Masuoka James, Hazen Kevin C
Department of Pathology, University of Virginia Health System, Charlottesville 22908-0904, USA.
Infect Immun. 2004 Nov;72(11):6230-6. doi: 10.1128/IAI.72.11.6230-6236.2004.
Cell surface hydrophobicity contributes to the pathogenesis of the opportunistic fungal pathogen Candida albicans. Previous work demonstrated a correlation between hydrophobicity status and changes in the acid-labile, phosphodiester-linked beta-1,2-oligomannoside components of the N-linked glycans of cell wall mannoprotein. Glycan composition also defines the two major serotypes, A and B, of C. albicans strains. Here, we show that the cell surface hydrophobicity of the two serotypes is qualitatively different, suggesting that the serotypes may differ in how they modulate cell surface hydrophobicity status. The cell wall mannoproteins from hydrophilic and hydrophobic cells of both serotypes were compared to determine whether the glycan differences due to serotype affect the glycan differences due to hydrophobicity status. Composition analysis showed that the protein, hexose, and phosphate contents of the mannoprotein fraction did not differ significantly among the strains tested. Electrophoretic profiles of the acid-labile mannan differed only with hydrophobicity status, not serotype, though some strain-specific differences were observed. Furthermore, a newly available beta-1,2-oligomannoside ladder allowed unambiguous identification of acid-labile mannan components. Finally, to assess whether the acid-stable mannan also affects cell surface hydrophobicity status, this fraction was fragmented into its component branches by acetolysis. The electrophoretic profiles of the acid-stable branches were very similar regardless of hydrophobicity status. However, differences were observed between serotypes. These results support and extend our current model that modification of the acid-labile beta-1,2-oligomannoside chain length but not modification of the acid-stable region is one common mechanism by which switching of cell surface hydrophobicity status of C. albicans strains occurs.
细胞表面疏水性有助于机会性真菌病原体白色念珠菌的发病机制。先前的研究表明，疏水性状态与细胞壁甘露糖蛋白N - 连接聚糖中酸不稳定、磷酸二酯连接的β - 1,2 - 寡甘露糖苷成分的变化之间存在相关性。聚糖组成还定义了白色念珠菌菌株的两种主要血清型，A和B。在这里，我们表明两种血清型的细胞表面疏水性在性质上是不同的，这表明血清型在调节细胞表面疏水性状态的方式上可能存在差异。比较了两种血清型亲水性和疏水性细胞的细胞壁甘露糖蛋白，以确定血清型引起的聚糖差异是否会影响疏水性状态引起的聚糖差异。组成分析表明，在所测试的菌株中，甘露糖蛋白部分的蛋白质、己糖和磷酸盐含量没有显著差异。酸不稳定甘露聚糖的电泳图谱仅因疏水性状态不同而不同，而非血清型，尽管观察到了一些菌株特异性差异。此外，一种新获得的β - 1,2 - 寡甘露糖苷阶梯图谱能够明确鉴定酸不稳定甘露聚糖成分。最后，为了评估酸稳定甘露聚糖是否也影响细胞表面疏水性状态，通过乙酰解将该部分片段化为其组成分支。无论疏水性状态如何，酸稳定分支的电泳图谱都非常相似。然而，血清型之间存在差异。这些结果支持并扩展了我们目前的模型，即酸不稳定的β - 1,2 - 寡甘露糖苷链长度的改变而非酸稳定区域的改变是白色念珠菌菌株细胞表面疏水性状态转换的一种常见机制。
