Breaking the bad: Bacillus blocks fungal virulence factors
Authors:François L. Mayer1 and James W. Kronstad1
doi: 10.15698/mic2017.11.599
Volume 4, pp. 384 to 386, published 30/10/2017.
1 Michael Smith Laboratories, Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
Keywords:
melanin, capsule, biofilm, filamentation, chitin, chitinase.
Corresponding Author(s):
Conflict of interest statement:
The authors declare that no competing interest exists.
Please cite this article as:
François L. Mayer and James W. Kronstad (2017). Breaking the bad: Bacillus blocks fungal virulence factors. Microbial Cell 4(11): 384-386. doi: 10.15698/mic2017.11.599
© 2017 Mayer and Kronstad. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Fungal pathogens rely on the production of specific virulence factors during infection. Inhibiting such factors generally results in reduced fungal pathogenicity. Most studies in the past have focused on understanding the molecular mechanisms of fungal virulence factor expression during mono-culture, or during interaction with the host. However, a potentially important, second type of interaction has been less well studied thus far – the interplay of fungal pathogens of humans with other microbes found in their natural habitat. Specifically, whether environmental bacteria may impact fungal virulence factor production is largely unknown. In our recent work, we have identified the soil bacterium, Bacillus safensis, as a potent inhibitor of virulence factor production by two major fungal pathogens of humans, Cryptococcus neoformans, and Candida albicans. We determined that the anti-virulence factor mechanism is, at least in part, based on production of bacterial chitinases that target and destabilize the fungal cell surface. These findings describe a cross-kingdom interaction between an environmental bacterium and pathogenic fungi, and highlight the fungal cell wall as an attractive antifungal drug target.