL-5 showed a relatively immature phenotype, determined by electron microscopy and the low content of eosinophil cationic protein. Contrary to its enhancing effect on Fc gamma RII expression, dbcAMP suppressed the IFN-gamma-induced Fc gamma RIII expression on peripheral eosinophils. Other cytokines examined did not show any effects on Fc gamma R expression. Fc epsilon RII/CD23 expression was neither detected nor induced. These results indicate that expression of Fc gamma RII and Fc gamma RIII on eosinophils is regulated differently and that cAMP and IFN-gamma play important roles in the regulation of Fc gamma R expression.

Blood Proteins↗
PubMed1993

Induction of phosphatidylinositol-linked Fc gamma receptor III expression on an eosinophilic cell line, EoL-1, by dibutyryl cyclic AMP and interferon-gamma.

The expression of Fc gamma receptor III (Fc gamma RIII) on a human eosinophilic leukemia cell line, EoL-1, was examined and compared with its expression on normal blood eosinophils. Surface Fc gamma RIII expression on EoL-1 cells could be induced in vitro with a combination of dibutyryl cAMP (dbcAMP) and gamma-interferon (IFN-gamma), but not with IFN-gamma or dbcAMP alone. Pretreatment of EoL-1 cells with dbcAMP induced EoL-1 cells to express Fc gamma RIII when stimulated with IFN-gamma, but EoL-1 cells pretreated with IFN-gamma and then stimulated with dbcAMP failed to express Fc gamma RIII. Cyclic AMP was shown to play a role in the effect of dbcAMP. Both the treatment with phosphatidyl-inositol-specific phospholipase C (PI-PLC) and the restriction enzyme digestion of Fc gamma RIII cDNA showed that the Fc gamma RIII on EoL-1 cells was a phosphatidylinositol-linked form. On the other hand, freshly isolated blood eosinophils constitutively expressed few, if any, Fc gamma RIII, and IFN-gamma induced Fc gamma RIII expression on them in vitro. Dibutyryl cAMP did not induce Fc gamma RIII expression and even suppressed the IFN-gamma-induced Fc gamma RIII expression on normal eosinophils. The EoL-1 cell line appears to be a useful in vitro model for the expression and function of the phosphatidylinositol-linked form of Fc gamma RIII on eosinophils.

Base Sequence↗
PubMed1993

Roles of eosinophils and catecholamines in pathophysiology of exercise-induced asthma.

To study the roles of eosinophils and catecholamines in the pathophysiology of exercise-induced asthma (EIA), an exercise challenge test was performed in 22 asthmatic children, using a bicycle ergometer, and the changes in lung function, plasma norepinephrine (NE), epinephrine (E) and eosinophil cationic protein (ECP) levels with exercise were evaluated. Subjects were classified into three groups from the results of lung function test, respectively: EIA-negative group. EIA-positive groups with good recovery and poor recovery. Eosinophil counts before exercise in the EIA-positive groups were significantly higher than those in the EIA-negative group. The ECP levels rose with exercise in all groups. Five minutes after exercise, ECP values fell to the pre-exercise level in the EIA-negative group, but rose to higher levels in EIA-positive groups. Plasma E levels rose with exercise and showed 4-fold increase in the EIA-negative group, whereas only 1.5-fold increase of plasma E levels was observed in the EIA-positive group with poor recovery. From these findings, a possible contribution of sympathoadrenal hypofunction and a probable involvement of eosinophils in the pathophysiology of EIA have been suggested.

Adolescent↗
PubMed1993

Inhibitory effects of azelastine hydrochloride on Ca2+ influx, actin polymerization and release of eosinophil cationic protein of an eosinophilic leukaemia cell line EoL-1.

