abstract
- Celiac disease (CeD) is an immune-mediated disease, triggered by gluten ingestion, in genetically susceptible individuals. The gluten-free diet (GFD) is the only current treatment for CeD, but is difficult to follow, has high non-adherence rates, and does not always lead to symptomatic or mucosal remission. Microbially-mediated mechanisms have been proposed to contribute to disease pathogenesis, and clinical studies support an association, but mechanistic insight has been difficult to obtain. Recent advances using translational approaches have provided clues to the mechanisms through which bacteria could contribute to CeD pathogenesis. In this review we discuss these bacterially mediated mechanisms, which include the modulation of pathogenic or protective pathways. Targeting these pathways through microbial therapeutics could provide adjuvant therapies to the GFD.