Celiac disease is the destruction of the lining of the upper gut, which occurs when a person with certain predisposing genes consumes gluten in the diet. However, not everyone with celiac genes and eating gluten will develop the disease.
Tryptophan is an essential amino acid, which cannot be produced by the body and needs to be consumed through foods such as poultry products, chocolate, bananas and cruciferous vegetables such as broccoli, cabbage and cauliflower.
The study, published in the journal Science Translational Medicine, investigated whether the breakdown of tryptophan by gut bacteria gets altered in celiac disease and if this pathway could be targeted as a potential therapy.
The findings highlighted the potential therapeutic value of targeting tryptophan metabolism in the gut in celiac disease to better control the symptoms, despite the gluten-free diet, and accelerate intestinal healing.
"The only treatment for celiac disease is a strict adherence to a gluten-free diet, which is difficult to follow, and doesn't always lead to complete recovery of the gut or symptom resolution," said study author Elena Verdu from the McMaster University in Canada.
According to the researchers, tryptophan is necessary for many functions in the body and can be broken down by bacteria in the gut, producing bioactive molecules (called "metabolites") that interact with receptors in the gut lining which control inflammation.
One of these receptors is the aryl hydrocarbon receptor, or AhR, and suboptimal activation of this receptor has been implicated in chronic intestinal inflammation, including inflammatory bowel diseases such as ulcerative colitis and Crohn's disease.
For the findings, the researchers studied three groups: patients with active celiac disease, patients two years after a gluten-free diet, and healthy people.
Celiac patients had evidence of lower bacterial metabolism of tryptophan, and their gut microbiota did not appropriately stimulate the AhR pathway which controls inflammation and protects the gut barrier.
These alterations were partially improved in patients after two years of a gluten-free diet.
Using mice that express the genes for celiac disease, the authors showed that two strains of lactobacilli, bacteria known to breakdown tryptophan, activated AhR and reduced inflammation caused by gluten.
The study findings highlight the potential therapeutic value of targeting tryptophan metabolism in the gut in celiac disease to better control symptoms.