Researchers Say They Have Identified Difference Between Celiac Disease, Gluten Sensitivity

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Researchers performed a study to examine the molecular-level differences between gluten-associated disorders celiac disease and gluten sensitivity.

Researchers from University of Maryland School of Medicine’s Center for Celiac Research performed a study to examine the molecular-level differences between gluten-associated disorders celiac disease and gluten sensitivity. The study, recently published online in BMC Medicine, found differences in levels of intestinal permeability and the response elicited from the immune system. The researchers say the study provides the first scientific evidence of a different mechanism leading to gluten sensitivity.

The study enrolled gluten-tolerant individuals, as well as those with celiac disease and gluten sensitivity. Intestinal permeability was evaluated using a lactulose and mannitol probe. Mucosal biopsy specimens were collected to study the expression of genes involved in barrier function and immunity.

The researchers said they found that, unlike celiac disease, gluten sensitivity is not associated with increased intestinal permeability. In fact, intestinal permeability was significantly reduced in those with gluten sensitivity compared to controls. Those with gluten sensitivity also showed significantly increased expression of claudin.

In those with celiac disease, relative to controls, adaptive immunity markers interleukin and IL-21 were expressed at higher levels, although they were not in those with gluten sensitivity. Expression of the innate immunity marker Toll-like receptor 2 was increased in those with gluten sensitivity, but not in those with celiac disease. Finally, the expression of the T-regulatory cell marker FOXP3 was significantly reduced in those with gluten sensitivity compared to controls and those with celiac disease.

The researchers say these differences contribute “to the characterization of gluten sensitivity as a condition associated with prevalent gluten-induced activation of innate, rather than adaptive, immune responses in the absence of detectable changes in mucosal barrier function.”

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