【葡萄球菌肠毒素的生物活性及催吐机制研究】。

Hisaya Ono
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摘要

1930年,ack等人发现金黄色葡萄球菌食物中毒是由金黄色葡萄球菌产生的葡萄球菌肠毒素(SE)引起的,而不是由细菌感染引起的。然而,SE的催吐机制尚不清楚。在本研究中,我们分析了SE在几种催吐动物模型中的催吐活性,试图阐明其催吐机制。我们建立了一种小型灵长类动物,普通狨猴,作为一种新的呕吐模型。我们还分析了普通狨猴胃肠道的免疫荧光分析,发现SE与胃肠道粘膜下肥大细胞结合,并诱导肥大细胞脱颗粒。此外,我们发现SE诱导组胺释放,而组胺释放被肥大细胞稳定剂抑制。此外,用肥大细胞稳定剂或组胺H1受体拮抗剂治疗普通狨猴可抑制SE诱导的呕吐反应。这些结果表明,口服SE与胃肠道粘膜下肥大细胞结合,引起脱颗粒,导致组胺释放,从而引起呕吐。
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[Studies on the biological activities and emetic mechanism of staphylococcal enterotoxins].

Staphylococcus aureus food poisoning was shown by Dack et al. in 1930 to be caused by staphylococcal enterotoxin (SE) produced by S. aureus, rather than by the bacterial infection. However, the emetic mechanism of SE has remained unclear. In this study, we analyzed the emetic activity of SE in several emetic animal models and tried to elucidate the mechanism of emesis. We established a small primate, common marmoset, as a novel emetic model for SE. We also analyzed the immunofluorescence analysis of the gastrointestinal tract of the common marmoset and found that SE binds to submucosal mast cells in the gastrointestinal tract and SE induces degranulation of the mast cells. Furthermore, we showed that SE induces histamine releases, which is inhibited by mast cell stabilizer. In addition, treatment of common marmosets with either mast cell stabilizer or histamine H1 receptor antagonists suppressed the emetic response induced by SE. These results indicate that orally administered SE binds to submucosal mast cells in the gastrointestinal tract and causes degranulation, resulting in the release of histamine, which in turn causes emesis.

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[Study on biofilm formation and heterogeneity in Clostridium perfringens]. [Wakate Colosseum for Bacteriology]. [Award Lecture]. [Workshop]. [Luncheon Seminar].
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