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Pathogenicity of phospholipase B1 of Trichosporon asahii in immunosuppressed mice

Background Trichosporon asahii is an opportunistic pathogenic yeast‐like fungus. Phospholipase B1 (PLB1) is an important virulence factor of pathogenic fungi such as Candida albicans and Cryptococcus neoformans, and there are few studies on the role of PLB1 in the pathogenicity of T. asahii. Objecti...

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Published in:Mycoses 2023-06, Vol.66 (6), p.467-476
Main Authors: Cheng, Xiaoxian, Zhu, He, Bai, Shuang, Zou, Yuekun, Xia, Zhikuan, Yang, Rongya
Format: Article
Language:English
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Summary:Background Trichosporon asahii is an opportunistic pathogenic yeast‐like fungus. Phospholipase B1 (PLB1) is an important virulence factor of pathogenic fungi such as Candida albicans and Cryptococcus neoformans, and there are few studies on the role of PLB1 in the pathogenicity of T. asahii. Objectives To investigate the role of PLB1 in the pathogenicity of T. asahii. Methods A strain with low secretion of PLB1 (4848) was screened, a PLB1 overexpression strain (PLB1OX) was constructed, and the differences in histopathology, fungal load of organ, survival time of mice, the levels of IL‐6, IL‐10, TNF‐α, and GM‐GSF in the serum and organs caused by the two strains were compared. Results Histopathology showed that spores and hyphae were observed in both groups, and PLB1OX led to more fungal invasion. The fungal loads in the kidney, lung, spleen and liver in the PLB1OXgroup were significantly higher than those in the 4848 group, and the survival time of mice was significantly lower than that in the 4848 group. The levels of TNF‐α in the serum, liver, spleen, lung and kidney of the PLB1OX group were lower than those of the 4848 group, while the level of IL‐10 in the serum was higher than that of the 4848 group. Conclusions These results suggest that PLB1 can enhance the invasive function of T. asahii and affect the secretion of TNF‐α and IL‐10 which may affect the host antifungal immune response, providing evidence that PLB1 plays a role in the pathogenic infection of T. asahii.
ISSN:0933-7407
1439-0507
DOI:10.1111/myc.13568