Much ado about EoE

In 1996, a landmark study from Kelly et al demonstrated that placement of children with oesophageal eosinophilia on an elemental diet, that is, a diet devoid of all food antigens, led to histological and symptomatic normalisation.1 Over the past three decades, this simple understanding of eosinophilic oesophagitis (EoE) has evolved from a one-act play to a highly complex drama involving multiple scenes and actors. Recently in Gut, Santacroce et al 2 carefully and elegantly illustrated an understandable and exciting view of the pathogenesis of EoE. Roughly, three acts were presented to advance the pathobiology of EoE: barrier dysfunction, inflammation and tissue remodelling. The observation that large protein antigens and pathogens can penetrate the oesophageal epithelium is a novel concept.3 Dysfunction of this barrier leading to antigen penetration is manifest pathologically by dilation of intracellular spaces, physiologically by methods that demonstrate increased permeability and mechanistically by disruption of cell–cell adhesion proteins such as tight junctions and desmosomes. The initiating events for this perturbation are unclear but they range from localised epithelial microbial effects on tight junctions to mucosal damage from environmental toxins and a hyperproliferative response of the epithelial basal zone. Specific gene variations such …