Li Fang, Svarovsky Michael J, Karlsson Amy J, Wagner Joel P, Marchillo Karen, Oshel Philip, Andes David, Palecek Sean P
Department of Chemical & Biological Engineering, University of Wisconsin-Madison, 1415 Engineering Drive, Madison, WI 53706, USA.
Eukaryot Cell. 2007 Jun;6(6):931-9. doi: 10.1128/EC.00049-07. Epub 2007 Apr 6.
Candida albicans is the leading cause of systemic fungal infections in immunocompromised humans. The ability to form biofilms on surfaces in the host or on implanted medical devices enhances C. albicans virulence, leading to antimicrobial resistance and providing a reservoir for infection. Biofilm formation is a complex multicellular process consisting of cell adhesion, cell growth, morphogenic switching between yeast form and filamentous states, and quorum sensing. Here we describe the role of the C. albicans EAP1 gene, which encodes a glycosylphosphatidylinositol-anchored, glucan-cross-linked cell wall protein, in adhesion and biofilm formation in vitro and in vivo. Deleting EAP1 reduced cell adhesion to polystyrene and epithelial cells in a gene dosage-dependent manner. Furthermore, EAP1 expression was required for C. albicans biofilm formation in an in vitro parallel plate flow chamber model and in an in vivo rat central venous catheter model. EAP1 expression was upregulated in biofilm-associated cells in vitro and in vivo. Our results illustrate an association between Eap1p-mediated adhesion and biofilm formation in vitro and in vivo.
白色念珠菌是免疫功能低下人群系统性真菌感染的主要病因。在宿主体内表面或植入的医疗设备上形成生物膜的能力增强了白色念珠菌的毒力，导致抗菌药物耐药性，并为感染提供了一个病灶。生物膜形成是一个复杂的多细胞过程，包括细胞黏附、细胞生长、酵母形态和丝状形态之间的形态发生转换以及群体感应。在这里，我们描述了白色念珠菌EAP1基因在体外和体内黏附和生物膜形成中的作用，该基因编码一种糖基磷脂酰肌醇锚定、葡聚糖交联的细胞壁蛋白。删除EAP1以基因剂量依赖的方式降低了细胞对聚苯乙烯和上皮细胞的黏附。此外，在体外平行板流动腔模型和体内大鼠中心静脉导管模型中，白色念珠菌生物膜形成需要EAP1表达。在体外和体内，生物膜相关细胞中EAP1表达上调。我们的结果说明了Eap1p介导的黏附与体外和体内生物膜形成之间的关联。
