We set out to explore how eicosapentaenoic acid (EPA), a type of healthy fat, can disrupt the mature biofilms formed by a significant human fungal pathogen. These biofilms are important since they enhance the pathogen's ability to cause infections. Our investigation focused on the effects of a 1 mM EPA treatment on these established biofilms.
Through various assays, we observed that EPA significantly reduced the viability of these preformed biofilms. The use of advanced microscopy techniques allowed us to see that EPA could block the transformation from yeast to a more invasive form and damaged the biofilm's structure.
We also found that EPA prompted changes at the genetic level. Specifically, it downregulated genes linked to the development of hyphae and biofilms. Additionally, EPA affected two key signaling pathways involved in biofilm formation. Notably, it reduced the production of a crucial messenger in one of these pathways.
Lastly, we noted that treatment with EPA downregulated genes related to ergosterol biosynthesis, suggesting it may lower the chances of developing resistance to existing antifungal treatments. Our findings emphasize the potential of EPA as a promising alternative or complementary option in treating yeast infections.