Not many people who are genetically prone to celiac disease actually develop the condition, even though the reason why have been unclear. Lately, a new research suggests that it may be close to making clear how certain gut bacteria respond to gluten.
What is celiac disease in the first place? It is an immune disease in which an individual is intolerant to gluten, the protein present in grains, such as rye, barley, and wheat. According to some estimation, about one percent of the American population has celiac disease.
If a person who suffers from celiac disease consumes gluten, their immune system responds by causing damage to the small intestine. This in turn may contribute to pain in the abdominal area, bloating, fatigue, and diarrhea, among other symptoms.
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Celiac disease is triggered by certain gene mutations. Nevertheless, just two to three percent of the people who have such mutations actually develop the condition.
Dr. Elena F. Verdu and her colleagues from the Digestive Health Research Institute at McMaster University in Canada conducted a researcher in attempt to address the reason for this, so they looked at the way the immune system responds to gluten with different populations of gut bacteria in mouse models of gluten intolerance.
The results and the findings of this research were published in the American Journal of Pathology.
Germ-free mice showed that a sign of celiac disease is response to gluten
The team investigated and observed here groups of mice that expressed a gene called DQ8, which is present in humans as well and makes them genetically prone to gluten intolerance.
Some facts about celiac disease
About 83 percent of the American population that suffers from celiac disease are undiagnosed or misdiagnosed with other diseases
You can only treat celiac disease if you consume a gluten-free diet
About 5-22 percent of the people with celiac disease have a first-degree relative who also has the same condition
Find out more things about celiac disease
In the study, each group of mice had different gut bacteria composition, or different gut micro biomes. There was also a group that was germ-free, as well as a group that was clean specific-pathogen-free (SPF); the gut of these mice was free of proteobacteria – a group of gram-negative bacteria – and devious pathogens.
The last group consisted of conventional SPF mice, which possessed a wide range of gut bacteria, such as Proteobacteria and devious pathogens such as Staphylococcus, Streptococcus, and Helicobacter.
The scientists exposed each group of mice to gluten. They discovered that the mice that were germ-free showed raised levels of intraepithelial lymphocytes (IELs) in the gut; proliferation and activation of IELs is an early sign of celiac disease. Raised IEL levels, though, were not noticed in the clean SPF mice.
Moreover, the mice which were germ-free experienced increased death of cells that line the gastrointestinal tract, named enterocytes. This was accompanied by anatomical alterations of the small, fingerlike projection that line the small intestine, known as the villi.
The team of researchers also noticed the development of antibodies in response to a component of gluten, also known as gliadin, among the germ-free mice, and these mice also showed T-cell responses specific to this component.
Another interesting thing that the team discovered was the fact that the development of gluten-induced pathology was stopped in the clean SPF mice compared to the germ-free mice, however, this was not the case when the clean SPF mice got enteroadherent Escherichia coli from a patient with celiac disease.
Increasing Proteobacteria worsened gluten-induced pathology
The researchers noticed that the conventional SPF mice showed greater gluten-induced pathology than the clean SPF mice, so they set out to investigate whether the presence of Proteobacteria, like Escherichia and Helicobacter, plays a role.
When it comes to increasing the presence of Proteobacteria among conventional SPF mice by administering an antibiotic known as vancomycin once they are born, the researchers discovered that gluten-induced pathology got worse. More precisely, the researchers noticed that the IELs levels increased.
Dr. Verdu stated that this research has shown that perturbation of early microbial colonization in life and induction of dysbiosis (microbial imbalance in the body), characterized by raised levels of Proteobacteria, boost the severity of gluten-induced responses in mice genetically predisposed to gluten sensitivity.
According to the researchers, their data argue that the identified increase in celiac disease prevalence in the general population over the last fifty years could be driven, at least partly, by perturbations in the intestinal microbial ecology. There are some specific therapies based on microbiota which may help in the prevention or treatment of celiac disease in subjects with moderate genetic risk.
According to Dr. Robin G. Lorenz from the University of Alabama at Birmingham, who made an editorial connected to this study, these findings which suggest the presence of Proteobacteria may play an important role in celiac disease pathology. However, they do not have to mean that this condition is caused by Proteobacteria. It may be that the Proteobacteria somehow improve the immune response to gluten or gliadin.
Recently, a study announced in the Medical News Today suggested that people with celiac disease may be facing an increased risk of nerve damage.