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M Hirashima

Publications and source records attributed to M Hirashima.

At least 73 records · Page 4Linked to original sources
PubMed1986

The regulation of tissue eosinophilia. IV. Purification and properties of eosinophil-directed chemotactic inhibitory factors from complete Freund's adjuvant-treated guinea pigs.

Eosinophil-directed chemotactic inhibitory factors (ECIF) from T lymphocytes of complete Freund's adjuvant-treated guinea pigs were recovered in two separate molecular weight (MW) fractions: the one is eluted near bovine serum albumin (MW about 70,000), and in pH range between 7.0 and 7.5 by chromatofocusing column, whereas the other is near cytochrome c (MW 12,500), and in pH range between 5.0 and 5.5. It was, however, found by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoadsorption that the high molecular ECIF is probably an aggregated form of the low molecular ECIF. It was subsequently confirmed that both the ECIF had similar physicochemical properties: sensitive to heating at 56 or 80 degrees C sensitive to enzyme treatment with trypsin and neuraminidase, sensitive in acid but not alkaline condition, and bind to peanut agglutinin-or Limulus polyphemus agglutinin-coupled agarose beads. The inhibitory activity of ECIF was suppressed by previous treatment of eosinophils with D-galactose and sialic acid. ECIF activity was specifically absorbed by eosinophils; the absorption was inhibited by pretreatment of eosinophils with D-galactose and sialic acid. Previous treatment of eosinophils with beta-galactosidase and neuraminidase led the cells not to respond to both ECIF. It was thus suggested that the inhibition by ECIF is receptor-mediating phenomenon, and that ECIF and ECIF receptors on eosinophils contain galactose and sialic acid residues which may play an essential role for the biological activity.

Adsorption↗
PubMed1986

Eosinophil chemotactic factors from granuloma of Kimura's disease, with special reference to T lymphocyte-derived factors.

The granuloma of patients with Kimura's disease characterized by tissue and peripheral blood eosinophilia was reviewed with respect to eosinophil infiltration. An infiltrate of inflammatory cells with histiocytes and a sprinkling of eosinophils were observed in the fibrous stroma surrounding the newly formed vessels. Mast cells were rarely seen in the areas where eosinophils were grouped together. Three different eosinophil chemotactic factors (ECF) were isolated from the granulomas of Kimura's disease. They were termed as low molecular weight (LMW), intermediate molecular weight (IMW), and high molecular weight (HMW)-ECF according to the profile on gel filtration (LMW-ECF, about 500; IMW-ECF, about 12,500; HMW-ECF, 45,000-70,000). In terms of their activity when extracted from the granuloma, LMW-ECF and HMW-ECF seemed to be major natural mediators for the tissue eosinophilia, whereas IMW-ECF was a minor one. In an in vitro system, it was shown that granuloma lymphoid cells produce spontaneously at least two ECF having similar properties to LMW- and HMW-ECF, respectively. By analysis with monoclonal antibodies, granuloma T cells, probably OKT4-positive cells, were shown to be responsible for the production of those two ECF. It was thus suggested that prolonged synthesis of LMW- and HMW-ECF by OKT4-positive T cells plays a crucial role in the local eosinophilia of Kimura's disease.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed1986

Spontaneous production of eosinophil chemotactic factors by T lymphocytes from patients with subcutaneous angioblastic lymphoid hyperplasia with eosinophilia.

