Gut takes care of friendly bacteria during illness

Date: Oct-06-2014 A new study led by the University of Chicago shows that when they get sick, mice

produce specialized sugars in the gut that feed their friendly bacteria. Reporting in

Nature, the scientists describe how they also found mice unable to do this took longer

to recover from illness.

Senior author Alexander Chervonsky, an Associate Professor in Chicago's Department of

Pathology and chair of the Committee on Immunology, says:

"Both hosts and their gut microbiota can suffer in the case of sickness, but this mutually

beneficial relationship is guarded by the host."

He and his colleagues suggest the mechanism they have discovered helps the host resist or be

less harmed by pathogens or harmful microbes, and when it fails, it may lead to chronic diseases

like Crohn's.

Ability to produce L-fucose may be key to faster recovery

When animals get sick, they tend to eat less - this helps conserve energy and deprives

pathogens of nutrients. However, it also means beneficial bacteria - whose health is important

to the host - can suffer from lack of nutrients.

The team found that sick mice lacking Fut2 had more switched on harmful microbial genes than normal sick mice.

To investigate this further, the team focused on a sugar called L-fucose that the body does

not use for energy but when bound to proteins, it becomes a food source for gut bacteria.

When mice are healthy, their gut contains hardly any L-fucose. So the team made the mice sick

by exposing them to a compound that produces a systemic reaction, causing illness all over the

body. As they got sicker, the mice drank less water, ate less and lost weight.

However, within only a few hours of becoming sick, the mice also began to produce L-fucose in

their gut - nearly all of their small intestine was lined with it.

In another experiment, the researchers bred mice lacking Fut2, the gene that controls L-fucose production, and also exposed them to the compound that induces systemic sickness.

As with the normal mice, the mice lacking Fut2 also drank and ate less and lost weight as

they got sicker. But unlike normal mice, their gut contained no L-fucose and they took longer to

recover.

Prof. Chervonsky explains, "Mice that can produce L-fucose recover better than those

that can't[...] if you remove bacteria the effect goes away."

Findings may explain link between Crohn's disease and gut bacteria

When they carried out a genetic analysis on the gut microbes in both groups of mice, the team

found sick mice lacking Fut2 had more switched on harmful microbial genes than normal sick

mice.

They then tested the idea that L-fucose somehow stops unfriendly bacteria from switching on

the genes that make them more harmful. They exposed normal and Fut2-deficient mice to

Citrobacter rodentium - a mild pathogen that causes a reaction similar to food

poisoning - and then 4 days later exposed them to the chemical that gave them a systemic

illness.

The Fut2-deficient mice lost more weight than the normal mice. The researchers suggest this

shows the ability to produce L-fucose helped the normal mice somehow resist or tolerate the mild

additional pathogen.

Prof. Chervonsky says about 20% of people don't have a gene for producing L-fucose, and this

has been linked to the inflammatory bowel disease known as Crohn's.

He suggests perhaps not being able to make L-fucose means the gut cannot block the virulence

genes in harmful pathogens explaining why bacteria are involved in Crohn's disease:

"Whether we can use this toward therapeutics in the future requires further study," he

adds.

The study follows research recently published in PLOS ONE where a team from Boston's

Brigham and Women's Hospital found gut bacteria changes may

predict infection and inflammation. In that study, the team analyzed what happens to gut

bacteria in mice during different stages of infection by C. rodentium.

Written by Catharine Paddock PhD

Not to be reproduced without permission.

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