Metabolome of human microbiota associated with the degradation of gluten: an approach involving bifidobacteria

Abstract

The human microbiota consists of hundreds of bacterial species from which the imbalance in their community (dysbiosis) can cause the emergence of several diseases. The intestinal dysbiosis has been associated with celiac disease (CD), a chronic disease characterized by an inflammatory process induced in genetically predisposed individuals by the ingestion of foods containing gluten, a protein complex found naturally in cereals such as wheat, barley and rye. As result, damages to the small bowel mucosa, villous atrophy and malabsorption of nutrients are observed. The main gluten proteins present in wheat are gliadins and glutenins, which due to the high content of proline and glutamine, are not fully digested by the gastro-intestinal system and some of them arrive intact to the intestine, where most of the bacterial community of the human body is present. There is a crescent consensus that the human microbiota plays a crucial role in the development of CD to metabolize the gluten proteins. The bifidobacteria, in particular the species B. animalis, B. longum, B. bifidum, B. adolescentis e B. breve, are among the main bacterial species observed in dysbiosis of celiac patients, which the action mechanism in the metabolism of gluten proteins and the metabolites generated by them are still poorly known. Thus, the present research project aims to investigate the effect of these bifidobacteria species in the metabolism of the gliadins and glutenins proteins. For that, the polypeptides (metabolites) will be chemically characterized by liquid chromatography coupled to mass spectrometry and by nuclear magnetic resonance spectroscopy, and their immunogenic response will be evaluated though the given effect in the expression of marker proteins of inflammatory process in the intestinal Caco-2 cell type. As results and perspectives, it is expected to better understand the chemical nature of the metabolites generated by these microorganisms and their immunogenic effect on the development or treatment of CD.