In a new study, researchers found a type of gut bacteria that causes intestinal inflammation in patients with Crohn’s disease, a type of inflammatory bowel disease that affects more than 4 million people worldwide.
They showed that patients with Crohn’s disease have an overabundance of a type of gut bacteria called adherent-invasive Escherichia coli (AIEC), which promotes inflammation in the intestine.
Their experiments revealed that a metabolite produced by the bacteria interacts with immune system cells in the lining of the intestine, triggering inflammation.
Interfering with this process, by either reducing the bacteria’s food supply or eliminating a key enzyme in the process relieved gut inflammation in Crohn’s disease.
The discovery may lead to more targeted therapies for the difficult to treat disease.
The research was conducted by a team at Weill Cornell Medicine and elsewhere.
In the study, the team targeted a process the AIEC bacteria uses to convert a byproduct of sugar fermentation in the gut to grow.
Specifically, the AIEC uses a byproduct of the breakdown of a type of sugar called fucose that is found in the lining of the intestines.
The team showed the bacteria interacts with a type of immune system cell called mononuclear phagocytes , which sets off a cascade of inflammation.
Next, they genetically engineered AIEC bacteria to lack a key enzyme in this process.
They found after that, the bacteria do not set off a cascade of inflammation in a mouse model of Crohn’s disease.
Reducing the available supply of fucose in the animal’s gut also reduced inflammation.
The finding shows that changing one metabolic pathway in one type of bacteria can have a big impact on intestinal inflammation.
The discovery could lead to better treatments for Crohn’s disease.
Currently, patients with Crohn’s disease are often treated with antibiotics, which can kill both beneficial and harmful bacteria causing unwanted side effects.
But treatments that precisely target the inflammatory cascade discovered by the current study might help reduce inflammation while preserving beneficial bacteria.
One author of the study is Dr. Randy Longman.
The study is published in Cell Host and Microbe.
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