The inhibitory effects of azelastine hydrochloride on PAF-induced and fMLP-induced Ca2+ influx, actin polymerization and calcium ionophore A23187-induced and aggregated IgG-induced release of eosinophil cationic protein (ECP) of an eosinophilic leukaemia cell line, EoL-1, were examined. EoL-1 cells cultured with 0.2 mM dibutyryladenosine-cyclic monophosphate for 48 hours showed an increase in intracellular free Ca2+ concentration ([Ca2+]i) and actin polymerization when stimulated by PAF and fMLP. Azelastine hydrochloride inhibited PAF-induced and fMLP-induced Ca2+ influx ([Ca2+]i) in a dose-dependent manner with an IC50 of 1 x 10(-8) M and 1 x 10(-7) M, respectively. It also inhibited PAF-induced and fMLP-induced actin polymerization in a dose-dependent manner up to 40% and 30%, respectively. EoL-1 cells were differentiated to contain ECP in their eosinophilic granules when cultured for 9 days with supernatants of a human adult T cell leukaemia cell line, HIL-3 (HIL-3 sup). Calcium ionophore A23187 and aggregated IgG induced the secretion of ECP by EoL-1 cells. Azelastine hydrochloride inhibited the secretion of ECP in a dose-dependent manner. These inhibitory effects were seen even at therapeutic concentrations of 10(-8) M to 10(-9) M. These results indicate that the therapeutic effects of azelastine hydrochloride as an anti-allergic agent may include inhibition of the accumulation of eosinophils into the locus of allergic inflammation and of the release of cytotoxic granules from eosinophils.

Actins↗
PubMed1992

Regulation of the expression of leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) on a human eosinophilic leukemia cell line EoL-3.

The effects of several cytokines and phorbol myristate acetate (PMA) on LFA-1 and ICAM-1 expression on a human eosinophilic leukemia cell line, EoL-3, were investigated and compared with those of a human monocytic leukemia cell line, U937. EoL-3 cells expressed large amounts of LFA-1 and small amounts of ICAM-1, and their expression was regulated similarly in EoL-3 cells and U937 cells. Interferon-gamma (IFN-gamma) enhanced ICAM-1 expression but not LFA-1 expression, and PMA augmented both LFA-1 and ICAM-1 expression. IFN-gamma and PMA showed an additive effect on ICAM-1 expression. These results collectively suggest that expression of LFA-1 and ICAM-1 is regulated differently and that IFN-gamma and PMA regulate the expression through different mechanisms. PMA but not IFN-gamma induced homotypic adhesion of EoL-3 and U937 cells, suggesting that PMA but not IFN-gamma activated the adhesive function of these cells. Staurosporin, an inhibitor of protein kinases (PKs), partly suppressed IFN-gamma- and PMA-augmented expression of ICAM-1 on EoL-3 and U937 cells, but did not affect PMA-augmented LFA-1 expression, suggesting that staurosporin-sensitive PKs are involved in IFN-gamma- and PMA-augmented ICAM-1 expression but not in PMA-augmented LFA-1 expression. The role of protein kinase C (PK-C) in these mechanisms was not revealed because a PK-C inhibitor, H-7, did not show any definitive effect on IFN-gamma- and PMA-induced expression of LFA-1 and ICAM-1. Moreover, cyclic AMP (cAMP)- and cGMP-dependent pathways were not shown to be involved in the augmentation of the expression of these molecules.

Antigens, CD↗
PubMed1991

Growth regulation of a human mature B cell line, B104, by anti-IgM and anti-IgD antibodies.

An EBNA- human B lymphoma cell line, B104, was established. B104 cells express IgD as well as IgM on their surface, which is thought to be a basic characteristic of mature B cells. The growth of B104 cells was inhibited by treatment with a panel of anti-IgM antibodies. Cell cycle analyses revealed that the transition of B104 cells from the G2/M to the G0/G1 phase of the cell cycle was markedly inhibited by treatment with anti-IgM antibodies. Progression of B104 cells to the M phase of the cell cycle was found to be suppressed in the presence of anti-IgM antibodies. In contrast, both the entrance of G0/G1 phase cells into the S phase and the progression of S phase cells to the G2/M phase of the cell cycle did not seem to be inhibited significantly by treatment with anti-IgM antibodies. These results indicate that the mechanism of the inhibition of growth of B104 cells by anti-IgM antibodies is blockage of the transition from the G2 to the M phase of the cell cycle. In contrast to anti-IgM antibodies, anti-IgD antibodies could not cause growth inhibition of B104 cells at all. B cell growth factors such as IL-4 and IL-6 had no effect on the inhibition of growth of B104 cells by anti-IgM antibody. IFN-alpha and -beta, which have no B cell growth factor activity, did increase the number of cells that survived the treatment with anti-IgM antibodies. B104 is an excellent experimental model for the study of the mechanism of signal transduction through sIg as well as the functional difference between sIgM and sIgD.

Antibodies, Anti-Idiotypic↗
PubMed1991

Regulation of Fc gamma receptor subtype expression on a human eosinophilic leukemia cell line EoL-3: participation of cAMP and protein kinase C in the effects of interferon-gamma and phorbol ester.

