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首页> 外文期刊>Infection and immunity >Glucose up-regulates expression of the differentiation-associated brush border binding site for enterotoxigenic Escherichia coli colonization factor antigen I in cultured human enterocyte-like cells.
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Glucose up-regulates expression of the differentiation-associated brush border binding site for enterotoxigenic Escherichia coli colonization factor antigen I in cultured human enterocyte-like cells.

机译：葡萄糖上调培养的人肠样细胞样细胞中产肠毒素的大肠杆菌定居因子抗原I的分化相关的刷状边界结合位点的表达。

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摘要

The association of enterotoxigenic Escherichia coli expressing colonization factor antigen I (CFA/I) with the cultured human colon adenocarcinoma cell, a model of the mature enterocyte of the small intestine, is dependent on the binding of CFA/I to a brush border-associated component. Binding of the purified radiolabeled [125I]CFA/I- and 14C-labeled CFA/I-positive bacteria could be displaced by an increasing concentration of unlabeled CFA/I. Moreover, we showed that expression of the specific CFA/I binding developed as a function of cell differentiation in Caco-2 cells, whereas expression of the nonspecific binding did not. Expression of the brush border differentiation-associated component acting as a binding site for CFA/I was up-regulated by glucose. Indeed, the enterocyte-like HT-29 glc- cell subpopulation not expressing the CFA/I binding site when cultured in dialyzed serum and hexose-free medium regained the ability to bind CFA/I when the cells were returned to culture medium containing glucose. Furthermore, expression of the brush border-associated CFA/I binding site in the enterocyte-like Caco-2 cells was repressed when the cells were cultured in hexose-free conditions.
机译：表达肠毒素的大肠杆菌表达定殖因子抗原I（CFA / I）与培养的人结肠腺癌细胞（小肠成熟肠细胞的模型）之间的关联取决于CFA / I与刷状缘相关的结合零件。纯化的放射性标记的[125I] CFA / I和14C标记的CFA / I阳性细菌的结合可以通过增加浓度的未标记CFA / I来取代。此外，我们表明在Caco-2细胞中特异性CFA / I结合的表达随细胞分化而发展，而非特异性结合的表达则没有。葡萄糖上调了与CFA / I的结合位点相关的刷状边缘分化相关成分的表达。实际上，当在透析的血清中培养时，不表达CFA / I结合位点的肠样细胞HT-29 glc-细胞亚群，并且当细胞返回含葡萄糖的培养基时，无己糖的培养基恢复了结合CFA / I的能力。此外，当在无己糖条件下培养细胞时，肠细胞样Caco-2细胞中与刷状缘相关的CFA / I结合位点的表达受到抑制。

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