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Blueberries and black tea can help your gut bacteria fight the flu


A common gut bacterium may break down compounds found in blueberries, black tea and other foods to boost interferon and help your immune system fight the influenza virus


A cup of black tea and some blueberries
Researchers have found that a particular gut microbe can prevent severe flu infections in mice, likely by breaking down naturally occurring compounds -- called flavonoids -- commonly found in foods such as black tea, red wine and blueberries.
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In news almost guaranteed to be joyfully and profitably misrepresented by the dietary supplement industry and natural health gurus, a species of gut bacteria has been found that breaks down blueberries and use the components to fight influenza.

In a report published in the journal Science, a team led by Thaddeus Stappenbeck of the Washington University School of Medicine in the US finds that the bacterium, Clostridium orbiscindens, degrades flavonoids – compounds that influence colour and flavour, notably found in blueberries, black tea and red wine – and produces a metabolite that, in turn, boosts the production of interferon, a key signalling mechanism for the immune system.

To test the idea that microbial activity might boost immune responses to the flu, Stappenbeck and colleagues first combed through human gut biome samples and identified C. orbiscindens as a bug that breaks down flavonoids and makes a metabolite called desaminotyrosine (DAT), known to be involved in interferon signalling.

DAT was then administered to one of two cohorts of mice. Both groups were then infected with the virus.

“When we gave DAT to mice and then infected them with influenza, the mice experienced far less lung damage than mice not treated with DAT,” says co-author Ashley Steed.

The scientists found that both groups developed identical viral loads, but the degrees of damage wrought were markedly different.

“The infections were basically the same,” says Stappenbeck. “The microbes and DAT didn’t prevent the flu infection itself; the mice still had the virus. But the DAT kept the immune system from harming the lung tissue.”

More research is needed before the exact mechanism induced by the microbe-derived metabolite is fully understood. The work will form another aspect to a wide range of research being conducted into the role of interferon in relation to influenza. (A 2012 paper, for instance, found that interferon increased the risk of secondary pneumonia in patients.)

Should further study and, eventually, human clinical trials confirm the team’s initial findings, C. orbiscindens and DAT might eventually be deployed as a method to lessen the severity of influenza infection.

“This strategy doesn’t target the virus. Instead, it targets the immune response to the virus,” says Steed. “That could be valuable, because there are challenges with therapies and vaccines that target the virus due to changes in the influenza virus that occur over time.”

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Andrew Masterson is news editor of Cosmos.
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