Celiac disease is an immune disease of the intestine that is characterized by gluten intolerance causing inflammation of the gut, diarrhoea, and abdominal pain. Affecting more than 1% of the global population, the condition can also lead to weight loss and nutrient deficiencies.
A team of researchers from McMaster University in Canada, INRAE, INSERM, Sorbonne University Paris, Paris Public Hospitals, and Wageningen University in Netherlands studied the intestinal microbiota of celiac patients. Their findings show that the patients exhibit a defect in the production of active compounds resulting from the breakdown of tryptophan, an amino acid found in the diet.
Their findings show that taking tryptophan or a supplement with probiotics can metabolize this amino acid, reducing the intestinal lesions of celiac disease in animals. These findings offer a new therapeutic prospect to treating celiac disease in humans.
A person suffering from celiac disease is intolerant to gluten, a protein widely present in our regular diet as it can be found in grains such as wheat. They need to follow a restrictive diet that excludes gluten, which is meant to alleviate their symptoms. It is believed that several factors are involved in triggering the condition, including immune and genetic factors.
The scientists decided to look into the role of the gut microbiota as the condition is characterized by inflammation of the gut. Studying healthy subjects, they found out that the function of some bacteria in the microbiota is to specifically utilize tryptophan to produce indole derivatives that activate AhR (Aryl hydrocarbon Receptors) that are present in the intestine.
Beneficial effects, such as reinforcing the intestinal barrier and stimulating immunity, happen upon activation of these receptors. These, then, attenuate gut inflammation as well as preserve the balance of gut microbiota. The research team had previously demonstrated changes to the microbiota in other inflammatory intestinal diseases such as Crohn’s disease and ulcerative colitis, and a defect in the production of these tryptophan derivatives resulted in a reduction in AhR activation.
The team analyzed stool samples from 29 patients who were either actively suffering from celiac disease or already had the disease and are being treated with a gluten-free diet for 2 years. They also had a group of healthy volunteers without celiac disease.
The results of their study revealed that among patients with active celiac disease, they detected a reduced quantity of tryptophan indole derivatives and a decreased activation of AhR. The team also observed changes to the intestinal microbiota that resulted in fewer microorganisms that metabolized tryptophan and produced the indole derivatives necessary to activate AhR.
Translating these findings to a possible treatment plan for celiac disease, the scientists conducted a study on model mice developing a condition similar to celiac disease. They altered the mice’s diet by either administering an additional intake of tryptophan (found in foods high in protein such as meat, fish, poultry, liver, dairy products, and soybean) or giving them the probiotic bacterium Lactobacillus reuteri, which produces indole derivatives.
Based on the study conducted, the team’s findings showed that a diet enriched with tryptophan can cause changes to the microbiota of the animals. These changes are characterized by an increase in the number of microorganisms that produce indole derivatives that activate AhR. Hence, when the mice were exposed to gluten, those given a tryptophan-enriched diet exhibited a lower level of intestinal inflammation compared to those fed a standard diet.
In addition, they also observed similar results among the mice given Lactobacillus reuteri. Thus, either a diet rich in tryptophan or taking the probiotic bacterium resulted in a significant improvement to the celiac disease lesions in mice upon exposure to gluten.
The study offers new possibilities in terms of therapeutic options for patients suffering from celiac disease. Further studies are needed to confirm these findings in humans.
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