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首页> 外文期刊>Infection and immunity >Bacterial Superantigen-Treated Intestinal Epithelial Cells Upregulate Heat Shock Proteins 25 and 72 and Are Resistant to Oxidant Cytotoxicity
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Bacterial Superantigen-Treated Intestinal Epithelial Cells Upregulate Heat Shock Proteins 25 and 72 and Are Resistant to Oxidant Cytotoxicity

机译：细菌超抗原处理的肠上皮细胞上调热休克蛋白25和72，并且抗氧化剂细胞毒性

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摘要

While the pathological events evoked by infection are commonly described, effective host responses to bacteria and their products should primarily be protective. Heat shock protein (Hsp) expression is upregulated by many stimuli and serves to maintain intracellular protein integrity. The ability of the prototypic superantigen, Staphylococcus aureus enterotoxin B (SEB) to induce Hsps was investigated with BALB/c mice and by in vitro addition to the murine small intestinal epithelial cell line MSIE. SEB-treated (5 or 100 μg intraperitoneally) mice revealed increased Hsp25 and Hsp72, but not Hsc73, in jejunal lymphocytes and epithelial cells. A similar Hsp response to SEB occurred in MSIE cells and was preceded by activation of the ERK1/2 and p38 mitogen-activated protein kinases but not the SAPK/JNK pathway; pharmacological inhibition of ERK1/2, but not p38, significantly reduced SEB-induced Hsps. Moreover, SEB-treated MSIE cells were protected against oxidant-induced cytotoxicity (measured by 51Cr release) and F-actin depolymerization. Thus, SEB exposure results in a rapid induction of the Hsp25 and Hsp72 in intestinal epithelial cells, both directly and through lymphocyte activation, and we suggest that this event is important in protecting the gut from damage by Staphylococcus infection or in the reparatory process and may be a generalized response to lumen-derived bacterial toxins.
机译：尽管通常描述了由感染引起的病理事件，但宿主对细菌及其产物的有效反应应主要是保护性的。热激蛋白（Hsp）的表达受许多刺激上调，并用于维持细胞内蛋白的完整性。用BALB / c小鼠并通过体外添加到鼠小肠上皮细胞系MSIE中研究了原型超抗原金黄色葡萄球菌肠毒素B（SEB）诱导Hsps的能力。 SEB处理的小鼠（腹膜内5或100μg）显示空肠淋巴细胞和上皮细胞中Hsp25和Hsp72升高，但Hsc73升高。 MSIE细胞中发生了对SEB的类似Hsp反应，并先激活了ERK1 / 2和p38丝裂原激活的蛋白激酶，但未激活SAPK / JNK途径。 ERK1 / 2而非p38的药理抑制作用显着降低SEB诱导的Hsps。此外，SEB处理的MSIE细胞具有抗氧化剂诱导的细胞毒性（通过 51 Cr释放测量）和F-肌动蛋白解聚的保护作用。因此，SEB暴露可直接或通过淋巴细胞激活快速诱导肠道上皮细胞中Hsp25和Hsp72的诱导，因此我们认为该事件对于保护肠道免受 Staphylococcus 感染的损害很重要。或在修复过程中，可能是对腔内细菌毒素的普遍反应。

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