Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tübingen, Germany; Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Juliet Jacobson
Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Elizabeth A Kennedy
Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Mary E Bell
Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Qiaojuan Shi
Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Jillian L Waters
Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tübingen, Germany; Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Peter Lawrence
Division of Nutritional Sciences, Cornell University, Ithaca, United States
J Thomas Brenna
Division of Nutritional Sciences, Cornell University, Ithaca, United States; Dell Pediatric Research Institute, Dell Medical School, University of Texas at Austin, Austin, United States
Robert A Britton
Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, United States
Department of Agricultural, Food, and Nutritional Science, University of Alberta, Edmonton, Canada; Department of Biological Sciences, University of Alberta, Edmonton, Canada
Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tübingen, Germany; Department of Molecular Biology and Genetics, Cornell University, Ithaca, United States
Over the past century, soybean oil (SBO) consumption in the United States increased dramatically. The main SBO fatty acid, linoleic acid (18:2), inhibits in vitro the growth of lactobacilli, beneficial members of the small intestinal microbiota. Human-associated lactobacilli have declined in prevalence in Western microbiomes, but how dietary changes may have impacted their ecology is unclear. Here, we compared the in vitro and in vivo effects of 18:2 on Lactobacillus reuteri and L. johnsonii. Directed evolution in vitro in both species led to strong 18:2 resistance with mutations in genes for lipid biosynthesis, acid stress, and the cell membrane or wall. Small-intestinal Lactobacillus populations in mice were unaffected by chronic and acute 18:2 exposure, yet harbored both 18:2- sensitive and resistant strains. This work shows that extant small intestinal lactobacilli are protected from toxic dietary components via the gut environment as well as their own capacity to evolve resistance.
