Exploiting interkingdom interactions for development of small-molecule inhibitors of Candida albicans biofilm formation
Reen, F. Jerry; Phelan, John P.; Gallagher, Lorna; Woods, David F.; Shanahan, Rachel M.; Cano, Rafael; Ó Muimhneacháin, Eoin; McGlacken, Gerard P.; O'Gara, Fergal
Citation:Reen, F. J., Phelan, J. P., Gallagher, L., Woods, D. F., Shanahan, R. M., Cano, R., Ó Muimhneacháin, E., McGlacken, G. P. and O'Gara, F. (2016) ‘Exploiting interkingdom interactions for the development of small molecule inhibitors of Candida albicans biofilm formation’, Antimicrobial Agents and Chemotherapy, 60(10), pp. 5894-5905. doi: 10.1128/AAC.00190-16
A rapid decline in the development of new antimicrobial therapeutics has coincided with the emergence of new and more aggressive multidrug-resistant pathogens. Pathogens are protected from antibiotic activity by their ability to enter an aggregative biofilm state. Therefore, disrupting this process in pathogens is a key strategy for the development of next-generation antimicrobials. Here, we present a suite of compounds, based on the Pseudomonas aeruginosa 2-heptyl-4(1H)-quinolone (HHQ) core quinolone interkingdom signal structure, that exhibit noncytotoxic antibiofilm activity toward the fungal pathogen Candida albicans. In addition to providing new insights into what is a clinically important bacterium-fungus interaction, the capacity to modularize the functionality of the quinolone signals is an important advance in harnessing the therapeutic potential of signaling molecules in general. This provides a platform for the development of potent next-generation small-molecule therapeutics targeting clinically relevant fungal pathogens.
This website uses cookies. By using this website, you consent to the use of cookies in accordance with the UCC Privacy and Cookies Statement. For more information about cookies and how you can disable them, visit our Privacy and Cookies statement