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Found 3 results

  1. Celiac.com 03/17/2014 - Researchers know a great deal about the function of human digestive proteases in gluten proteins, but they know very little about the role of intestinal microbes in metabolizing those proteins. A team of researchers recently set out to examine the isolation and characterization of human gut bacteria involved in the metabolizing gluten proteins. The researchers include Alberto Caminero, Alexandra R. Herrán, Esther Nistal, Jenifer Pérez-Andrés, Luis Vaquero, Santiago Vivas, José María G. Ruiz de Morales, Silvia M. Albillos, and Javier Casqueiro. They are variously affiliated with the Instituto de Biología Molecular, Genómica y Proteómica (INBIOMIC), and the Instituto de Biomedicina (IBIOMED) at the Campus de Vegazana of the Universidad de León, with the Área de Microbiología, Facultad de Biología y Ciencias Ambientales at the Universidad de León, with the Departamento de Inmunología y Gastroenterología, Hospital de León, León, Spain, and with the Instituto de Biotecnología (INBIOTEC) de León, all in León, Spain. For their study, the team cultured 22 human fecal samples, with gluten as the principal nitrogen source, and isolated 144 strains belonging to 35 bacterial species that may play a role in gluten metabolism in the human gut. They found that 94 of the isolated strains were able to metabolize gluten, 61 strains showed an extracellular proteolytic activity against gluten proteins, while several strains showed a peptidasic activity toward the 33-mer peptide, which is an known peptide trigger in celiac disease patients. Most of the isolated strains belong to the phyla Firmicutes and Actinobacteria, mainly from the genera Lactobacillus, Streptococcus, Staphylococcus, Clostridium and Bifidobacterium. They found that the human gut hosts a wide variety of bacteria capable of using gluten proteins and peptides as nutrients. These bacteria could play an important role in gluten metabolism and could offer promising new treatment possibilities for celiac disease. Source: Onlinelibrary.wiley.com. DOI: 10.1111/1574-6941.12295
  2. Celiac.com 08/16/2016 - Celiac disease changes the composition and differentiation potential of the duodenal intraepithelial innate lymphocyte compartment, specifically, the composition and function of duodenal intraepithelial T cells. The intestinal tract is also home to four types of CD3-negative intraepithelial lymphocytes (IELs) with largely unknown function: CD56(-)CD127(-); CD56(-)CD127(+); CD56(+)CD127(-) and CD56(+)CD127(+). A team of researchers wanted to gain insight into the potential function of these innate IELs in health and disease. Specifically, they wanted to assess how the composition and differentiation potential of the duodenal intraepithelial innate lymphocyte compartment is altered in celiac disease. The research team included F Schmitz, Y Kooy-Winkelaar, AS Wiekmeijer, MH Brugman, ML Mearin, C Mulder, S Chuva de Sousa Lopes, CL Mummery, FJ Staal, J van Bergen, F Koning. They are variously affiliated with the Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands, the Department of Immunohematology and Blood Transfusion at Leiden University Medical Center in Leiden, The Netherlands, the Department of Pediatrics, Leiden University Medical Center, Leiden, The Netherlands, the Department of Gastroenterology at the Free University Medical Center, Amsterdam, The Netherlands, and with the Department of Anatomy and Embryology at Leiden University Medical Center in Leiden, The Netherlands. For their study, the team measured the phenotypes, relative abundance and differentiation potential of these innate IEL subsets in duodenal biopsies from controls and patients with celiac disease or patients with refractory celiac disease type II (RCDII). Hierarchical clustering analysis of the expression of 15 natural killer and T cell surface markers showed that innate IELs differed markedly from innate peripheral blood lymphocytes and divided innate IEL subsets into two main branches: a CD127(-) branch expressing high levels of interleukin (IL) 2/15Rβ but no IL-21R, and a CD127(+) branch with the opposite phenotype. While celiac disease was characterized by the contraction of all four innate IEL subsets, a selective expansion of CD56(-)CD127(-) and CD56(-)CD127(+) innate IEL was detected in RCDII. In vitro, in the presence of IL-15, CD56(-)CD127(-) IEL from controls and patients with celiac disease differentiated into functional natural killer and T cells, the latter largely dependent on notch-signaling. This did not occur in patients with RCDII. Furthermore, compared with non-celiac controls, CD56(-)CD127(-) IEL from patients with celiac disease expressed more intracellular CD3ε and CD3γ and gave more pronounced T cell differentiation. RCDII changes the normally diverse and plastic innate IEL compartment, and encourages a loss of differentiation potential. Source: Gut. 2016 Aug;65(8):1269-78. doi: 10.1136/gutjnl-2014-308153.
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