We investigated the effects of interferon-gamma (IFN-gamma), phorbol myristate acetate (PMA), and dibutyryl cAMP (Bt2cAMP) on Fc gamma R subtype expression on a human eosinophilic leukemia cell line, EoL-3. Unstimulated EoL-3 cells expressed Fc gamma RII as determined by monoclonal antibody (mAb) IV-3, whereas there was little or no Fc gamma RI and Fc gamma RIII expression as determined by mAbs 32.2 and 3G8, respectively. IFN-gamma induced Fc gamma RI expression, and Bt2 cAMP, which did not induce Fc gamma RI expression by itself, showed an additive effect on IFN-gamma-induced Fc gamma RI expression. Fc gamma RII expression was augmented by IFN-gamma, PMA, and Bt2 cAMP. Bt2 cAMP also showed an additive effect on IFN-gamma-augmented Fc gamma RII expression. Fc gamma RIII expression could be induced only by IFN-gamma plus Bt2 cAMP. H-7, a protein kinase C (PK-C) inhibitor, suppressed the enhancement of Fc gamma R subtype expression induced by these reagents. These results show that Fc gamma R subtype expression on EoL-3 cells is regulated differently in each subtype and that cAMP and PK-C play important roles in the regulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Dibutyryl cyclic AMP induces formyl peptide receptor expression and chemotactic responses in a human eosinophilic cell line, EoL-1.

We investigated actin polymerization and the increase of cytosolic free calcium concentration ([Ca2+]i) in a human eosinophilic leukemia cell line, EoL-1, in response to stimulation with chemotactic factors; we also investigated the effect of dibutyryl cyclic AMP (dbcAMP) on the responses. EoL-1 cells under normal culture conditions did not show either actin polymerization or an increase in [Ca2+]i when stimulated with formyl-methionyl-leucyl-phenylalanine (fMLP). Expression of formyl peptide receptors was not detectable on untreated EoL-1 cells, either. Dibutyryl cAMP induced the expression of formyl peptide receptors and the responsiveness to fMLP. The responsiveness of EoL-1 cells to the complement fragment C5a and platelet-activating factor (PAF) was also induced or enhanced by dbcAMP. The growth of EoL-1 cells was decreased and the proportion of cells in the G0/G1 phase of the cell cycle was increased by the treatment of EoL-1 cells with dbcAMP. The proportion of eosinophilic granule-containing cells and the content of eosinophil cationic protein (ECP) in EoL-1 cells was also increased when they were stimulated with dbcAMP for a longer period. The responsiveness of EoL-1 cells to fMLP, C5a, and PAF was shown to be regulated independently. EoL-1 cells and dbcAMP seem to be useful for examining chemotactic receptor expression and its signal transduction mechanisms.

Actins↗
PubMed1991

[An operative case of solitary interruption of the aortic arch in adult].

A 43-year-old lady was hospitalized due to easy fatiguability in the legs during exercise, and for evaluation of an abnormal shadow in the chest X-ray, and hypertension. Her blood pressure was 200/80 mmHg in the right arm, 140/70 mmHg in the left, and 110/70 mmHg in both lower extremities. Systolic vascular bruit radiating to her neck and back was audible in the Erb's area. DSA and aortogram disclosed extremely dilated vessels around the origin of the left common carotid artery. The left subclavian artery was opacified retrogradely as a subclavian blood steal via the left vertebral artery, and mild stenosis was seen at its origin. There was no evidence of associated congenital anomaly such as VSD, PDA, or ASD. The final diagnosis, solitary interruption of the aortic arch (S-IAA, type B), was made by MRI. The patient had an extra-anatomical bypass operation by using Cooley woven dacron graft from the ascending to the abdominal aorta. The result was good. S-IAA is a very rare congenital anomaly. As far as we know, only 21 patients with S-IAA including this case have been reported. A physician should be aware that a patient with S-IAA tends to have a difference of blood pressure not only between the upper and lower extremities but also between both arms, and pressure in the right arm is usually higher than that in the left. These are good signs to suspect S-IAA. And they also can be helpful to differentiate S-IAA from coarctation of the aorta.

Angiography, Digital Subtraction↗
PubMed1990

Indocyanine green (ICG) test before and after exercise in patients with chronic liver diseases.