Subcutaneous angioblastic lymphoid hyperplasia with eosinophilia (SALH) was reviewed with respect to eosinophil chemotaxis. Lymphoid cells separated from the granuloma spontaneously released at least two different eosinophil chemotactic factors (ECF): low-molecular-weight and high-molecular-weight ECF according to the profile on gel filtration (LMW-ECF, about 500; HMW-ECF, 45,000 to 70,000). The cells, however, failed to produce chemotactic activity for macrophages and neutrophils. By analysis with monoclonal antibodies against lymphocyte subpopulations, the granuloma T cells, probably OKT4-positive cells, were shown to be responsible for spontaneous production of these two ECF. Furthermore, the blood mononuclear leukocytes were separated from the patients with SALH. An ECF closely resembling HMW-ECF was also spontaneously produced by the blood OKT4-positive T lymphocytes, whereas no LMW-ECF was released. Mononuclear leukocytes from healthy donors, however, could produce an ECF resembling HMW-ECF and chemotactic activities for macrophages and neutrophils by stimulation with concanavalin A (Con A). Protein synthesis appeared to be essential for spontaneous ECF and for Con A-induced ECF production. These results suggest that the granuloma OKT4-positive T lymphocytes of the patients with SALH are in activated condition to release LMW- and HMW-ECF, whereas the blood OKT4-positive T lymphocytes are in activated condition to release only HMW-ECF. Such spontaneous and prolonged production of HMW-ECF by the cells can be one of the diagnostic means of SALH.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed1986

An adhesive glycoprotein from rat ascites hepatoma cells potentiates natural cytotoxic activity by rat spleen cells.

In a previous paper, we have described a cell-surface associated adhesive glycoprotein (AF) that has been separated and highly purified from rat ascites hepatoma AH136B cells. AF was found to induce the aggregation and adhesiveness of hepatoma cells. AF was also shown to have a mitogenic activity on rat T lymphocytes, and to stimulate them to produce a lymphokine chemotactic for macrophages. In the present paper, we have examined the effects of AF on natural killing (NK) activity by rat spleen cells against NK-sensitive YAC-1 cells using 51Cr-release cytotoxicity assay. NK activity of spleen cells was potentiated by AF treatment in a dose-dependent manner. A short incubation with AF was sufficient for the potentiation of NK activity, whereas the potentiation by OK-432, which is well known as a potentiator of anti-tumour activity, required a longer stimulation. Macrophage depletion from spleen cells resulted in the decreased potentiating effects of OK-432, whereas the depletion failed to influence the effects of AF. IN subsequent experiments, it was found that AF could potentiate NK activity of the NK-cell enriched fraction. We further found that culture supernatants from spleen cells and peritoneal exudate cells treated with OK-432 potentiate the NK activity, whereas those from AF-treated cells fail. It was thus suggested that AF acts directly on the cells responsible for NK activity, and that the mechanisms of AF-induced potentiation of NK activity differ from those of OK-432-induced potentiation.

Animals↗
PubMed1986

[Left ventricular function in hypertrophic cardiomyopathy: a Tc-99m radionuclide angiographic study during exercise].

Hypertrophic cardiomyopathy (HCM) generally shows increased systolic function of the left ventricle at rest, although patients with HCM often have decreased exercise tolerance and develop dyspnea or chest pain. The present study was to investigate of left ventricular (LV) function during exercise in 26 patients with HCM using Tc-99m equilibrium angiocardiography, and to elucidate the mechanism of impaired functional reserve during exercise. Controls consisted of 11 normal volunteers and 12 patients with chest pain syndrome who had no abnormality on coronary arteriography or left ventriculography. In patients with HCM, LV ejection fraction decreased from 65 +/- 8 (mean +/- SD)% at rest to 59 +/- 18% at peak exercise, in contrast to an increase among controls (from 56 +/- 9% to 64 +/- 9%). As compared with resting values, cardiac output increased to 168 +/- 24% at peak exercise in HCM, but the increase was significantly less than that in controls (215 +/- 47%). Stroke volume decreased gradually to 83 +/- 16% during exercise in HCM, while it increased to 114 +/- 10% at an exercise level of half intensity, and it decreased slightly to 106 +/- 16% at peak exercise. LV end-systolic volume decreased among controls to 78 +/- 27% at peak exercise, but remained unchanged in HCM (118 +/- 58%). An increase in peak ejection rate at peak exercise was less in HCM than in controls (143 +/- 26% vs 170 +/- 42%). No significant differences were observed between the two groups concerning changes in indices of LV diastolic function including LV end-diastolic volume, peak filling rate or 1/3 filling rate during exercise. In the analysis of LV function curves, pulmonary arterial diastolic pressure increased to a greater extent in HCM than in controls (19 +/- 6 mmHg vs 11 +/- 6 mmHg); whereas, an increase in the stroke work index was less in HCM (80 +/- 26 g.m/m2/beat vs 121 +/- 21 g.m/m2/beat) at peak exercise. Thus, the LV function curve shifted downward and to the right in patients with HCM. The above findings indicate that LV functional reserve during exercise is impaired, especially as to systolic function in patients with HCM, while deterioration of diastolic function may be partly compromised by elevated filling pressure.

