University of Washington

By constructing models of the microbial communities inside the human digestive system, a team led by SFI External Professor Elhanan Borenstein has revealed key differences between the microbial network interactions in the guts of lean and obese people.

The collection of microbes inside the human gut is a bustling network of genetic interplays and energy use. The microbiome in which they live is essential for human development, immunity, and nutrition.

In the Proceedings of the National Academy of Sciences, researchers report that they modeled the network of multiple microbial species in the human gut as a complex, integrated biological system rather than as many separate species.

"Our research introduces a novel framework, applying systems biology and in-silico (computer) modeling to study the human microbiome -- the complex ensemble of microorganisms that populate the human body -- as a single cohesive system," says Borenstein.

Their models helped identify enzymes that are peripheral to the functioning of the microbe network but that may serve as an important interface between microbial and human metabolism. These enzymes may play an important role in obesity and inflammatory bowel disease, the researchers say.

Comparisons between the obese and lean microbiome network models also showed that obese microbiomes are associated with lower levels of a topological trait called "modularity."

While the associations drawn from the study may not clearly implicate a specific mechanism for complex and poorly understood diseases such as obesity and inflammatory bowel disease, Borenstein noted that they demonstrate the promise of using a systems biology approach to study the human microbiome and its contribution to human health.

The research was funded by the National Human Genome Research Institute, the National Institutes of Health, and the Alfred P. Sloan Foundation.

Read the PNAS paper (published online December 19, 2011, subscription required)

Read the University of Washington news release (January 10, 2012)