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Superantigenic activity of toxic shock syndrome toxin-1 is resistant to heating and digestive enzymes

机译:毒性休克综合征毒素-1的超抗原活性对加热和消化酶具有抵抗力

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Aims:To elucidate the stability of superantigenic activity and pathogenesis of toxic shock syndrome toxin 1 (TSST-1) and staphylococcal enterotoxin A (SEA) against heating and digestive enzymes.Methods and Results:Purified TSST-1 and SEA were treated with heating, pepsin and trypsin that are related to food cooking, stomach and intestine conditions. The integrity, superantigenic activity and toxicity of treated TSST-1 and SEA were analysed by Western blotting, spleen cell culture, cytokine assay and toxic shock models. Both TSST-1 and SEA showed strong resistance to heating, pepsin and trypsin digestion. Furthermore, the treated TSST-1 showed significant higher induction of interferon-gamma and toxic shock compared with that of SEA. Pepsin- or trypsin-digested TSST-1 fragments still showed significant superantigenic and lethal shock toxicities.Conclusions:The superantigenic activity of TSST-1 was stable to heating and digestive enzymes. Pepsin- and trypsin-digested TSST-1 fragments still showed superantigenic and lethal shock activities, indicating that digested TSST-1 could cross epithelial cells and induce systemic toxicity.Significance and Impact of the Study:This study found, for the first time, that pepsin- or trypsin-digested smaller TSST-1 retained significant superantigenic and lethal shock activities. The different resistance of TSST-1 and SEA participates in the different pathogenic activities during food poisoning and toxic shock syndrome.
机译:目的:阐明中毒性休克综合征毒素1(TSST-1)和葡萄球菌肠毒素A(SEA)对加热和消化酶的超抗原活性和发病机理。方法与结果:对纯TSST-1和SEA进行加热处理,胃蛋白酶和胰蛋白酶与食物烹饪,胃和肠的状况有关。通过蛋白质印迹,脾细胞培养,细胞因子测定和毒性休克模型分析处理过的TSST-1和SEA的完整性,超抗原活性和毒性。 TSST-1和SEA均显示出对加热,胃蛋白酶和胰蛋白酶消化的强烈抵抗力。此外,与SEA相比,经处理的TSST-1表现出明显更高的干扰素-γ诱导和毒性休克。胃蛋白酶或胰蛋白酶消化的TSST-1片段仍显示出明显的超抗原和致命的休克毒性。结论:TSST-1的超抗原活性对加热和消化酶稳定。胃蛋白酶和胰蛋白酶消化的TSST-1片段仍显示超抗原性和致死性休克活性,表明消化的TSST-1可以穿过上皮细胞并诱导全身毒性。本研究的意义和影响:这项研究首次发现胃蛋白酶或胰蛋白酶消化的较小的TSST-1保留了显着的超抗原性和致死性休克活性。在食物中毒和中毒性休克综合症期间,TSST-1和SEA的不同抗性参与了不同的致病活动。

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