DOI: 10.1101/477117Nov 22, 2018Paper

Fungal symbionts produce prostaglandin E2 to promote their intestinal colonization

BioRxiv : the Preprint Server for Biology
Tze Guan TanNorman Pavelka

Abstract

Candida albicans is a ubiquitous fungal symbiont that resides on diverse human barrier surfaces. Both mammalian and fungal cells can convert arachidonic acid into the lipid mediator, prostaglandin E2 (PGE2), but the physiological significance of fungal-derived PGE2 remains elusive. Here we report that a C. albicans mutant deficient in PGE2 production suffered a loss of competitive fitness in the murine gastrointestinal (GI) tract and that PGE2 supplementation mitigated this fitness defect. Impaired fungal PGE2 production affected neither the in vitro fitness of C. albicans nor hyphal morphogenesis and virulence in either systemic or mucosal infection models. Fungus-derived PGE2 improved intra-GI fitness of C. albicans by diminishing the killing of C. albicans by phagocytes. Consequently, ablation of colonic phagocytes abrogated the fitness boost conferred by fungal PGE2. These observations suggest that C. albicans has evolved the capacity to produce PGE2 from arachidonic acid, a host-derived precursor, to promote its own colonization of the host gut. Analogous mechanisms might undergird host-microbe interactions of other symbiont fungi.

Related Concepts

Arachidonic Acid
Candida albicans
Fungi
Intestines
Phagocytes
Prostaglandins
Virulence
Surface
Ablation
Mutant

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