PNNL

Abstract

Salmonella enterica provokes intestinal inflammation to gain access to nutrients. One of these nutrients is fructose-asparagine (F-Asn), and its availability to Salmonella during infection is dependent upon the pathogenicity islands, SPI1 and SPI2, that are required to provoke inflammation. Here we found that F-Asn is found in mouse chow at approximately 400 pmol/mg dry weight, in the intestinal tract of germ-free mice at 2700 pmol/mg dry weight, and in the intestinal tract of conventional mice at 15 pmol/mg. This suggests that the mice themselves do not have the capability to utilize F-Asn, while the mouse intestinal microbiota does. We ruled out the possibility of F-Asn formation in the intestine, in the presence or absence of inflammation, using heavy-labeled precursors. Finally, we determine that some members of the Clostridia class encode F-Asn utilization pathways and are eliminated from highly inflamed Salmonella-infected mice. Thus, the source of F-Asn is the diet, and Salmonella-mediated inflammation is required to eliminate competitors for this nutrient source.