(PhSe)₂ and (pCl-PhSe)₂ organochalcogen compounds inhibit Candida albicans adhesion to human endocervical (HeLa) cells and show anti-biofilm activities

Abstract

Adhesion capacity on biological surfaces and biofilm formation is considered an important step in the infection process by Candida albicans. The ability of (PhSe)₂ and (pCl-PhSe)₂, two synthetic organic selenium (organochalcogen) compounds, to act on C. albicans virulence factors related to adhesion to human endocervical (HeLa) cell surfaces and their anti-biofilm activities was analyzed. Both organochalcogen compounds inhibited C. albicans adhesion to HeLa cells, dependent on compound concentrations. (PhSe)₂ (at 20 µM; p = 0.0012) was significantly more effective than (pCl-PhSe)₂ (at 20 µM; p = 0.0183) compared with the control. (PhSe)₂ inhibited biofilm formation and decreased biofilm viability in both early and mature biofilms more efficiently than (pCl-PhSe)₂. Overall, the organochalcogen compounds, especially (PhSe)₂, were demonstrated to be effective antifungal drugs against C. albicans virulence factors related to epithelial cell surface adhesion and the formation and viability of biofilms.

Graphical Abstract

Keywords:

• Candida albicans
• organochalcogen compounds
• biofilm
• antifungal therapy
• cell adhesion
• HeLa cells

Compliance with ethical standards

Conflict of interest statement

The authors have no financial, personal, or other conflicts of interest related to this work.

Role of funding source

The authors would like to thank FAPESP.

Ethical approval

In this study, all experiments were performed using Cultures of Candida albicans (ATCC 10231), therefore there was no need for approval by local authorities.

Informed consent

The authors have obtained permission from all the authors, and declare that the material has not been published in whole or in part elsewhere; the paper is not currently being considered for publication elsewhere.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) and by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES) – Finance Code 001.