The indocyanine green (ICG) test (serum disappearance rate: K and 15 min. retention rate: R15) was performed in 15 patients with chronic hepatitis (CH) and 22 patients with liver cirrhosis (LC) before and after exercise (Master's two step method for three min.). In LC, ICG K was 0.063 +/- 0.026 (mean +/- SD) before exercise and 0.083 +/- 0.028 after exercise. ICG R15 was 31.6 +/- 15.6% and 23.3 +/- 15.3%, respectively. In CH, ICG R15 before exercise was 8.2 +/- 4.0%, as compared with that (5.7 +/- 3.6%) after exercise. Namely, the ICG test significantly (P less than 0.05) improved after exercise in chronic liver diseases. Excretion of ICG into bile after exercise increased both in gallstone patients without abnormal liver function and LC, and it markedly increased in patients with decompensated LC. There was no significant difference in ICG excreted into urine before and after exercise. These results suggest that hepatic blood flow increases through moderate exercise in chronic liver diseases.

Bile↗
PubMed1990

Transforming growth factor beta and dexamethasone suppress the expression of Fc epsilon receptor 2 (CD23) on a human eosinophilic cell line EoL-3.

The effects of interferon-alpha (IFN-alpha), INF-gamma, transforming growth factor beta (TGF-beta) and dexamethasone on low-affinity Fc receptors for IgE (Fc epsilon R2/CD23) expression on a human eosinophilic leukemia cell line, Eol-3, were examined. Fc epsilon R2/CD23 expression was enhanced by both IFN-alpha and IFN-gamma, and suppressed by TGF-beta and dexamethasone. Northern blot analysis revealed that these reagents regulate the Fc epsilon R2/CD23 expression from mRNA level: both IFN-alpha and IFN-gamma increased the amount of Fc epsilon R2/CD23 mRNA, while both dexamethasone and TGF-beta decreased Fc epsilon R2/CD23 mRNA, where the effect of dexamethasone was much stronger than that of TGF-beta. In comparison with IFN-alpha, IFN-gamma seemed to enhance preferentially the release of surface Fc epsilon R2/CD23, which resulted in the increase of soluble Fc epsilon R2/CD23. These results suggest that these reagents may play important regulatory roles in allergy and in helminth infections via their effects on Fc epsilon R2/CD23 expression on eosinophils.

Antigens, CD↗
PubMed1989

Regulation of Fc gamma receptor expression and phagocytosis of a human monoblast cell line U937. Participation of cAMP and protein kinase C in the effects of IFN-gamma and phorbol ester.

We investigated the positive and negative effects of IFN-gamma, PMA, dibutyryl cAMP (Bt2cAMP), dexamethasone and transforming growth factor-beta (TGF-beta) on Fc gamma R subtype expression and phagocytosis of a human monoblast cell line, U937. IFN-gamma increased and Bt2cAMP decreased Fc gamma RI expression determined by a mAb 32.2, whereas PMA and Bt2cAMP increased Fc gamma RII expression determined by a mAb IV-3. Phagocytosis was measured microscopically by counting ingested aggregated human IgG- or BSA-treated ox E (Eo'-IgG or Eo'-BSA). IFN-gamma increased the phagocytosis of Eo'-IgG but not that of Eo'-BSA, and PMA increased the phagocytosis of both Eo'-IgG and Eo'-BSA. Bt2cAMP decreased both basal and IFN-gamma- and PMA-augmented phagocytosis of U937 cells. Dexamethasone also inhibited both basal and IFN-gamma-augmented Fc gamma RI expression and PMA-augmented Fc gamma RII expression and phagocytosis, but did not affect IFN-gamma-augmented phagocytosis of Eo'-IgG. The augmentation of phagocytosis of Eo'-IgG by IFN-gamma thus seems to be due mainly to the increased internalizing process rather than to increased Fc gamma RI expression. TGF-beta slightly decreased Fc gamma R expression. In a study of the participation of protein kinase C (PK-C), it was found that H-7, a PK-C inhibitor, did not inhibit either IFN-gamma- or PMA-enhanced Fc gamma RI and Fc gamma RII expression, respectively, and 1-oleoyl-2-acetylglycerol and N-(6-phenylhexyl)-5-chloro-1-naphthalenesulfonamide, both PK-C activators, did not show any apparent increase in Fc gamma R expression and phagocytosis. These results show that Fc gamma RI and Fc gamma RII expression on U937 cells is regulated by different mechanisms and that IFN-gamma and PMA play their roles in Fc gamma R expression and phagocytosis by different pathways. It is possible that cAMP but not PK-C plays an important role in the regulation of Fc gamma R expression and phagocytosis.

Antigens, Differentiation↗