They used a mouse model of respiratory influenza, giving mice a combination of antibiotics in their drinking water to deplete the bacterial composition in the gut and then infecting the mice with the flu virus. The animals exhibited a significantly impaired immune response compared to the control group. The bacteria-deficient mice had reduced levels of T-cells and influenza-specific antibodies, which play a key role in fighting infection. As a result, the animals had high amounts of virus in the lungs. Together with Ichinohe, they uncovered an unexpected role of the commensal bacteria's contribution to host sensing of viral-inflicted damage and adaptive immunity to flu. It is a bit difficult to determine exactly what the experiment was, since this article was written in simplified language for a wide audience. However, one of my guesses as to what is going on here is that the gut flora typically induces a certain amount of inflammation, keeping the immune system running at low speed. When they killed off the gut flora in the experimental mice, they removed the source of inflammation and the immune system activity dropped as a result. So when the mice were challenged with the influenza virus, they had to start building up an immune response from scratch, instead of from its normal state of activity.