白色念珠菌细胞壁蛋白参与芽孢粘附人颊上皮细胞

Christine Imbert-Bernard, Alexis Valentin, Michèle Mallie, Jean-Marie Bastide
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引用次数: 9

摘要

Imbert-Bernard, C., Valentin, A., Mallie, M.和Bastide, J.-M.。1995. 白色念珠菌细胞壁蛋白参与胚孢子与人颊上皮细胞的粘附。真菌学通报,19(2):444 - 444。白色念珠菌对上皮细胞的粘附是念珠菌病发展的第一步,因此可能构成预防感染的有趣靶点。利用高度粘附于口腔上皮细胞(BECs)的白色念珠菌分离株(ivp1453)制备酵母细胞壁提取物。通过刀豆蛋白a亲和层析将该细胞壁提取物分离为Fr1(蛋白质部分)和Fr2(甘露蛋白部分)两个部分。粘附活性主要与蛋白质组分有关。因此,这个部分被保留下来,并通过离子交换色谱进一步分离成另外两个部分,称为Fr1a和Fr1b。粘附活性主要与Fr1b片段相关(56.4%的粘附抑制);对细胞壁提取物制备过程中使用的白色念珠菌分离株不具有特异性。Fr1b片段包含4种主要蛋白,分子量分别为30、38、47和54 kDa。在这4种蛋白中,分子量为38和54 kDa的蛋白可能参与了白色念珠菌对人BECs的粘附机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Involvement of Candida albicans Cell Wall Proteins in the Adherence of Blastospores to Human Buccal Epithelial Cells

Imbert-Bernard, C., Valentin, A., Mallie, M., and Bastide, J.-M. 1995. Involvement of Candida albicans cell wall proteins in the adherence of blastospores to human buccal epithelial cells. Experimental Mycology 19, 247-253. The adherence of Candida albicans to epithelial cells is one of the first steps in the development of candidiasis and therefore could constitute an interesting target for the prevention of infection. A yeast cell wall extract was prepared by using a C. albicans isolate (IVP 1453) highly adherent to buccal epithelial cells (BECs). This cell wall extract was separated by concanavalin A-affinity chromatography into two fractions referred to as Fr1 (proteic fraction) and Fr2 (mannoproteic fraction). The adhesion activity was mostly associated with the proteic fraction. This fraction was therefore retained and further fractionated by ion-exchange chromatography into two other fractions, referred to as Fr1a and Fr1b. The adhesion activity was mostly associated with the Fr1b fraction (56.4% adherence inhibition); it was not specific to the C. albicans isolate used during the cell wall extract preparation. The Fr1b fraction contained four major proteins with molecular masses of 30, 38, 47, and 54 kDa. Among these four proteins, those with molecular masses of 38 and 54 kDa could be involved in adherence mechanisms of C. albicans to human BECs.

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