Oral administration of Bifidobacterium longum CECT 7347 modulates jejunal proteome in an in vivo gliadin-induced enteropathy animal model.

Celiac disease is an immune-mediated disorder triggered by gluten proteins of wheat (gliadins) and other cereals. Gliadin-mediated effects on weanling animals, sensitized or not with interferon (IFN)-γ, were investigated. Also, the influence of the co-administration of Bifidobacterium longum CECT 7347 was studied together with changes in the proteome of jejunal sections, using 2DE and MALDITOF-TOF peptide fingerprinting. Findings were compared to results for control animal groups. In the principal component analysis (PCA) of proteome pattern, two components were extracted accounting for 79.8% of variability in the expression of the identified proteins. PCA analysis clearly discriminated between the proteome of animals fed gliadins alone and those fed gliadins and B. longum simultaneously. However, the proteome patterns from animals sensitized with IFN-γ and fed gliadins together with B. longum, or alone, could not be discriminated. Gliadin feeding caused inflammatory effects as well as changes in proteins involved in intracellular ionic homeostasis, lipid turnover, cell motility and redox regulation in intestinal sections. After feeding gliadins to animals sensitized with IFN-γ, changes were also detected in proteins involved in recruitment and function of inmunocompetent cells, trophic effect on the intestine and organization of myofibers reflecting the more marked gliadin-mediated injury in jejunal sections. The administration of the bacterial strain to rats fed gliadins seemed to ameliorate the inflammation caused by gliadin feeding alone, although, in sensitized animals the co-administration of B. longum had less marked effects, which was probably due to the more extensive intestinal mucosal damage. The proteome patterns in animals administered B. longum alone did not reveal any changes reflecting impairment of jejunal functions.

Unraveling the ties between celiac disease and intestinal microbiota.

Celiac disease is a multifactorial disorder that involves interactions between genetic and environmental factors. Gluten proteins are responsible for the symptoms of celiac disease, but other environmental factors that influence the intestinal ecosystem, including the milk-feeding type and gastrointestinal infections, may also play a role. Moreover, intestinal dysbiosis, characterized by increased Gram-negative bacteria and reduced bifidobacteria, has been detected in celiac disease patients. This review summarizes current knowledge of the associations between the intestinal microbiota and celiac disease and its possible modes of action in pathogenesis. Deeper understanding of these interactions can help redefine how this disorder is investigated.

Influence of Bifidobacterium longum CECT 7347 and gliadin peptides on intestinal epithelial cell proteome.

Celiac disease is an enteropathy caused by an abnormal immune response to cereal gluten proteins (gliadin). To unravel the possible role of the interactions between gliadin peptides and specific intestinal bacteria, the response of intestinal epithelial (Caco-2) cells to gliadin subjected to gastrointestinal digestion in the presence or absence of Bifidobacterium longum CECT 7347 has been studied. Changes in the proteome of Caco-2 cells were determined by 2DE and MALDI-TOF. Gliadins digested without B. longum altered the expression of a higher number of proteins than in the presence of the bacterium (21 versus 9), and these proteins were involved in disorganization of cell cytoskeleton, inflammation, and apoptosis. Gliadins digested in the presence of the bacterium influenced the production of proteins involved in calcium homeostasis and cell survival and function. Therefore, B. longum CECT 7347 might ameliorate gliadin toxicity and modify the responses of intestinal epithelial cells to the gliadin challenge.