초록
<P>Elimination of specific enteropathogenic microorganisms is critical to gut health. However, the complexity of the gut community makes it challenging to target specific bacterial organisms. Accumulating evidence suggests that various foods can change the abundance of intestinal bacteria by modulating prophage induction. By using pathogenic <I>Escherichia coli</I> (<I>E. coli</I>) ATCC 25922 as a model in this research, we explored the potential of dietary modulation of prophage induction and subsequent bacterial survival. Among a panel of sugars tested in vitro, <SMALL>D</SMALL>-xylose was shown to efficiently induce prophages in <I>E. coli</I> ATCC 25922, which depends, in part, upon the production of <SMALL>D</SMALL>-lactic acid. In an enteric mouse model, prophage induction was found to be further enhanced in response to propionic acid. Dietary <SMALL>D</SMALL>-xylose increased the proportion of Clostridia which converted <SMALL>D</SMALL>-lactic acid to propionic acid. Intestinal propionic acid levels were diminished, following either oral gavage with the dehydrogenase gene (<I>ldhA</I>)-deficient <I>E. coli</I> ATCC 25922 or depletion of intestinal Clostridia by administration of streptomycin. <SMALL>D</SMALL>-Xylose metabolism and exposure to propionic acid triggered <I>E. coli</I> ATCC 25922 SOS response that promoted prophage induction. <I>E. coli</I> ATCC 25922 mutant of RecA, a key component of SOS system, exhibited decreased phage production. These findings suggest the potential of using dietary components that can induce prophages as antimicrobial alternatives for disease control and prevention by targeted elimination of harmful gut bacteria.</P>