Journal Article
Infection and Immunity, vol. 86, iss. 5, 2018
Authors
Jikang Wu, Anice Sabag-Daigle, Mikayla A. Borton, Linnea F. M. Kop, Blake E. Szkoda, Brooke L. Deatherage Kaiser, Stephen R. Lindemann, Ryan S. Renslow, Siwei Wei, Carrie D. Nicora, Karl K. Weitz, Young-Mo Kim, Joshua N. Adkins, Thomas O. Metz, Prosper Boyaka, Venkat Gopalan, Kelly C. Wrighton, Vicki H. Wysocki, Brian M. M. Ahmer, Vincent B. Young
Abstract
ABSTRACT
Salmonella enterica
elicits intestinal inflammation to gain access to nutrients. One of these nutrients is fructose-asparagine (F-Asn). The availability of F-Asn to
Salmonella
during infection is dependent upon
Salmonella
pathogenicity islands 1 and 2, which in turn are required to provoke inflammation. Here, we determined that F-Asn is present in mouse chow at approximately 400 pmol/mg (dry weight). F-Asn is also present in the intestinal tract of germfree mice at 2,700 pmol/mg (dry weight) and in the intestinal tract of conventional mice at 9 to 28 pmol/mg. These findings suggest that the mouse intestinal microbiota consumes F-Asn. We utilized heavy-labeled precursors of F-Asn to monitor its formation in the intestine, in the presence or absence of inflammation, and none was observed. Finally, we determined that some members of the class
Clostridia
encode F-Asn utilization pathways and that they are eliminated from highly inflamed
Salmonella
-infected mice. Collectively, our studies identify the source of F-Asn as the diet and that
Salmonella
-mediated inflammation is required to eliminate competitors and allow the pathogen nearly exclusive access to this nutrient.
