Saville Stephen P, Lazzell Anna L, Chaturvedi Ashok K, Monteagudo Carlos, Lopez-Ribot Jose L
Department of Biology, The University of Texas at San Antonio, San Antonio, TX 78249, USA.
Infect Immun. 2008 Jan;76(1):97-102. doi: 10.1128/IAI.00982-07. Epub 2007 Oct 29.
The pathogenesis of Candida albicans systemic infection is complex and results from the balance between its intrinsic virulence attributes and the host immune responses. Morphogenetic transitions between yeast cell and filamentous forms are considered one of the main virulence attributes in C. albicans. We have examined the pathogenesis of a genetically engineered C. albicans strain in which morphogenetic conversions can be externally manipulated in immunodeficient mice; these included B-cell deficient, nude (T cell deficient), SCID (lacking both functional T and B cells), and DBA/2N (C5 deficient with impaired neutrophil activity) mice. We also tested mice severely immunosuppressed by cyclophosphamide-cortisone acetate treatment. Mice with specific immune defects were able to survive an infection by yeast cells but not filamentous forms. However, yeast cells displayed a pathogenic effect leading to lethality in the severely immunosuppressed mice.
白色念珠菌全身感染的发病机制很复杂,是由其内在毒力属性与宿主免疫反应之间的平衡所致。酵母细胞与丝状形态之间的形态发生转变被认为是白色念珠菌的主要毒力属性之一。我们研究了一种基因工程改造的白色念珠菌菌株的发病机制,在免疫缺陷小鼠中,其形态发生转变可通过外部手段进行操控;这些小鼠包括B细胞缺陷、裸鼠(T细胞缺陷)、重症联合免疫缺陷小鼠(缺乏功能性T细胞和B细胞)以及DBA/2N小鼠(C5缺陷且中性粒细胞活性受损)。我们还测试了经环磷酰胺 - 醋酸可的松治疗而严重免疫抑制的小鼠。具有特定免疫缺陷的小鼠能够在酵母细胞感染中存活,但不能在丝状形态感染中存活。然而,酵母细胞在严重免疫抑制的小鼠中显示出导致死亡的致病作用。