Gluten Digestion and the Microbiome: Gluten-Eating Bacteria

It is often assumed, and sometimes defended fanatically by certain “groups”, that humans cannot digest gluten, and therefore no single human (with or without CD) should be eating gluten-containing foods, such as wheat. For them the story ends here. But there is a lot more to it.

Abstract

There is a large variety of bacteria capable of digesting gluten with gluten-degrading proteases naturally present in the upper human gastro-intestinal tract. The oral cavity is colonised with microorganisms that produce proteases capable of hydrolysing peptides rich in proline and glutamine residues. Intestinal dysbiosis is present in celiac disease patients, characterized by increased Gram-negative bacteria, other potentially pro-inflammatory bacteria and reduced bifidobacteria.

Small-intestinal bacterial overgrowth (SIBO) and infections have been suggested to contribute to CD pathogenesis with persistence of gastrointestinal symptoms after gluten withdrawal. Pathogenic enterobacteria could play a role in the switch from tolerance to an inflammatory immune response to gluten, by altering the permeability of the intestinal mucosa.

A lack of maturation of the gut microbiota is observed within the first 2 years of life in infants at risk of CD. The early introduction of gluten and the lack of maturity in the GI microbiota could trigger or accelerate the development of autoimmunity. Bacterial groups related to gluten metabolism are altered in patients with CD.

Either Bifidobacterium could protect against CD, or inherent features of the CD intestine influence Bifidobacterium colonization. Reduced IgA-coated bacteria is associated with intestinal dysbiosis suggesting the existence of a barrier defect, which fails to stabilize the gut microbiota and prevent the host from the invasion of harmful antigens and pathogens.

The induction of gliadin proteolysis in the human gut might not be the solution but the origin of CD, since gliadinases are CD specific. Gliadinases might have a bacterial origin within the duodenum of patients with CD. Gliadin-metabolising bacteria could be absent, or present to a much lower degree, in the duodenum of all non-predisposed individuals.

In CD the mucosal tolerance to the gut microbiota is deregulated. Reductions in beneficial Gram-positive bacteria could favor the residence and interactions of harmful Gram-negative bacteria within the mucosal surface thereby contributing to loss of gluten tolerance.

Either a particular glycosylation pattern in predisposed individuals favors harmful bacterial adhesion, which contributes to CD pathogenesis or modifications in the composition of the intestinal microbiota lead to alterations in the glycosylation pattern and its defensive role of the mucus layer against infections and CD.

Read the Free Full Article @ http://sciencedrivennutrition.com/gluten-manisfesto/ and learn a ton about gluten with myself and Brad Dieter, PhD 

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