Cardiomyopathy, Hypertrophic↗
PubMed1985

Selective regulation of chemotactic lymphokine production. I. Selective potentiation of eosinophil chemotactic lymphokine production in alum hydroxy gel- and Bordetella pertussis vaccine-treated guinea pigs.

Delayed tissue eosinophilia in DNP-ovalbumin-induced allergic inflammatory skin lesions of guinea pigs was markedly enhanced by previous treatment with alum hydroxy gel (Alum) or Bordetella pertussis vaccine. This enhancement seemed due to increased production of a lymphocyte-derived eosinophil chemotactic factor (ECF) at the skin site. Treatment of animals with Alum potentiated antigen-induced in vitro ECF production by lymphoid cells from spleen and mesenteric lymph node of sensitized animals. The co-culture supernatants of lymphoid cells from Alum-treated animals also potentiated concanavalin A (Con A)-induced in vitro ECF production. The potentiating effect of Alum on ECF production seemed to be ascribed to the release of soluble factors from macrophages of the Alum-treated animals. The macrophage-derived soluble factor ECF-potentiating factor (ECF-PF) selectively potentiated ECF production but not macrophage chemotactic lymphokine production by Con A-stimulated lymphoid cells from normal animals. ECF-PF activity was associated with two separate m.w. fractions: one was 50,000 to 70,000 and the other was 10,000 to 20,000. The present study provides one of the explanations for enhanced ECF production by adjuvants, such as Alum and Bordetella pertussis vaccine.

Adjuvants, Immunologic↗
PubMed1985

Dexamethasone suppresses concanavalin A-induced production of chemotactic lymphokines by releasing a soluble factor from splenic T lymphocytes.

Treatment of guinea-pig spleen cells with glucocorticoids, such as dexamethasone (DEX), reduces concanavalin A (Con A)-induced production of chemotactic lymphokines (CLK), such as eosinophil chemotactic factor and macrophage chemotactic factor. The decreased CLK production is not caused by a direct effect of DEX on the spleen cells producing CLK, because Con A-induced CLK production is suppressed when the cells are cultured together with cell-free culture supernatants of the spleen cells which had been pretreated with DEX. A soluble suppressive factor, termed CLK-SF, with a MW of about 20,000, seems to be responsible for the suppression of both CLK production. CLK-SF is produced from DEX-treated T lymphocytes. CLK-SF probably exerts a critical role in the early stage of CLK production. In contrast, CLK-SF fails to inhibit Con A-induced lymphocyte proliferation, although DEX itself suppresses lymphocyte proliferation. This suggests that DEX suppresses Con A-induced CLK production by a different mechanism from that for lymphocyte proliferation.

Animals↗
PubMed1985

The regulation of tissue eosinophilia. III. In vitro production of eosinophil-directed chemotactic inhibitory factor by T lymphocytes of complete Freund's adjuvant-treated guinea-pigs.

Guinea-pig spleen cells treated with complete Freund's adjuvant (CFA) produce eosinophil-directed chemotactic inhibitory factors (ECIF). The inhibition is selective for the response of eosinophils to delayed ECF-a, which had been isolated from 24-hr-old inflamed skin lesions induced by DNP-Ascaris extract in sensitized animals and had been confirmed as being a T lymphocyte-derived lymphokine. ECIF activity is absorbed by incubation with eosinophils, but not with macrophages or neutrophils. The cells spontaneously release ECIF; pretreatment with a protein synthesis inhibitor reduces ECIF production, indicating that protein synthesis is essential. The source of ECIF seems to be lymphocytes, probably T lymphocytes. ECIF activity is recovered in two separate fractions: one elutes near bovine serum albumin (MW 70,000) and the other near cytochrome c (MW 12,500). ECIF binds to peanut agglutinin- or Limulus polyphemus agglutinin-coupled agarose beads. Furthermore, ECIF activity is blocked when eosinophils are incubated with D-galactose or sialic acid. These results suggest that ECIF derived from T lymphocytes of CFA-treated animals modulate the delayed ECF-a-mediated tissue eosinophilia, and that terminal galactose and/or sialic acid residues are essential for ECIF activity.

