Sciadonic acid modulates prostaglandin E2 production by epithelial cells during infection with C. albicans and C. dubliniensis.

Candida albicans is an important opportunistic pathogen in humans. During infection, arachidonic acid (ω6) is released from host phospholipids, leading to the production of host and yeast derived prostaglandin E(2) (PGE(2)). This stimulates yeast hyphal formation, is immunomodulatory and causes cell damage during infection. Although supplementation of mammalian cells with ω3 fatty acids has received attention due to their immunomodulatory and anti-inflammatory activities, increased production of ω3 fatty acid metabolites could lower the host's ability to combat infections. Since mammalian cells cannot produce PGE(2) from sciadonic acid (SA), a non-methylene interrupted ω6 fatty acid (NMIFA), supplementation of cells with SA may decrease the production of PGE(2) without increasing levels of ω3 fatty acid metabolites. Our study evaluated PGE(2) production by SA supplemented epithelial cells in response to Candida albicans and C. dubliniensis. We show that PGE(2) production during infection can be modulated by incorporation of SA into host lipids and that this does not influence the levels of ω3 fatty acids in the epithelial cells.