Superoxide dismutases are involved in Candida albicans biofilm persistence against Miconazole
- Author
- Anna Bink, Davy Vandenbosch (UGent) , Tom Coenye (UGent) , Hans Nelis (UGent) , Bruno PA Cammue and Karin Thevissen
- Organization
- Abstract
- We investigated the cellular mechanisms responsible for the occurrence of miconazole-tolerant persisters in Candida albicans biofilms. Miconazole induced about 30% killing of sessile C. albicans cells at 75 mu M. The fraction of miconazole-tolerant persisters, i.e., cells that can survive high doses of miconazole (0.6 to 2.4 mM), in these biofilms was 1 to 2%. Since miconazole induces reactive oxygen species (ROS) in sessile C. albicans cells, we focused on a role for superoxide dismutases (Sods) in persistence and found the expression of Sod-encoding genes in sessile C. albicans cells induced by miconazole compared to the expression levels in untreated sessile C. albicans cells. Moreover, addition of the superoxide dismutase inhibitor N,N'-diethyldithiocarbamate (DDC) to C. albicans biofilms resulted in an 18-fold reduction of the miconazole-tolerant persister fraction and in increased endogenous ROS levels in these cells. Treatment of biofilms of C. albicans clinical isolates with DDC resulted in an 18-fold to more than 200-fold reduction of their miconazole-tolerant persister fraction. To further confirm the important role for Sods in C. albicans biofilm persistence, we used a Delta sod4 Delta sod5 mutant lacking Sods 4 and 5. Biofilms of the Delta sod4 Delta sod5 mutant contained at least 3-fold less of the miconazole-tolerant persisters and had increased ROS levels compared to biofilms of the isogenic wild type (WT). In conclusion, the occurrence of miconazole-tolerant persisters in C. albicans biofilms is linked to the ROS-detoxifying activity of Sods. Moreover, Sod inhibitors can be used to potentiate the activity of miconazole against C. albicans biofilms.
- Keywords
- CELLS, LOCK THERAPY, CHEMOSENSITIZATION, INFECTION, GENE
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-1899747
- MLA
- Bink, Anna, et al. “Superoxide Dismutases Are Involved in Candida Albicans Biofilm Persistence against Miconazole.” ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, vol. 55, no. 9, 2011, pp. 4033–37, doi:10.1128/AAC.00280-11.
- APA
- Bink, A., Vandenbosch, D., Coenye, T., Nelis, H., Cammue, B. P., & Thevissen, K. (2011). Superoxide dismutases are involved in Candida albicans biofilm persistence against Miconazole. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 55(9), 4033–4037. https://doi.org/10.1128/AAC.00280-11
- Chicago author-date
- Bink, Anna, Davy Vandenbosch, Tom Coenye, Hans Nelis, Bruno PA Cammue, and Karin Thevissen. 2011. “Superoxide Dismutases Are Involved in Candida Albicans Biofilm Persistence against Miconazole.” ANTIMICROBIAL AGENTS AND CHEMOTHERAPY 55 (9): 4033–37. https://doi.org/10.1128/AAC.00280-11.
- Chicago author-date (all authors)
- Bink, Anna, Davy Vandenbosch, Tom Coenye, Hans Nelis, Bruno PA Cammue, and Karin Thevissen. 2011. “Superoxide Dismutases Are Involved in Candida Albicans Biofilm Persistence against Miconazole.” ANTIMICROBIAL AGENTS AND CHEMOTHERAPY 55 (9): 4033–4037. doi:10.1128/AAC.00280-11.
- Vancouver
- 1.Bink A, Vandenbosch D, Coenye T, Nelis H, Cammue BP, Thevissen K. Superoxide dismutases are involved in Candida albicans biofilm persistence against Miconazole. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY. 2011;55(9):4033–7.
- IEEE
- [1]A. Bink, D. Vandenbosch, T. Coenye, H. Nelis, B. P. Cammue, and K. Thevissen, “Superoxide dismutases are involved in Candida albicans biofilm persistence against Miconazole,” ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, vol. 55, no. 9, pp. 4033–4037, 2011.
@article{1899747, abstract = {{We investigated the cellular mechanisms responsible for the occurrence of miconazole-tolerant persisters in Candida albicans biofilms. Miconazole induced about 30% killing of sessile C. albicans cells at 75 mu M. The fraction of miconazole-tolerant persisters, i.e., cells that can survive high doses of miconazole (0.6 to 2.4 mM), in these biofilms was 1 to 2%. Since miconazole induces reactive oxygen species (ROS) in sessile C. albicans cells, we focused on a role for superoxide dismutases (Sods) in persistence and found the expression of Sod-encoding genes in sessile C. albicans cells induced by miconazole compared to the expression levels in untreated sessile C. albicans cells. Moreover, addition of the superoxide dismutase inhibitor N,N'-diethyldithiocarbamate (DDC) to C. albicans biofilms resulted in an 18-fold reduction of the miconazole-tolerant persister fraction and in increased endogenous ROS levels in these cells. Treatment of biofilms of C. albicans clinical isolates with DDC resulted in an 18-fold to more than 200-fold reduction of their miconazole-tolerant persister fraction. To further confirm the important role for Sods in C. albicans biofilm persistence, we used a Delta sod4 Delta sod5 mutant lacking Sods 4 and 5. Biofilms of the Delta sod4 Delta sod5 mutant contained at least 3-fold less of the miconazole-tolerant persisters and had increased ROS levels compared to biofilms of the isogenic wild type (WT). In conclusion, the occurrence of miconazole-tolerant persisters in C. albicans biofilms is linked to the ROS-detoxifying activity of Sods. Moreover, Sod inhibitors can be used to potentiate the activity of miconazole against C. albicans biofilms.}}, author = {{Bink, Anna and Vandenbosch, Davy and Coenye, Tom and Nelis, Hans and Cammue, Bruno PA and Thevissen, Karin}}, issn = {{0066-4804}}, journal = {{ANTIMICROBIAL AGENTS AND CHEMOTHERAPY}}, keywords = {{CELLS,LOCK THERAPY,CHEMOSENSITIZATION,INFECTION,GENE}}, language = {{eng}}, number = {{9}}, pages = {{4033--4037}}, title = {{Superoxide dismutases are involved in Candida albicans biofilm persistence against Miconazole}}, url = {{http://doi.org/10.1128/AAC.00280-11}}, volume = {{55}}, year = {{2011}}, }
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