Physiological functions of fungus-derived prostaglandin E₂ in Candida albicans
Candida albicans is a polymorphic fungus that colonizes various barrier tissue sites in humans asymptomatically. However, under specific conditions, the fungus can turn pathogenic and provoke diseases. C. albicans has been observed to produce the lipid molecule, prostaglandin E2 (PGE2), both in vitr...
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| Format: | Final Year Project |
| Language: | English |
| Published: |
2017
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| Online Access: | http://hdl.handle.net/10356/72847 |
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| Institution: | Nanyang Technological University |
| Language: | English |
| Summary: | Candida albicans is a polymorphic fungus that colonizes various barrier tissue sites in humans asymptomatically. However, under specific conditions, the fungus can turn pathogenic and provoke diseases. C. albicans has been observed to produce the lipid molecule, prostaglandin E2 (PGE2), both in vitro and in vivo upon colonization of the host. PGE2 exerts diverse immunomodulatory effects in humans and has been implicated as a virulence factor for C. albicans. In this study, we investigated the role of fungus-derived PGE2 in modulating the status of C. albicans as a symbiont when colonizing the gastrointestinal tract or a pathogen in the host. Neither PGE2 supplementation nor blockade altered the in vitro growth or virulence of C. albicans, and an ole2/ole2 fungal mutant defective in PGE2 production manifested similar virulence as the wild-type strain in a mouse model of disseminated candidiasis. However, the ole2/ole2 mutant exhibited decreased competitive fitness in the murine gut. Thus, fungus-derived PGE2 might promote the ability of C. albicans to colonize the intestines but is not an essential virulence determinant. Our work identified PGE2 secretion as a novel mechanism employed by C. albicans to colonize the host gut as a symbiont and suggests the possibility of targeting PGE2 to modulate fungal commensalism versus pathogenicity in susceptible individuals. |
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