Studying host-microbiome interactions can be complex. In addition to genetic differences between hosts, the composition of intestinal microbial communities can be wildly diverse. This can be affected by many things, including genetics, infection, diet and circadian rhythms (plus others!). Despite the complexity and the dynamic nature of the gut microbiota, the research community has established that the bacterial communities of healthy subjects and people with chronic inflammatory disorders, such as inflammatory bowel disease (IBD), multiple sclerosis or metabolic syndrome, tend to be quite distinct.
In order to address questions related to intestinal microbial ecology and immune homeostasis, inflammation and response to infectious pathogens, we take reductionist approaches to model the interactions we're interested in. Using 'germ-free' mice (that are born and develop in the absence of any detectable microbes) as a starting point, we can selectively colonize mice with individual or communities of microbes. The power of this approach is that we can start to address questions related to causality - does development of a given disease drive microbial changes, or are different populations of microbes necessary to drive disease?
Importantly, we're expanding our studies beyond the bacterial microbiome. Our goal is to make meaningful contributions to the understanding of the 'multibiome' - the collection of not only bacteria but also viruses, fungi, protists and even parasitic worms that can colonize the mammalian intestine.