Animals↗
PubMed1984

The appearance of eosinophil-directed chemotactic inhibitory factor in the serum of complete Freund's adjuvant-treated guinea pigs.

When guinea pigs were treated by complete Freund's adjuvant (CFA), eosinophil-directed chemotactic inhibitory factor (ECIF) appeared in the serum of the treated animals. The inhibition of the response of eosinophils by ECIF was selective for the T cell-derived chemotactic factor, which has been isolated from DNP-ascaris extract-induced skin lesions (termed delayed ECF-a) but not for another ECF (termed delayed ECF-b), which was also isolated from the same skin lesions. ECIF was detected in the serum after a single CFA injection, and no significant increase of ECIF activity was observed in the serum of animals injected with CFA twice. The ECIF activity in the serum was associated with fractions of MW 70,000 and 12,500, and failed to bind to Con A-Sepharose. Furthermore, ECIF was absorbed by eosinophils but not by macrophages suggesting that eosinophils have receptor sites for ECIF. On the other hand, chemotactic inhibitor against delayed ECF-b was not detected in the serum. It was thus suggested that inhibition of eosinophil reaction by CFA treatment is related to ECIF, inhibition being selective for the eosinophil response to delayed ECF-a.

Adjuvants, Immunologic↗
PubMed1984

The regulation of tissue eosinophil chemotactic factor and inhibitor in allergic skin lesions of Freund's complete adjuvant-treated guinea-pigs.

The regulation of tissue eosinophilia induced by dinitrophenyl-ascaris extract (DNP-As) was investigated in guinea-pigs. Biphasic tissue eosinophilia peaking at 6 and 24 hr was observed in the skin lesions in Bordetella pertussis vaccine (Bp)-treated animals. In contrast, only the early phase of tissue eosinophilia was observed in Freund's complete adjuvant (FCA)-treated animals. Although less eosinophil chemotactic activity was detected in 24-hr-old skin extract of FCA-treated animals (FCA-extract), evident activity was recovered in the concanavalin A eluate (Con A-eluate) when FCA-extract was fractionated by Con A Sepharose. The chemotactic factor in Con A-eluate of FCA-extract was confirmed to be the T cell-derived eosinophil chemotactic factor, termed Delayed ECF-a, which has been isolated from allergic skin lesions by immunoadsorption. Another factor from the same skin lesions, Delayed ECF-b (which is a serum-derived one), was not detected in the FCA-extract. When eosinophils were mixed or pretreated with Con A-effluent of FCA-extract, the treated cells failed to be attracted by Delayed ECF-a, while the response to Delayed ECF-b was not affected, indicating that the inhibition was selective for Delayed ECF-a but not for Delayed ECF-b, and the eosinophil chemotactic inhibitory factor (ECIF) acts on eosinophils directly. Major ECIF activity was associated with a mol. wt. of 70,000 and minor with 12,500. Furthermore, the activity was absorbed by eosinophils but not by macrophages suggesting that eosinophils have receptor sites for ECIF. It was thus suggested that the appearance of ECIF, which is selective for the response of eosinophils to Delayed ECF-a, and decreased Delayed ECF-b production resulted in the inhibition of delayed tissue eosinophilia in FCA-treated guinea-pigs.

Animals↗
PubMed1984

Isolation of an eosinophil chemotactic lymphokine as a natural mediator for eosinophil chemotaxis from concanavalin A-induced skin reaction sites in guinea-pigs.

