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Biomedical subjects

Y Kamagata

Publications and source records attributed to Y Kamagata.

44 records · Page 3Linked to original sources
PubMed1989

[Dental radiographic survey of rapidly progressive periodontitis].

The purpose of this study was to determine the prevalence of rapidly progressive periodontitis (RPP) by radiographic evaluation in patient at the department of conservative dentistry, Ohu University hospital during two years from 1987 to 1988. The survey was conducted on 370 patients. The radiographic evaluation was done by the method of Schei. The results obtained were as follows. 1. The number of RPP patient was eight. The prevalence of RPP in all patients and periodontitis patients were 2.1%, 6.0%, respectively. RPP patients consisted of 4 females and 4 males. 2. The age of RPP patients ranged from 34 to 41 (mean age 37.5) years old. 3. The number of affected and missed teeth ranged from 4 to 19 (mean 12.1), 0 to 23 (mean 8.0), respectively in RPP patients. 4. Severe alveolar bone loss (more than 50%) was observed in the teeth except canine.

Adult↗
PubMed1989

Relative strength of the mitogenic and interleukin-2-production-inducing activities of staphylococcal exotoxins presumed to be causative exotoxins of toxic shock syndrome: toxic shock syndrome toxin-1 and enterotoxins A, B and C to murine and human T cells.

Several observations suggest that staphylococcal enterotoxins A, B and C (SEA, SEB and SEC, respectively), in addition to toxic shock syndrome toxin-1 (TSST-1), are causative exotoxins of toxic shock syndrome (TSS). Based on the view that polyclonal T cell activation with the causative exotoxins, resulting in over-production of lymphokines, is involved in the development of the pathological changes observed in TSS, we investigated the activities of these four exotoxins to induce proliferation and interleukin 2 production in murine and human lymphocytes by using in vitro culture systems. The results showed that all these exotoxins are strong polyclonal inducers of proliferation and interleukin 2 production in human T cells, whereas TSST-1 and SEA are strong and SEB and SEC are weak polyclonal inducers in murine T cells. These results suggest that SEA, SEB and SEC, in addition to TSST-1, are possibly involved as causative exotoxins in the development of the pathological changes observed in TSS.

Adult↗
PubMed1987

Study of the biological activities of toxic shock syndrome toxin-1: II. Induction of the proliferative response and the interleukin 2 production by T cells from human peripheral blood mononuclear cells stimulated with the toxin.

Toxic shock syndrome toxin-1 (TSST-1) is an exotoxin produced by Staphylococcus aureus isolated from patients with toxic shock syndrome. We investigated the proliferative response of human lymphocytes and their interleukin 2 (IL-2) production after stimulation with TSST-1 in vitro. Human cord blood mononuclear cells (HCBM) and human peripheral blood mononuclear cells (HPBM) could proliferate with TSST-1 stimulation. T cell-depleted HPBM showed only a marginal response to this toxin. A IL-2-like factor with a molecular weight of 15-18 kD was obtained from the supernatants of TSST-1-stimulated HPBM cultures. The factor was absorbed by CTLL-2 cells but not by T cell-depleted murine spleen cells, indicating that it is IL-2. HPBM are very sensitive to TSST-1: a low concentration of TSST-1 (0.01 ng/ml in 36 h stimulation) and a short period of stimulation (8 h at 10 ng/ml of the toxin) were fully effective for HPBM to produce substantial amounts of IL-2. Removal of T cells abrogated the TSST-1-induced IL-2 production by HPBM. Reconstituted cell cultures of nylon wool column-passed T cells and macrophages produced IL-2 by TSST-1 stimulation and, furthermore, the accessory activity of the macrophages could be partially replaced by a macrophage-derived factor containing interleukin 1. These findings indicate that T cells require macrophages or IL-1 for TSST-1-induced production of IL-2. The roles of lymphokines, including IL-2, in the development of this illness are discussed.

Bacterial Toxins↗
PubMed1986

Study of the biological activities of toxic shock syndrome toxin-1. I. Proliferative response and interleukin 2 production by T cells stimulated with the toxin.

The mitogenic and interleukin 2 (IL 2) production-inducing effects of toxic shock syndrome toxin-1 (TSST-1) on murine lymphocytes were investigated. TSST-1, an exotoxin produced by Staphylococcus aureus recovered from patients with toxic shock syndrome (TSS), is thought to be a causative agent of the syndrome. TSST-1 was mitogenic for splenic T cells and peanut agglutinin (PNA)-negative thymocytes, but not for T cell-depleted spleen cells, PNA-positive thymocytes or IL 2-dependent CTLL 2-cells. A factor mitogenic for CTCC-2 cells with a molecular weight of 30-35 kdaltons was obtained by stimulating spleen cells with TSST-1 and it was absorbed by CTLL-2 cells, indicating that the factor is IL 2. For substantial amounts of IL 2 to be produced, 10 ng or more of TSST-1 per ml and 48 hr or more of incubation were required. Removal of T cells abrogated the IL 2 production by spleen cells. T cells obtained by the nylon wool column method alone produced IL 2 on TSST-1 stimulation in the presence of either macrophages or a macrophage lysate containing interleukin 1. However, T cells obtained by a combination of the nylon wool column method and anti-Ia antibody treatment produced IL 2 in the presence of macrophages but not of the macrophage lysate, indicating that IL 2 production by TSST-1-stimulated T cells is absolutely dependent on the presence of accessory cells.

Animals↗
PubMed1984

Mechanism of lipopolysaccharide-induced immunosuppression: immunological activity of B cell subsets responding to T-dependent or T-independent antigens in lipopolysaccharide-preinjected mice.

Spleen cells from mice preinjected with high doses of bacterial lipopolysaccharide did not generate anti-trinitrophenyl (TNP) plaque-forming cells in vitro to the T-dependent antigen, TNP-sheep erythrocytes, but did generate fully plaque-forming cells to the T-independent antigens, TNP-Ficoll and TNP-Brucella abortus. The immunological activity of B cells from such lipopolysaccharide-preinjected mice was analyzed in the present study. T cell-depleted spleen cells from mice injected with 30 micrograms of lipopolysaccharide 3 days previously did not respond to combined stimulation with TNP-sheep erythrocytes and concanavalin A-induced T cell-replacing factor and had no suppressive activity on normal T cell-depleted spleen cells. Splenic B cells, which were separated from T cells and macrophages from mice injected with 30 micrograms of lipopolysaccharide 3 days previously, responded only partially (about 25% of the control response) to combined stimulation with TNP-sheep erythrocytes and concanavalin A-induced cell-replacing factor in the presence of normal macrophages, but responded fully to TNP-B. abortus, regardless of the presence of normal macrophages. These results indicate that B cells responding to the T-dependent antigens are rendered unresponsive to antigenic stimulation in mice preinjected with lipopolysaccharide, whereas B cells responding to the T-independent antigens are kept intact.

Animals↗