Woongjae Yoo

7Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN 37232, USA. 1Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA. 7Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN 37232, USA. 8Vanderbilt Center for Immunobiology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

Gut bugs and systemic disease risk What people eat has an immediate selective effect on the microbial populations resident in the gut. A high-fat diet is associated with the occurrence of microbes that catabolize choline and the accumulation of trimethylamine N-oxide (TMAO) in the bloodstream, a contributing factor for heart disease. Yoo et al. explored the microbial organisms and pathways that convert choline into TMAO in mice.

Metabolic adaptation plays a key role in determining the composition of microbial ecosystems. A new study shows that in the inflamed gut, pathogenic Enterobacteriaceae can reprogramme their metabolism towards diet-derived l-serine utilization to outcompete the resident microbiota and cause disease. Fig. 1: Dietary l-serine fuels Enterobacteriaceae expansion in the inflamed gut. References 1. Brestoff, J. R. & Artis, D. Nat. Immunol. 14, 767–684 (2014). 2. Winter, S. E. & Baumler, A. J.