Abstract

Background: Candida albicans is the most common pathogen in patients with vulvovaginitis. Secretory aspartyl proteinases (SAPs) are potential factors in the virulence of C. albicans. Antimicrobial peptides (AMPs) are recognized as a promising antimicrobial group of drugs with a membrane degradation mechanism. Occurrence of resistance to these drugs is quite rare. The impact of rapid membrane degradation on AMPs is relative to the prevention or delay in drug resistance mechanisms in different microbes. Objectives: The purpose of this study was to compare the inhibitory effects of the designed NK95 peptide and caspofungin on expression of SAP4-SAP6 genes from clinical vaginal isolates of C. albicans. Methods: In this experimental study, samples were collected from 350 women, who were suspected of vulvovaginal candidiasis and were referred to Zahedan gynecology clinics during 6 months. The clinical specimens were cultured in Sabouraud glucose agar (SGA). Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to identify the vaginal isolates of C. albicans. Afterwards, the NK95 peptide was designed and synthesized. Drug susceptibility test was carried out at different concentrations of NK95 peptide and caspofungin. RNA extraction, cDNA synthesis, and quantitative Real-time PCR were performed on the clinical isolates before and after treatment with the designed peptide and caspofungin. Results: Based on the findings of this study, the minimum inhibitory concentration (MIC90), MIC50, and minimum fungicidal concentration (MFC) of C. albicans isolates were 62.5, 31.25, and 125 mu g/mL for the designed peptide, respectively. The SAP4 (45), SAP5 (85), and SAP6 (73) genes expressions significantly reduced at 48 hours after treatment with the designed peptide (P < 0.05). Conclusions: Our findings showed that the designed NK95 peptide has antifungal effects on the clinical vaginal isolates of C. albicans. Moreover, it has potential down-regulating on expression of SAP4, SAP5 and SAP6 genes.