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.
Keyphrases
- candida albicans
- cell wall
- biofilm formation
- cell cycle
- staphylococcus aureus
- reactive oxygen species
- cell proliferation
- end stage renal disease
- ejection fraction
- newly diagnosed
- mouse model
- oxidative stress
- prognostic factors
- cell death
- risk factors
- pseudomonas aeruginosa
- escherichia coli
- amino acid
- saccharomyces cerevisiae
- methicillin resistant staphylococcus aureus