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Eicosapentaenoic acid influences the pathogenesis of Candida albicans in Caenorhabditis elegans via inhibition of hyphal formation and stimulation of the host immune response

N. Z. Mokoena; H. Steyn; A. Hugo; T. Dix-Peek; C. Dickens; O. M. N. Gcilitshana; O. Sebolai; J. Albertyn; C. H. Pohl
Medical Microbiology and Immunology · Vol. 212, Issue 5 · pp. 349-368 · 2023

Abstract

The intake of omega-3 polyunsaturated fatty acids, including eicosapentaenoic acid (EPA), is associated with health benefits due to its anti-inflammatory properties. This fatty acid also exhibits antifungal properties in vitro. In order to determine if this antifungal property is valid in vivo , we examined how EPA affects Candida albicans pathogenesis in the Caenorhabditis elegans infection model, an alternative to mammalian host models. The nematodes were supplemented with EPA prior to infection, and the influence of EPA on C. elegans lipid metabolism, survival and immune response was studied. In addition, the influence of EPA on hyphal formation in C. albicans was investigated. It was discovered that EPA supplementation changed the lipid composition, but not the unsaturation index of C. elegans by regulating genes involved in fatty acid and eicosanoid production. EPA supplementation also delayed killing of C. elegans by C. albicans due to the inhibition of hyphal formation in vivo, via the action of the eicosanoid metabolite of EPA, 17,18-epoxyeicosatetraenoic acid. Moreover, EPA supplementation also caused differential expression of biofilm-related gene expression in C. albicans and stimulated the immune response of C. elegans . This provides a link between EPA and host susceptibility to microbial infection in this model.

Bibliographic Information

JournalMedical Microbiology and Immunology
PublisherSpringer
Publication Date2023-10-01
Publication Year2023
Volume212
Issue5
Pages349-368
Document TypeJournal Article
Print ISSN0300-8584
eISSN1432-1831
DOI10.1007/s00430-023-00777-6

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NARA Access Coverage1886-01-01~Current
Journal Homepagehttps://www.springer.com/journal/430
Publisher PageOpen Publisher Page
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