Ryo Kobayashi

Gifu Pharmaceutical University, Gihu, Gifu, Japan

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Publications (7)13.6 Total impact

  • Toxicology Letters 06/2012; 211:S137. · 3.36 Impact Factor
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    ABSTRACT: Trichloroethylene (TCE) is suspected as a potent immunomodulator that accelerates the development of allergic diseases. We previously reported that TCE promotes ovalbumin (OVA)-induced active cutaneous anaphylaxis, including enhancing antigen-specific serum IgE levels and splenic lymphocyte proliferation. However, the target cells and molecular mechanism through which TCE modulates antigen-specific immune responses remain unclear. To identify a potential underlying mechanism, we investigated whether TCE modulates T cell receptor (TCR)-induced T cell activation and proliferation in vitro. TCE enhanced T cell proliferation primed by anti-CD3 antibody, but not concanavalin A, in a dose-dependent fashion. In addition, TCE enhanced anti-CD3-primed proliferation of CD8(+) rather than CD4(+) T cells. Consistent with this result, TCE markedly enhanced the Lck phosphorylation mediated by anti-CD3 antibody in CD8(+) but not CD4(+) T cells. Furthermore, we analyzed the effect of TCE exposure via drinking water for 2 weeks on splenocyte populations in non-immunized and OVA-immunized mice. In OVA-immunized mice, TCE (3 mg/l) significantly expanded CD3(+), CD8(+) and CD4(+) cell populations, however the effect at the lower concentration was significant only in the CD8(+) populations, whereas TCE had no effect on these cells population in non-immunized mice. These findings suggest that TCE enhances TCR-CD3-induced proliferation of CD8(+) rather than CD4(+) cells and disrupts various activities of peripheral T cells.
    The Journal of Toxicological Sciences 01/2012; 37(2):381-7. · 1.38 Impact Factor
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    ABSTRACT: Trichloroethylene (TCE) and tetrachloroethylene (perchloroethylene; PCE) are commonly identified as environmental contaminants of groundwater. Previously, we investigated the enhancing effects of TCE and PCE on antigen-induced histamine release and inflammatory mediator production in rat mast cells. In this study, to examine the potential effect of TCE and PCE on antigen-induced histamine release from mouse mast cells, mouse bone marrow-derived mast cells (BMMC) were sensitized with anti-dinitrophenol (DNP) monoclonal IgE antibody and then stimulated with DNP-BSA containing with TCE or PCE. Both TCE and PCE significantly enhanced antigen-induced histamine release from BMMC. Next we investigated the effects of TCE and PCE on the passive cutaneous anaphylaxis (PCA) reaction in vivo using ICR mice. TCE and PCE significantly enhanced the PCA reaction in a dose-dependent manner. In addition, we examined the enhancing effects of ingesting small amount of TCE and PCE in drinking water on antigen-stimulated allergic responses. After the ICR mice had ingested TCE or PCE in their drinking water for 2 or 4 weeks, we performed the PCA reaction. Both TCE and PCE ingestion enhanced the PCA reaction in a dose-dependent manner for 4 weeks. These results suggest that exposure to TCE and PCE leads to the augmentation of type I allergic responses in many species.
    The Journal of Toxicological Sciences 01/2012; 37(2):439-45. · 1.38 Impact Factor
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    Makoto Seo, Ryo Kobayashi, Hisamitsu Nagase
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    ABSTRACT: Allergic diseases have been increasing worldwide in industrialized countries. The interplay of genetic and environmental factors is involved in the induction and progression of several types of allergic diseases. Recently, there have been many reports that the increase and spread of allergic diseases are related to chronic exposure to several environmental pollutants, such as diesel exhaust particles and formaldehyde. Trichloroethylene (TCE) and tetrachloroethylene (PCE) are categorized into chlorinated organic compounds, and are the most widely used ex-tensively in various industrial processes. As a consequence of their widespread use, TCE and PCE are becoming environmental pollutants. Generally, TCE and PCE exposure causes organ toxicological effects on the liver, kidney, and the central nervous system; however, studies of TCE and PCE exposure-induced immune modulations are lim-ited. In this review, we summarize research into immunotoxic effects, such as allergy hypersensitivity, autoimmune disease, and immunosuppression, of TCE and PCE from experimental animal studies and human epidemiological studies.
