Antibiotic resistance is one of the most pressing threats to public health. Intrinsic resistance to many antimicrobials in Gram-negative bacteria is accomplished by naturally occurring efflux pumps. Efflux pumps are transmembrane proteins that can extrude antimicrobials from bacterial cytoplasm. Efflux pumps recognize a wide range of compounds including antibiotics, antiseptics, pesticides, and hormones. The upregulation of efflux pump genes in response to increasing concentrations of substrates has shown to increase resistance to toxic substrates. We hypothesize that efflux pump substrates other than antimicrobials, such as steroid hormones, will also induce the expression of efflux pump genes and consequently increase resistance to antibiotics. In this study, uropathogenic Escherichia coli strain CFT073 and its isogenic deletion mutant ΔtolC were exposed to the primary synthetic estrogen found in oral hormonal contraceptives, ethinylestradiol (EE). Using the Baker Koob Endowment, we successfully completed our first goal, analyzing multidrug resistance after exposure to EE. Multidrug resistance was analyzed by assessing the minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) of 16 different antibiotics with or without previous exposure to EE. Both strains demonstrated multidrug resistance after EE exposure when compared to the unexposed control. Also using the Baker Koob Endowment, we started and purchased all necessary materials to fulfill our second goal, quantifying the expression of efflux pump genes and the entire transcriptome after exposure to EE. RNA sequencing is currently underway.
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