Sap2在白念珠菌致病机制中的作用

The Role of Sap2 in Pathogenicity of Candida Albicans

Sap2是白念珠菌感染宿主后在天冬氨酸蛋白酶(secreted aspartyl proteinase, Saps)家族中表达最强的酶,受多个系统的共同调控,包括环境中的氮源、氨基酸浓度、自身调节、Ecm33蛋白、OPI1因子和其他菌属微生物。白念珠菌可通过Sap2的多种特性(炎性体的激活、抗菌肽的分解、激肽的释放、补体系统的抑制和中性粒细胞的诱导迁移)发挥其黏附和侵袭功能,因此认为Sap2是白念珠菌感染宿主后主要的致病因子。现就Sap2的研究现状进行总结,旨在进一步了解Sap2在白念珠菌中的表达调控和致病机制,从而为抗真菌药物的研发提供新思路。

Sap2 is the most strongly expressed enzyme from the Secreted aspartyl proteinase(Saps) family in Candida albicans during host infection.Sap2 is co-regulated by multiple systems, including environmental nitrogen sources, amino acid concentrations, self-regulation, Ecm33 protein, OPI1 factors and other microorganisms of the genus.Candida albicans can exert its adhesive and invasive functions through a variety of properties of Sap2(activation of the inflammasome, catabolism of antimicrobial peptides, release of kinins, inhibition of the complement system and induction of neutrophil migration).Therefore, Sap2 is thought to be the main pathogenic factor in Candida albicans infection.This review aims to present the regulation of Sap2 expression and pathogenic mechanisms in Candida albicans to provide new directions for developing antifungal drugs.