Abstract
With the extensive utilization of antifungal drugs, the drug resistance of Candida albicans is progressively intensifying, and the effect of empirical treatment for C. albicans infection is not evident. There is an urgent need for novel strategies and methods for the treatment of C. albicans infection. Our study utilized the previously constructed C. albicans Ire1 double gene deletion strain to explore the influence of the Ire1 on endoplasmic reticulum (ER) stress and pathogenicity of C. albicans through drug stress phenotype testing, biofilm and hyphomycete formation testing, and mouse systemic infection testing. The results indicate that Ire1 is involved in maintaining the integrity of the C. albicans cell wall and influencing the hyphal formation ability of C. albicans. Concurrently, the deletion of the Ire1 increased the sensitivity of C. albicans to the ER stress agents tunicamycin and dithiothreitol and diminished the biofilm formation ability of C. albicans in vitro, resulting in significant inhibition of the growth of C. albicans. In mouse models, the deletion of Ire1 completely nullified the virulence and pathogenicity of C. albicans in the tail vein infection. In conclusion, Ire1 might be a key target for the potential development of new therapeutic drugs and vaccines.