Speaker
Description
The basic evolutionary principle of adaptation by natural selection applies to the natural microbial populations in our microbiomes. Disease-mediated changes in the intestinal environment would impose different selection pressures on the microbiome to what we would expect in healthy individuals, resulting in selection for disease-specific microbial traits. Inflammatory bowel disease (IBD) result in drastic changes in the gut environment, and individuals with IBD are known to have significantly different microbiome compositions to healthy individuals. In this study, we performed an evolution experiment with Escherichia coli in a mouse model of IBD to study the adaptation of the gut microbiome to chronic inflammation within a host’s lifetime. Bacteria were allowed to adapt to two alternative mouse intestinal environments (healthy wild-type vs. inflamed Il10-/-) for a period of three months. Subsequently, the growth of the evolved bacterial populations in a range of metabolites was systematically analyzed. We used Biolog GEN III MicroPlates to systematically assess the growth of bacterial populations in the presence of different metabolites. We performed kinetic growth measurements on bacterial populations isolated from fecal samples collected at early and late time points from gnotobiotic healthy and chronically inflamed mice. We found that bacterial populations that evolved in healthy and chronically inflamed mice showed differential growth in multiple metabolites. Notably, populations isolated from chronically inflamed mice at a late time point showed more susceptibility to antibacterial compounds such as fusidic acid and lithium chloride than those isolated at an early time point. Our results suggest that adaptation of bacterial populations to the inflamed intestinal environment could lead to changes in their metabolic repertoire, which in turn may provide new opportunities for therapeutic interventions.
