Title Alpha‑Hemolysin from Staphylococcus aureus Obstructs Yeast‑Hyphae Switching and Diminishes Pathogenicity in Candida albicans
Author Xiaoyu Yu1*, Yinhe Mao2, Guangbo Li1, Xianwei Wu2, Qiankun Xuan1, Simin Yang1, Xiaoqing Chen2, Qi Cao3, Jian Guo1, Jinhu Guo4, and Wenjuan Wu1*
Address 1Department of Laboratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200123, People’s Republic of China, 2Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai 200031, People’s Republic of China, 3Pharmaceutical Analysis Center, School of Pharmacy, The Naval Military Medical University, Shanghai 200433, People’s Republic of China, 4Department of Clinical Laboratory, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, People’s Republic of China
Bibliography Journal of Microbiology, 61(2),233-243, 2023,
DOI 10.1007/s12275-022-00006-4
Key Words Candida albicans · Hemolysin · Hyphal development · Cell wall · Mitochondria · Cell cycle · Pathogenicity
Abstract The use of antibiotics can disrupt the body’s natural balance and increase the susteptibility of patients towards fungal infections. Candida albicans is a dimorphic opportunistic fungal pathogen with niches similar to those of bacteria. Our aim was to study the interaction between this pathogen and bacteria to facilitate the control of C. albicans infection. Alpha-hemolysin (Hla), a protein secreted from Staphylococcus aureus, causes cell wall damage and impedes the yeast–hyphae transition in C. albicans. Mechanistically, Hla stimulation triggered the formation of reactive oxygen species that damaged the cell wall and mitochondria of C. albicans. The cell cycle was arrested in the G0/G1 phase, CDC42 was downregulated, and Ywp1 was upregulated, disrupting yeast hyphae switching. Subsequently, hyphae development was inhibited. In mouse models, C. albicans pretreated with Hla reduced the C. albicans burden in skin and vaginal mucosal infections, suggesting that S. aureus Hla can inhibit hyphal development and reduce the pathogenicity of candidiasis in vivo.