The rise in allergic diseases has been attributed to the ‘hygiene hypothesis’, according to which changes in the commensal microbiome in populations residing in industrial countries may trigger immune reactions. Indeed, associations have emerged between allergic diseases to variables that affect the microbiome assembly, such as history of cesarean delivery, premature birth,early antibiotic exposure and formula feeding.  Eosinophilic esophagitis (EoE) is a chronic allergic disease, which causes significant impairment in the quality of life due to pain on swallowing, food impaction, esophageal stricture formation, and in extreme cases, esophageal rupture.  Although previous literature has elucidated that EoE involves a breech to the gut barrier and activation of bacteria-sensing immune receptors, such as Toll-like receptors, only few studies have hitherto focused on the role of the microbiome in the disease. The association between EoE and an altered composition of the microbiome along the GI tract, from salivary through esophageal to fecal microbiome, has been shown repeatedly, however no insights into the cellular immune mechanisms that link between the microbiome to EoE development have been studied to date, partially owing to a lack of a reliable animal model for the disease.

In our lab we study the role of the microbiota in EoE using a unique mouse model for the disease developed by the Munitz lab (TAU) in various conditions, including treatment with antibiotics and under germ-free conditions, and attempt to ameliorate the disease using probiotic and post-biotic interventions. We employ an artificial esophagus culture system to systematically assess barrier function and the effect of microbiota- and host-derived compounds. We set out to validate our findings in human specimens by establishing an EoE human biobank, consisting of esophageal tissue biopsies, saliva and stool samples for microbiome analysis.