Celiac disease, an autoimmune disorder that can seriously damage the intestinal system, can appear in genetically pre-disposed people, however, it is triggered via environmental factors, the article explains.
“When people suffering from celiac disease eat gluten, their immune system triggers a response against their body’s own cells, damaging the mucosal surface of the small intestine,” the article says.
Roughly 1 in every 100 people suffer from celiac disease, and the occurrence of celiac disease is roughly three times higher in patients who suffer from cystic fibrosis, a condition in which the lungs and intestines are affected by a build-up of thick, sticky mucus.
Cystic fibrosis develops due to mutartions of the gene coding for “cystic fibrosis transmembrane conductance regulator (CFTR) … an ion transport protein that plays an important role in keeping mucus fluid – when it fails, the mucus clogs up … CFTR malfunction triggers a number of additional reactions in the lungs and other organs including intestine by activation of the immune system. These effects are very similar to the responses triggered by gluten in celiac patients,” the article says.
There may be hope, however. An international research team from Italy and France recently discovered a molecular component in the development of gluten intolerances, with their findings being published in The EMBO Journal. Their research “suggests potential targets for the development of therapeutic approaches for the disease,” the article says.
As gluten is difficult to digest, long protein parts called peptides enter the intestine.
“Using human intestinal cell lines that are sensitive to gluten, the researchers found that one specific peptide, P31-43, directly binds to CFTR and impairs its function. This interaction triggers cellular stress and inflammation, suggesting that CFTR plays a central role in mediating gluten sensitivity in celiac patients.
“Moreover, the interaction between P31-43 and CFTR can be inhibited by a potentiator of CFTR, called VX-770. When intestinal cells or tissue samples collected from celiac disease patients were pre-incubated with VX-770 before being exposed to P31-43, the peptide did not elicit an immune reaction. Thus, VX-770 protects gluten-sensitive epithelial cells from the detrimental effect of gluten. In addition, the researchers found that VX-770 could protect gluten-sensitive mice from gluten-induced intestinal symptoms.”
While these findings offer hope for those who suffer from celiac disease and gluten intolerances, they do not guarantee a cure. The study is, however, a step in the right direction in terms of coming to a cure for this condition. The study’s findings suggest “that CFTR potentiators, which have been developed to treat cystic fibrosis, may also be explored as a starting point for the development of a remedy for celiac disease.”
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