    Journal of health science 01/2011; 57(6). · 0.80 Impact Factor
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    ABSTRACT: The prevalence of allergic disorders is increasing in industrial areas and countries. Recent reports suggest that some environmental pollutants are related to the increase in allergic diseases, and we reported that trichloroethylene (TCE) is a candidate chemical for causing the increase of allergic diseases, as TCE ingestion is associated with allergic reaction enhancement. TCE is widely used in many industries, and it is commonly detected as an environmental contaminant. This study aimed to clarify the immunotoxicity of TCE in detail. BALB/c mice were treated with TCE dissolved in drinking water for 2 and 4 weeks, and the mice were immunized with ovalbumin (OVA)/aluminum hydroxide (alum) twice. On the final day of the TCE exposure period, we measured the active cutaneous anaphylaxis (ACA) reaction and the antigen- specific IgE level in serum as well as the histamine level at the allergic reaction site and assayed the proliferation rates of splenocytes collected from the animals. The ACA reaction was enhanced by TCE ingestion. The OVA specific IgE level in mice was enhanced by TCE exposure for 4 weeks. The proliferation rate of the splenocytes was enhanced by TCE ingestion for 2 and 4 weeks. The enhancement of the ACA reaction by TCE ingestion via drinking water may be related to the increase in splenocyte proliferation. On the other hand, it may be weakly related to antigen-specific IgE production.
    The Journal of Toxicological Sciences 01/2010; 35(5):699-707. · 1.38 Impact Factor
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    ABSTRACT: In previous report, we have shown that trichloroethylene (TCE) increases histamine release and inflammatory cytokine production from antigen-stimulated mast cells. In this study, we examined the enhancing effect of a small amount of TCE ingestion from drinking water on antigen-stimulated allergic responses. After exposure of Wistar rats to TCE ingestion for 2 or 4 weeks, we performed a passive cutaneous anaphylaxis (PCA) reaction. TCE ingestion for 2 and 4 weeks enhanced PCA reaction in a dose-dependent manner. On histological examination, TCE ingestion for 2 weeks exacerbated inflammation characterized by infiltration of lymphocytes and accumulation of mast cells around the vessel in the skin. After TCE ingestion for 4 weeks, the mesenteric lymph nodes (MLNs) showed increase of the size and wet weight, and germinal centers changed distinctly. The interleukin-4 (IL-4) mRNA levels on spleen, MLNs and leukocytes were increased. Moreover, serum total IgE levels of TCE ingestion increased in a time-dependent manner. Our results suggest that TCE ingestion induces pro-inflammatory responses and causes Th1/Th2-type helper T-cell imbalance. And more, a small amount of TCE ingestion may lead to the initiation and acceleration of type I allergic reaction.
    Regulatory Toxicology and Pharmacology 09/2008; 52(2):140-6. · 2.13 Impact Factor
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    ABSTRACT: Previously, we observed that tetrachloroethylene (perchloroethylene, PCE) increased histamine release and inflammatory mediator production from antigen-stimulated mast cells. In this study, we examined the enhancing effect of low concentrations of PCE in drinking water on antigen-stimulated allergic responses. After exposure of Wistar rats to PCE in drinking water for 2 or 4 weeks, we performed a passive cutaneous anaphylaxis (PCA) reaction. PCE exposure for 4 weeks enhanced PCA reaction in a dose-dependent manner. In pathological studies, PCE exposure for 2 weeks exacerbated inflammation characterized by infiltration of lymphocytes and accumulation of mast cells around the vessel. Non-purified mast cells (NPMCs) from rats treated with 1mg/L PCE in drinking water for 2 weeks increased antigen-stimulated histamine release. Furthermore, the leukocytes of rats treated with PCE in drinking water for 4 weeks showed increased interleukin (IL)-4 expression. The mechanism of enhancing the PCA reaction is assumed to be that PCE increases IL-4 production and PCE causes T helper (Th) 1/Th2-type helper T-cell imbalance and increases histamine release from excessively accumulated mast cells. The results suggest that the intake of PCE in drinking water, even at a low concentration, leads to the initiation and acceleration of allergic diseases.
    Immunobiology 02/2008; 213(8):663-9. · 3.18 Impact Factor