Antimicrobial peptide AMP-17 exerts anti-Candida albicans effects through ROS-mediated apoptosis and necrosis

Abstract

Background: New anti-candida albicans drugs need to be developed due to the emergence of drug-resistant cases in recent years. AMP-17 (Musca. domestica antimicrobial pepitide-17) is an antimicrobial peptide from M. domestica, which inhibits many fungal pathogens including Candida albicans (C. albicans) effectively. In this article, we discuss the potential mechanism of AMP-17 against C. albicans from the perspective of affecting its cell internal structure.Methods: After AMP-17 treatment, we examined the ultrastructure of C. albicans by transmission electron microscopy (TEM) and detected the cell cycle using flow cytometry. Fluorescent probes were used to examine the reactive oxygen species (ROS) accumulation in C. albicans cells and to analyze the correlation between ROS accumulation and C. albicans cell necrosis. The JC-1 kit was used to measure the effect of AMP-17 on the mitochondrial membrane potential (MMP) of C. albicans cells. AMP-17-induced apoptosis and necrosis was investigated using an Annexin V-FITC apoptosis detection kit.Results: Morphological observations showed that the shape of C. albicans treated with AMP-17 was irregular, and vacuoles were found in the cytoplasmic region. The treatment of C. albicans with AMP-17 resulted in the elevation of reactive oxygen species (ROS), depolarization of mitochondrial membrane potential (MMP), and changes in cell cycle, which promoted apoptosis and necrosis of C. albicans cells. The level of apoptosis increased in a dose-dependent manner after AMP-17 treatment.Conclusions: AMP-17 inhibited the growth and proliferation of C. albicans cells by altering the cell cycle of C. albicans. In addition, AMP-17 stimulated mitochondria to produce excess ROS for anti-stress, but the excess ROS damages the function of mitochondria in return and results in the alteration of MMP. All of these ultimately contributes to the death of C. albicans.