Celiac

Information

Celiac disease is a systemic autoimmune disease with a pronounced genetic predisposition which may affect different organ systems. Celiac disease is triggered by the consumption of gluten, which makes up about 90% of the protein contents of many cereal grains. In most cases, the disease manifests as severe inflammation and damage to the mucous membrane of the small intestine (enteropathy).

Both genetic and environmental factors contribute to the development of celiac disease. Enteropathy, which is characteristic of celiac disease, is caused by an overreaction of the immune system to gluten components, especially the so-called gliadin. Gliadin is only partially digested in the small intestine. If there are gaps in the intestinal epithelium, as is typical in patients with celiac disease, the resulting gliadin fragments (peptides, consisting of 33 amino acids, 33-mer) can pass through the intestinal barrier and reach the connective tissue underneath. There, the enzyme tissue transglutaminase (tTG) modifies (deamidates) the amino acid glutamine (Q) into the amino acid glutamate (E) at certain sites of the gliadin peptides. This modification brings on an immunological reaction in the case of genetic predisposition. The activation of B cells leads to the production of antibodies against the deamidated gliadin peptides and against the body’s own tissue transglutaminase. In addition, the T cells secrete pro-inflammatory cytokines which cause an inflammatory reaction in the tissue. The immunological overreaction and the inflammation of the epithelium of the small intestine lead to apoptosis of the enterocytes, atrophy of the villi and widening of the intestinal crypts (hyperplasia). These damages mean the intestinal mucosa is no longer able to absorb sufficient nutrients from the digested food and to transport them into the bloodstream.