Home >

news Help

Publication Information


Title
Japanese:Fungal Reactive Oxygen Species Secreted by Candida albicans Induce Barrier Disruption and Cell Death in HaCaT Keratinocytes 
English:Fungal Reactive Oxygen Species Secreted by Candida albicans Induce Barrier Disruption and Cell Death in HaCaT Keratinocytes 
Author
Japanese: Jayshree Low Jit Sze, ChenXinyue, Kanami Orihara, Susumu Kajiwara.  
English: Jayshree Low Jit Sze, Xinyue Chen, Kanami Orihara, Susumu Kajiwara.  
Language English 
Journal/Book name
Japanese:Journal of Fungi 
English:Journal of Fungi 
Volume, Number, Page        
Published date Jan. 2, 2026 
Publisher
Japanese: 
English: 
Conference name
Japanese: 
English: 
Conference site
Japanese: 
English: 
Official URL http://dx.doi.org/10.3390/jof12010038
 
DOI https://doi.org/10.3390/jof12010038
Abstract <jats:p>Candida albicans is a pathogenic fungus that expresses a fungal NADPH oxidase known as C. albicans Cfl11, which produces reactive oxygen species (ROS). Secretion of these ROS triggers caspase 3–mediated cell death in hepatocytes, which was attenuated in a mutant with a disrupted CaCFL11 gene (designated Cacfl11Δ mutant). Here, we compared the effects of the C. albicans wild-type strain and the Cacfl11Δ mutant. Our findings revealed that C. albicans reduces the viability of HaCaT keratinocytes in a contact-independent manner. Furthermore, exposure to C. albicans increased intracellular ROS production and caspase 3 activity in HaCaT keratinocytes. These changes were attenuated when HaCaT keratinocytes were exposed to the Cacfl11Δ mutant or when HaCaT keratinocytes were treated with the known antioxidant N-acetylcysteine. Furthermore, wild-type C. albicans, but not the Cacfl11Δ mutant, disrupted transepithelial electrical resistance and modulated the downregulation of the tight-junction genes occludin and junction adhesion molecule 1 in HaCaT keratinocytes. Collectively, these results show that fungal ROS secretion via CaCFL11 is a potent virulence factor in mediating keratinocyte viability and barrier function.</jats:p>

©2007 Institute of Science Tokyo All rights reserved.