An intradermal injection with 20 micrograms concanavalin A (Con A) induce a marked tissue eosinophilia peaking at 24 h after the injection in guinea-pigs. Two different eosinophil chemotactic factors (ECFs) were isolated from the Con A-induced skin reaction sites. A non-dialysable ECF with mol. wt of about 70,000 closely resembled delayed ECF-a, which had been isolated from active cutaneous anaphylactic skin lesions and confirmed to be a product of T lymphocytes by antigenic stimulation, by virtue of the antigenicity, the chromatographic profiles on Sephadex G-100 and on DEAE-Sephadex, affinity to Con A-Sepharose, and other physicochemical properties. The activity of the factor paralleled the intensity of tissue eosinophilia, suggesting that the factor may function for the tissue eosinophilia as a natural mediator. Although another ECF with a low mol. wt (dialysable) was isolated from the same skin lesions, the dialysable factor may not contribute to the tissue eosinophilia because the activity of the factor paralleled the intensity of tissue basophilia but not that of eosinophilia.

Animals↗
PubMed1984

Difference in requirement of macrophage products for concanavalin A-induced production of eosinophil chemotactic factor and macrophage chemotactic factor from guinea pig lymphocytes in vitro.

Differences between the conditions for an eosinophil chemotactic factor (ECF) and macrophage chemotactic factor (MCF) production by lymphoid cells of mesenteric lymph nodes and spleen were studied in guinea pigs. If lymphoid cells were washed less than 4 hr after concanavalin A (Con A) stimulation and were cultured for an additional 24 hr, they failed to produce ECF, whereas Con A stimulation for 1 hr before washing was sufficient to stimulate them to produce MCF. Subsequently, it was shown that heat-labile soluble factors (termed ECF-PF) with potentiating activity for ECF production are produced from macrophages by 5 micrograms/ml Con A activation. When ECF-PF were added to the cell culture with 5 micrograms/ml Con A, the lymphoid cells could produce ECF even when they were washed 2 hr after Con A stimulation and were cultured for an additional 24 hr, suggesting that ECF-PF plays a critical role in the early stage of ECF production. The lymphoid cells were also able to produce ECF even when they were cultured with ECF-PF and a suboptimal dose of Con A (1 microgram/ml) for ECF production. Protein synthesis seemed to be essential for ECF-PF production. The ECF-PF activity was associated with two separated molecular fractions with m.w. of about 50,000 to 70,000 and of 10,000 to 20,000. It is thus suggested that ECF is produced from T cells by Con A stimulation under conditions which differ, at least, from those for MCF in the requirement of ECF-PF.

Animals↗
PubMed1984

Regulation of eosinophilia in rats infected with Nippostrongylus brasiliensis. I. Eosinophil chemotactic factor produced spontaneously by mesenteric lymph node cells of infected rats.

The possible mechanism of eosinophilia was studied in rats undergoing primary infection with Nippostrongylus brasiliensis (Nb). In vivo studies showed that the kinetics of intestinal tissue eosinophilia was not directly related to those of the intestinal worm burden. Furthermore, Nb worm extract has no or only very weak in vitro eosinophil chemotactic activity, suggesting that parasite-derived eosinophil chemotactic factor (ECF) is, if at all, not a major regulator for intestinal tissue eosinophilia in this Nb rat system. On the other hand, when mesenteric lymph node (MLN) cells obtained various days after infection were cultured, potent ECF activity was detected in the cell-free supernatant from the cultures of MLN cells 15-20 days after infection, at which time marked intestinal tissue eosinophilia was observed in vivo. Production of ECF by MLN cells from Nb-infected rats seems to be spontaneous, since these cultures were performed without adding worm antigen. ECF-producing activity of day-20 MLN cells was suppressed by adding various metabolic inhibitors such as cycloheximide, mitomycin C, or puromycin. After Sephadex G-75 gel filtration, ECF activity produced by day-20 MLN cells was associated with two different molecules.

Animals↗
PubMed1984

[Mechanism of exercise-induced ST segment deviation in myocardial infarction: a 201T1-myocardial scintigraphic study].

