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. Author manuscript; available in PMC: 2014 Jul 21.
Published in final edited form as: Gastroenterology. 2009 Aug 15;137(4):1238–1249. doi: 10.1053/j.gastro.2009.07.007

Figure 1. Molecular and cellular mechanisms involved in EE pathogenesis, eotaxin-3-associated eosinophil recruitment and treatments.

Figure 1

Aeroallergen, food allergen and skin sensitization have been implicated in EE pathogenesis. Elemental diet, glucocorticoids, and anti-IL-5 treatments improve the microscopic features of EE acting at different levels on the disease pathogenesis. Proton pomp inhibitors (PPI) are important in establishing the diagnosis of EE as inflammation should be present on PPIs therapy. Hyperplasic epithelial cells of the esophagus overexpress eotaxin-3 in response to IL-13. Fibroblasts overexpress periostin and downregulate filaggrin likelyin response to IL-13. Eotaxin-3 and periostin overexpression cooperatively chemoattract CCR3+ cells, a process primed by IL-5 which regulates eosinophil responsiveness to eotaxin-3 and the circulating level of eosinophils. Inheritance of EE disease suggests a genetic predisposition. A SNP in the eotaxin-3 gene has been associated with EE. In addition to eosinophils, mast cells and lymphocytes including B cells accumulate in the esophagus of EE patients and likely contribute to the local inflammatory responses.