麻豆淫院

Some things just go together in your belly: peanut butter and jelly, salt and pepper, bacteria and bacteria-eating viruses. For the bacterial species that inhabit your gut, there's a frenzy of viruses called bacteriophages that naturally infect them. Although they co-evolved with bacteria, phages get far less glory. They're harder to classify and so deeply entangled with the bacteria they target that scientists struggle to understand what functions they serve.

But what if there was a way to compare the exact same gut microbiome conditions with and without phages?

Virginia Tech biologist Bryan Hsu's team found a way to do just that.

Hsu and graduate student Hollyn Franklin built a model that allows them to diminish phage communities from a mouse gut microbiome鈥攁nd then bring them back鈥攚ithout affecting the bacteria. On a test run of their model, researchers found evidence that phages may increase gut bacteria's sensitivity to antibiotics. Their results were in the journal Cell Host and Microbe.

What could inhibit a bacteria's viruses but not the bacteria itself? In her early search through the literature, Franklin found a chemical compound called acriflavine that fit the bill. It's a component of a widely available medication used in Brazil to treat urinary tract infections (UTI).

Fortuitously, a member of Hsu's lab and paper co-author, Rogerio Bataglioli, is a native Brazilian. He shipped a massive order of acriflavine to his parents' house. Franklin began administering acriflavine to lab mice. Over a period of 12 days, there was a dramatic reduction in the concentration of viral particles. And they didn't bounce back when she stopped administering the drug.

But when Franklin reintroduced a tiny sample of the mouse's own gut microbiome, extracted before treatment, the natural phage populations sprang back to life.

"It goes away when we wanted it to, and came back when we wanted it to," said Hsu. "Which means we have a bacteriophage conditional mouse model." Or, more fun: BaCon mouse model.

Exacerbating antibiotic damage

To see if the mouse model had some significance for health, Hsu's research team went straight to one of the hottest topics in the field: the collateral damage that antibiotics have on a patient's resident microbial population.

Could phages be playing a role in the destructive wake of an antibiotic treatment? Hsu and Franklin used their BaCon mouse model to ask this question and administered antibiotics to mice with and without phage populations.

Their results suggest that phages increase the sensitivity of bacteria to antibiotics.

"It's hard to make definitive conclusions, but these results are telling us that phages have some significance for how we respond to antibiotics," Hsu said.

The next questions, according to Franklin, will explore if phages cause these effects or are simply correlated with them, and what role phages play in diseases鈥攚hich would open new doors in microbiome studies.