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.
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EPA reduces yeast infection severityEicosapentaenoic acid influences the pathogenesis of Candida albicans in Caenorhabditis elegans via inhibition of hyphal formation and stimulation of the host immune response.
Significant relevance to yeast infections
We investigated how eicosapentaenoic acid (EPA), an omega-3 fatty acid known for its health benefits, influences yeast infections, specifically those caused by Candida albicans. Using the Caenorhabditis elegans model, which provides a simpler system to study these interactions, we observed the effects of EPA supplementation on the nematode’s response to the fungal pathogen.
Our findings revealed that EPA not only altered lipid metabolism in these tiny worms but also significantly affected their survival during infection. Notably, we found that EPA inhibited the formation of hyphae—the structure that allows C. albicans to invade and damage host tissues—leading to a delay in the death of C. elegans. This effect seems to stem from a specific metabolite of EPA, called 17,18-epoxyeicosatetraenoic acid.
Furthermore, EPA prompted changes in gene expression related to biofilm formation in C. albicans, alongside stimulating the immune response in the worms. These results highlight a fascinating connection between dietary components like EPA and host defenses against infections, suggesting that incorporating omega-3 fatty acids could play a role in enhancing our resilience to such pathogens.
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