Preventing the Activation of a Stress Gene Response in Escherichia coli Using Acetate, Butyrate, and Propionate

Regulation of microbial symbiosis in the human intestinal tract is imperative to maintain overall human health and prevent dysbiosis-related diseases, such as inflammatory bowel disease and obesity. Short-chain fatty acids (SCFA) in the intestine are produced by bacterial fermentation and aid in inflammation reduction, dietary fiber digestion, and metabolizing nutrients for the colon. SCFA, notably acetate, butyrate, and propionate, are starting to be used in clinical interventions for GI diseases. While acetate has been shown to mitigate a stress response in the proteome of Escherichia coli cells, little is known about the effects of butyrate and propionate on the same cells. This study aims to evaluate the effects that butyrate and propionate have on the activation of stress promoters in E. coli when induced with a known stressor. Three different strains of E. coli containing the pUCD615 plasmid were used, each with a different promoter fused to the structural genes of the lac operon on the plasmid. Each promoter detected a unique stress response: grpE’::lux fusion (heat shock), recA’::lux fusion (SOS response), and katG’::lux fusion (oxidative damage). Activation of these stress promoters by treatment groups resulted in the emission of bioluminescence which was quantified and compared across treatment groups. All three SCFAs at 25 mM added to cultures prior to stressing the bacteria caused significantly lower bioluminescence levels when compared to the stressed culture without prior addition of SCFA. This indicates that these SCFAs may reduce the stress response in E. coli. KEYWORDS: Short-chain fatty acids; acetate; butyrate; propionate; Escherichia coli; stress response; Vibrio fischeri luxCDABE; grpE; katG; recA