Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity
BMC Medicine 2011, 9:23
Adapted from the 'discussion' section of the above paper:
Coeliac disease, an autoimmune condition, results from an inappropriate T-cell-mediated reaction to gliadin. In the past few years though, it has become apparent that "classic" CD represents the tip of a disease iceberg. An emerging problem is the clinical characterization of a group of gluten-reactive patients, accounting for roughly 10% of the general population, presenting with symptoms similar, but clinically different to CD.
As in CD, these gluten-sensitive (GS) patients experience distress when eating gluten-containing products and show improvement when following a gluten-free diet but in GS the adverse
reactions that develop while eating gluten are not followed by the appearance of autoantibodies and by persisting damage to the small intestine. Their symptoms may resemble some of the gastrointestinal symptoms associated with CD or wheat allergy, but objective diagnostic tests for this condition are currently missing. Therefore, a diagnosis of GS is commonly made by exclusion.
In itself, the absence of autoantibodies and intestinal damage does not mean that gluten may not be toxic for GS patients as, even in non-CD individuals, gluten has been associated with damage to
other tissues, organs and systems besides the intestine.
In the present study, the researchers sought to identify what it is that differentiates GS from CD and to try to understand its pathophysiology.
They found that, unlike CD, GS does not appear to increase the permeability of the lining of the gut; in fact, gut permeability in the GS patients was not only lower than in the CD patients but lower than in the controls who had neither condition. Increased intestinal permeability is thought to be an early biological change that precedes the onset of several autoimmune diseases as the loss of an effective intestinal barrier allows antigens (potential allergy triggers) to escape continually from the gut thereby, possibly, triggering an allergic response.
Patients with GS do not appear to suffer from other allergies or related conditions, and shared a similar blood antibody profile with schizophrenia patients and those on the autistic spectrum.
While there seems to be a strong genetic element in CD, this does not appear to be the case in GS which may also suggest a more limited involvement of the adaptive immune system in GS and may explain why this condition does not appear to trigger an autoimmune response.
It appears that GS may be an inflammatory condition triggered by innate immune mechanisms reacting to a microbial invasion which may or may not progress into a learned allergic response.
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