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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 (PGE 2 ), but the physiological significance of fungus-derived PGE 2  remains elusive. Here we report that a  C. albicans  mutant deficient in PGE 2  production suffered a loss of competitive fitness in the murine gastrointestinal (GI) tract and that PGE 2  supplementation mitigated this fitness defect. Impaired fungal PGE 2  production affected neither the  in vitro  fitness of  C. albicans  nor hyphal morphogenesis and virulence in either systemic or mucosal infection models. Instead, fungal production of PGE 2  was associated with enhanced fungal survival within phagocytes. Consequently, ablation of colonic phagocytes abrogated the intra-GI fitness boost conferred by fungal PGE 2 . These observations suggest that  C. albicans  has evolved the capacity to produce PGE 2  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.

Fungal Symbionts Produce Prostaglandin E2 to Promote Their Intestinal Colonization