No, the gut won't be defending the virtues of some microbes with impassioned speeches of grumblings and gurgles. However, when a person grows sick, the gut will still fight to support the good microbial community that helps keep its digestive processes regulated and infection-free.

According to a study recently published in the journal Nature, when an animal grows sick, its intestines will naturally start producing specialized sugars intended to keep beneficial microbial communities fed and healthy for as long as possible, even while the rest of the body grows tired in illness.

"Both hosts and their gut microbiota can suffer in the case of sickness, but this mutually beneficial relationship is guarded by the host," the study's senior author, Alexander Chervonsky of Chicago's Committee on Immunology, explained in a recent statement.

This was determined after Chervonsky and his team investigated the production of a kind of sugar - L-fucose - that cannot be used by an animal's body for energy, and yet is still produced, especially during illness. Observations showed that when bound to proteins, the unusual sugar can be used by microbes as a food source.

According to the study, two groups of lab mice were exposed to a molecule that mimicked a systemic infection. One group of mice were normal, but a second group was genetically designed to be lacking the Fut2 gene that is responsible for L-fucose production.

Unsurprisingly, without the key sugars to keep "good" gut bacteria happy and healthy, the fucose-deprived group took much longer to recover from their "illness" than the standard group.

A follow-up genetic analysis showed that the group of mice lacking Fut2 had experienced a microbial civil war in their intestines, where "bad" bacteria were beginning to overpower the "good" communities.

The researchers theorized that not only does L-fucose feed beneficial bacteria, but it also prevents harmful ones from switching to a more dangerous state.

Interestingly, Chervonsky says about a fifth of the human population doesn't have a gene for producing L-fucose, and this has been linked to the inflammatory bowel disease known as Crohn's.

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