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 (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.