Celiac disease is an autoimmune disorder which occurs when a person is intolerant to gluten, a protein found in grains such as rye, wheat and barley. Scientists are speculating that the root of the problem is how some gut bacteria respond to gluten, but the exact cause is still a mystery.
Thankfully, only a small group of people who are genetically predisposed to the disease can actually develop it, and it is estimated that about 1% of the American population is currently suffering from the disease.
When a gluten intolerant person ingests the protein, the immune system responds by damaging the small intestine, resulting in abdominal pain, bloating and fatigue besides other symptoms. Some medical experts claim that some gene mutations can also cause celiac disease, but only 2-3% of the people with the mutations develop the disease.
These are the main factors of celiac disease:
– About 83% of the Americans suffering from celiac disease are misdiagnosed with other conditions;
– A gluten-free diet is the only way to fight the disease;
– 5-22% of the people suffering from gluten intolerance have a first-degree relative suffering from the same condition.
– A gluten-free diet is the only way to fight the disease;
– 5-22% of the people suffering from gluten intolerance have a first-degree relative suffering from the same condition.
Dr. Elena F. Verdu is the head of a team of scientists at the Digestive Health Research Institute at the McMaster University in Canada who are currently trying to determine what causes celiac disease. She and her team are looking at how the immune system responds to gluten varied with different populations of intestinal bacteria in animal models of gluten intolerance. The findings from the study were published in the American Journal of Pathology.
The study examined mice divided into 3 groups that expressed the DQ8 gene found in humans, which makes them genetically predisposed to the condition. Each of the three groups had different gut bacteria variations. The first group was germ-free; the second was clean specific-pathogen free (SPF), with their gut microbiomes free of Proteobacteria. The third group consisted of conventional SPF mice which had a wide range of gut bacteria such as Proteobacteria, and pathogens such as Staphylococcus and Helicobacter. When subjected to gluten, this happened:
The germ-free mice showed increase levels of intraepithelial lymphocytes (IELs) in the gut – proliferation and activation of IELs is the earliest sign of celiac disease. They also experienced death of the cells that line the GI tract called enterocytes as well as in the small fingerlike projections inside the small intestine known as villi. The clean SPF mice did not experience the same thing.
The germ-free mice also developed antibodies as a response to a component of gluten called gliadin, while the same group demonstrated T-cell responses specific to this component. Dr. Verdu and her team discovered that the development of gluten-induced pathology was stopped in the clean SPF mice compared to the germ-free mice, but this didn’t occur when the SPF mice were injected with Escherichia Coli from a gluten intolerant patient.
The conventional SPF mice demonstrated better gluten-induced pathology than the clean SPF mice. The team started investigating whether the presence of Proteobacteria such as E. Coli or Helicobacter play a role in this. When they increased the presence of Proteobacteria in clean SPF mice, the gluten-induced pathology got worse, and there was a noticeable increase in the IEL levels. Here’s what Dr. Verdu said: “These studies demonstrate that perturbation of early microbial colonization in life and induction of dysbiosis (microbial imbalance inside the body), characterized by increased Proteobacteria, enhances the severity of gluten-induced responses in mice genetically predisposed to gluten sensitivity. Importantly, our data argue that the recognized increase in celiac disease prevalence in the general population over the last 50 years could be driven, at least in part, by perturbations in intestinal microbial ecology. Specific microbiota-based therapies may aid 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 Brimingham, these findings suggest that the presence of Proteobacteria may be crucial for celiac disease pathology, although they are not causing the condition. Proteobacteria probably boosts the immune system’s response to gluten.
A recent study published by Medical News showed that gluten intolerant people are more prone to nerve damage.
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