Exercise-induced ST segment deviation was investigated using thallium-201 myocardial scintigraphy and correlated with coronary artery lesions in 25 patients with old myocardial infarction. Seven of eight patients without ST deviation showed no reversible perfusion defect by near maximal exercise, and six had no significant stenosis in the coronary arteries perfusing the non-infarcted area. During exercise, ST segment depression was induced in 12 patients and six of them developed a reversible perfusion defect in the non-infarcted area, associated with significant stenosis of the corresponding coronary arteries. Remaining six patients, however, did not show a reversible perfusion defect and four of them had no significant stenosis of the coronary arteries perfusing the non-infarcted area. In nine patients with exercise-induced ST segment elevation in leads with Q waves, a reversible perfusion defect was not detected in seven (78%) and five (71%) of them had no significant coronary artery stenosis as well. Four patients developed both ST segment elevation in leads with Q waves and ST segment depression in other leads. One patient who had significant coronary artery stenosis in the non-infarcted area and showed a reversible perfusion defect developed 1.5 mm ST elevation in II, III, a VF leads and 4 mm ST depression in precordial leads. In the remaining three patients who did not show a reversible perfusion defect and significant coronary artery stenosis in the non-infarcted area, ST depressions were less than 2 mm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

A C5-derived macrophage chemotactic factor from DNP-Ascaris extract-induced skin lesion in guinea pigs.

In complement-depleted condition induced by cobra venom factor (CoF), tissue macrophage reaction and macrophage chemotactic activity (MCA) in skin extract from skin lesions induced by DNP-Ascaris extract (DNP-As) were decreased, respectively. MCA in the fraction containing macrophage chemotactic factor b (B fraction) was decreased completely. While MCA in the fraction containing macrophage chemotactic factor a and c (A fraction) was affected only slightly. These results suggested that the decrease of MCA of B-fraction might be associated with depletion of complement system by CoF. Using anti-C5 antibody, it was confirmed that macrophage chemotactic factor-b (MCF-b) (MW 14,000: thermostable) might be derived from C5 fragment in vivo.

Anaphylaxis↗
PubMed1983

Glycogen storage disease. Studies related to the mechanism of glycogenosome formation.

Glycogen storage diseases of type I, II, III, IV, V and the other muscle types, were examined electron microscopically, biochemically and physicochemically. Glycogenosomes (glycogen containing vacuoles) were found in the affected tissues of type II, type III variant of muscle glycogen storage disease, type IV and muscle type phosphorylase b kinase deficiency (disorder of the phosphorylase b kinase activation mechanism). The acid alpha-glucosidase activity was decreased only in the case of type II glycogen storage disease (Pompe's disease). The other types of glycogen storage disease showed no decrease in acid alpha-glucosidase activity. Moreover, one patient with type II disease also revealed a decrease in neutral alpha-glucosidase activity. In all cases where glycogenosomes were found, the extracted glycogen macromolecules showed some molecular abnormality or deviation when compared with normal native glycogen macromolecules.

1,4-alpha-Glucan Branching Enzyme↗
PubMed1983

The mediation of tissue eosinophilia in hypersensitivity reactions. III. Separation of two different delayed eosinophil chemotactic factors and transfer of these factors by serum or cells from sensitized guinea-pigs.

Two different eosinophil chemotactic factors (delayed ECF-a and ECF-b) were isolated from the delayed phase (24 hr old) of eosinophil-rich inflammatory reaction sites induced by DNP-ascaris extract, which could be separated by DEAE-Sephadex. Both the factors were thermolabile (56 degrees, 30 min) and had a mol. wt of about 70,000, whereas they were clearly different in antigenicity. Delayed tissue eosinophilia was shown to be mediated by peritoneal exudate cells (PEC) and serum from immunized donors to recipients. A chemotactic factor, closely resembling a delayed ECF-a, was isolated from the skin lesions of recipients transferred by sensitized PEC and challenged. Another factor, closely resembling a delayed ECF-b, was isolated from those of recipients transferred by immune serum and challenged. Furthermore, we have shown that delayed ECF-b, but not delayed ECF-a, shared a common antigenicity with some guinea-pig serum component. Thus we concluded that delayed tissue eosinophilia was mediated by the combined actions of two different factors, delayed ECF-a and ECF-b.

Animals↗