School of Medical Sciences, Institute of Medical Sciences, Foresterhill University of Aberdeen, Aberdeen AB25 2ZD, UK.
Curr Opin Microbiol. 2012 Aug;15(4):406-12. doi: 10.1016/j.mib.2012.04.005. Epub 2012 May 18.
An imbalance of the normal microbial flora, breakage of epithelial barriers or dysfunction of the immune system favour the transition of the human pathogenic yeast Candida albicans from a commensal to a pathogen. C. albicans has evolved to be adapted as a commensal on mucosal surfaces. As a commensal it has also acquired attributes, which are necessary to avoid or overcome the host defence mechanisms. The human host has also co-evolved to recognize and eliminate potential fungal invaders. Many of the fungal genes that have been the focus of this co-evolutionary process encode cell wall components. In this review, we will discuss the transition from commensalism to pathogenesis, the key players of the fungal cell surface that are important for this transition, the role of the morphology and the mechanisms of host recognition and response.
正常微生物菌群失衡、上皮屏障破裂或免疫系统功能障碍，有利于人类致病性酵母白色念珠菌从共生菌转变为病原体。白色念珠菌已经进化为适应黏膜表面的共生菌。作为共生菌，它还获得了一些特性，这些特性对于避免或克服宿主防御机制是必要的。人类宿主也进化到可以识别和消除潜在的真菌入侵者。在这个协同进化过程中，许多真菌基因一直是关注的焦点，这些基因编码细胞壁成分。在这篇综述中，我们将讨论从共生到发病机制的转变，讨论对这种转变很重要的真菌细胞表面的关键因子，以及形态和宿主识别与反应的机制的作用。
