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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Cell. Infect. Microbiol. | doi: 10.3389/fcimb.2019.00359

Fungal symbionts produce prostaglandin E2 to promote their intestinal colonization

  • 1Singapore Immunology Network (A*STAR), Singapore

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 fungus-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. Instead, fungal production of PGE2 was associated with enhanced fungal survival within phagocytes. Consequently, ablation of colonic phagocytes abrogated the intra-GI 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.

Keywords: Prostaglandin E2, Candida albicans, symbiont, Host-Microbe Interactions, Phagocyte, Virulence, Arachidonic acid (AA)

Received: 24 Aug 2019; Accepted: 03 Oct 2019.

Copyright: © 2019 Tan, Lim, Tan, Leong, Pavelka and Pavelka. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Dr. Tze Guan Tan, Singapore Immunology Network (A*STAR), Singapore, Singapore, tgtan01@gmail.com
Dr. Norman Pavelka, Singapore Immunology Network (A*STAR), Singapore, Singapore, normanpavelka@gmail.com
Dr. Norman Pavelka, Singapore Immunology Network (A*STAR), Singapore, Singapore, normanpavelka@gmail.com