An acquired mechanism of antifungal drug resistance simultaneously enables Candida albicans to escape from intrinsic host defenses.

ABSTRACT: The opportunistic fungal pathogen Candida albicans frequently produces genetically altered variants to adapt to environmental changes and new host niches in the course of its life-long association with the human host. Gain-of-function mutations in zinc cluster transcription factors, which result in the constitutive upregulation of their target genes, are a common cause of acquired resistance to the widely used antifungal drug fluconazole, especially during long-term therapy of oropharyngeal candidiasis. In this study, we investigated if C. albicans also can develop resistance to the antimicrobial peptide histatin 5, which is secreted in the saliva of humans to protect the oral mucosa from pathogenic microbes. As histatin 5 has been shown to be transported out of C. albicans cells by the Fl

SUBMITTER: Hampe IAI 

PROVIDER: S-EPMC5633205 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature