Vaginal fatty acid response mechanisms reveal a novel strategy for bacterial vaginosis treatment.

Bacterial vaginosis (BV), a common syndrome characterized by -deficient vaginal microbiota, is associated with adverse health outcomes. BV often recurs after standard antibiotic therapy in part because antibiotics promote microbiota dominance by instead of , which has more beneficial health associations. Strategies to promote and inhibit are thus needed. We show that oleic acid (OA) and similar long-chain fatty acids simultaneously inhibit and enhance growth. These phenotypes require OA-inducible genes conserved in and related species, including an oleate hydratase () and putative fatty acid efflux pump (). FarE mediates OA resistance, while OhyA is robustly active in the human vaginal microbiota and sequesters OA in a derivative form that only -harboring organisms can exploit. Finally, OA promotes dominance more effectively than antibiotics in an model of BV, suggesting a novel approach for treatment.