Candida albicans is responsible for conditions ranging from superficial
infections such as oral or vaginal
candidiasis to potentially fatal systemic
infections. It produces pathogenic factors contributing to its virulence.
Iturin A, a
lipopeptide derived from Bacillus sp., exhibits a significant inhibitory effect against C. albicans. However, its exact mechanism in mitigating the pathogenic factors of C. albicans remains to be elucidated. This study aimed to explore the influence of
iturin A on several pathogenic attributes of C. albicans, including hypha formation, cell membrane permeability, cell adhesion, biofilm formation, and therapeutic efficacy in an oral C. albicans
infection model in mice. The minimal inhibitory concentration of
iturin A against C. albicans was determined to be 25 µg/mL in both YEPD and RPMI-1640 media.
Iturin A effectively inhibited C. albicans hyphal formation, decreased cell viability within biofilms, enhanced cell membrane permeability, and disrupted cell adhesion in vitro. Nonetheless,
iturin A did not significantly affect the
phospholipase activity or hydrophobicity of C. albicans. A comparative study with
nystatin demonstrated the superior therapeutic efficacy of
iturin A in a mouse model of oral C. albicans
infection, significantly decreasing C. albicans count and inhibiting both fungal hypha formation and tongue surface adhesion. High-dose
iturin A treatment (25 µg/mL) in mice had no significant effects on blood indices, tongue condition, or
body weight, indicating the potential for
iturin A in managing oral
infections. This study confirmed the therapeutic potential of
iturin A and provided valuable insights for developing effective antifungal
therapies targeting C. albicans pathogenic factors.