Acute liver failure is a health concern worldwide. Stemming from a range of causes, such as viral, drug-induced, alcoholic, or autoimmune, the rate of progression is highly variable, and the environmental factors dictating the outcome remain poorly identified. Through working with an animal model of acute liver failure, our laboratory has found that gut microbiota is a critical modulator of liver injury.
The gut microbiota encompasses the bacteria that reside naturally in the intestines. A growing body of basic and clinical research reveals that microbiota not only modulates diseases in the gut, but it can also impact the course of disease in extra-intestinal disorders such as influenza, rheumatoid arthritis, cardiovascular disease, and type I diabetes. Despite the close interplay between the gut and liver through the portal system, very few studies have connected the microbiota to the regulation of acute liver injury.
Therefore, we investigated the role of the microbiome in determining the extent of hepatic damage. By comparing mice with different commensal composition, and manipulating the microbiota status in germ free and conventionally raised mice, our lab found that the microbiome dictates host susceptibility to hepatic damage. Most importantly, this phenomenon can be readily modulated through the use of antibiotics or probiotics as putative interventions.
In order to elucidate the composition of the microbiota, a complex research process is required. The Dartmouth Graduate Alumni Research Award has contributed with covering some of the costs of the sequencing of samples, allowing us to determine the bacterial species that harbor in the intestines of differentially susceptible mice. This work has been recently submitted for publication.