Shuai was a postdoc in the lab from June 2017 to October 2019, during which time he focused on using animal models to identify mechanisms that regulate dysbiosis. Using an infection model in mice, he showed that strong immune responses to infection can also promote pathogenic changes in gut microbiome composition. His first paper describing this work, showed that nitric oxide produced by macrophages during infection serves as a substrate for E. coli expansion in the small intestine, ultimately leading to barrier breakdown and subsequent sepsis. His second project in the lab used a canine model of diet-responsive inflammatory bowel disease (IBD) to dissect relationship between the microbiome and remission from IBD. His paper on this topic showed that diet therapy induced a structural change in the microbiome, marked by expansion of the bile acid producer, Clostridium hiranonis, and a comensurate decrease in levels of potential pathobionts such as E. coli and C. perfringens. He then showed that C. hiranonis was sufficient to ameliorate inflammation and E. coli expansion in a mouse model of GI disease. These findings set the stage for future work in the lab that will examine bile acid producers in modulating inflammation.