MYCOLab Ai Logo - gold and army green

Overexpression of efflux pump and biofilm associated genes in itraconazole resistant Candida albicans isolates causing onychomycosis

Summary

This research examines why some fungal infections of the nails resist treatment with the antifungal drug itraconazole. Scientists found that resistant fungi produce more proteins that pump the drug out of their cells (efflux pumps) and form protective biofilm structures. Understanding these resistance mechanisms could help develop better combination treatments that work alongside antifungal drugs to overcome resistance.

Background

Candida albicans is a common cause of onychomycosis (nail infections) with increasing antifungal resistance. Itraconazole resistance compromises treatment efficacy and understanding the underlying mechanisms is crucial for developing better therapeutic strategies.

Objective

This study investigates the role of efflux pump genes (CDR1, CDR2, MDR1) and biofilm-associated genes (ALS1, ALS3) in itraconazole resistance in C. albicans isolates from onychomycosis patients by comparing gene expression between resistant and sensitive isolates.

Results

CDR1, CDR2, and ALS3 genes showed statistically significant upregulation in resistant isolates (p-values 0.049, 0.023, 0.010 respectively). Resistant isolates demonstrated significantly higher efflux activity (p=0.001). Itraconazole reduced biofilm formation when present during biofilm development but had limited effect on pre-formed biofilms.

Conclusion

CDR1, CDR2, and ALS3 are implicated as key mediators of itraconazole resistance in C. albicans onychomycosis. These findings suggest potential therapeutic targets for combination therapies involving efflux pump inhibitors and biofilm-disrupting agents to improve treatment outcomes.
  • Published in:Scientific Reports,
  • Study Type:Experimental In Vitro Study,
  • Source: 10.1038/s41598-025-17359-6, PMID: 40855185
Scroll to Top