白念珠菌线粒体功能缺陷对胞壁结构及毒力的影响

摘要

Objective:To determine the effects of Candida albicans mitochondrial dysfunction on cell wall structure, virulence and pathogenicity. Methods:The differences of cell wall structure between the wild-type strain and the deficient strain were observed under transmission electron microscopy. The expression of cell wall components MNN4, PHR3, adhesion factors ALS1, ALS3 and virulence factors SAP9, SAP10 in the wild-type and deficient strain were detected using qPCR. The differences of the fatality rate and organ CFU load between the wild-type and deficient strain were detected in mice system infection model. Results:Com-pared with the wild-type strain, the deficient strain showed that the cell wall was thinner, the structure was looser and the realm of inner and outer membrane of cell wall was fuzzier under transmission scanning electron microscope. The expression of cell wall components, adhesion factors and virulence factors reduced significant-ly and there was no mice death in the deficient strain group. The CFU in liver, spleen and kidney of the mice treated with the deficient strain after 3 days reduced significantly. Conclusion: Mitochondrial dysfunction in candida albicans damage the cell wall integrity, reduce the expression of the major cell wall components and virulence factors, resulting in reduction of the pathogenicity of strain.%目的：明确白念珠菌线粒体功能缺陷对菌株细胞壁结构及致病力的影响。方法：通过透射电镜观察野生株与缺陷株胞壁结构的差异；利用 qPCR检测野生株与缺陷株细胞壁成分 MNN4、PHR3,常见黏附因子ALS1、ALS3及毒力因子SAP9、SAP10的表达；利用小鼠系统感染模型明确缺陷株与野生株在小鼠致死率及脏器菌载量等方面的差异。结果：与野生株相比,透射电镜显示缺陷株细胞壁整体结构较为疏松,胞壁较薄,胞壁内外膜境界模糊；qPCR显示缺陷株细胞壁成分、黏附因子、毒力因子表达显著降低；动物模型显示缺陷株无法导致小鼠系统性感染死亡,肝、脾、肾脏器菌载量在接种后第3日明显降低。结论：白念珠菌线粒体功能缺陷会导致其胞壁完整性,并下调主要胞壁成分及毒力因子的表达,从而导致菌株致病力显著减弱。