Eosinophilic esophagitis (EOE)
● Symptoms and Causes
Early-life exposures, genetic factors, and an atopic state likely increase disease susceptibility in eosinophilic esophagitis. Exposure to antigens causes the esophageal epithelium to release alarmins, IL-33, and thymic stromal lymphopoietin (TSLP). These cytokines in turn stimulate T-helper type 2 (Th2) cells’ secretion of IL-13, IL-4, and IL-5. IL-13 and IL-4 stimulate the changes seen in the esophageal epithelium, including basal cell hyperplasia and dilated intracellular spaces. Chemotaxins, eotaxin-3 and IL-5, lead to granulocyte infiltration. The mixed cytokine milieu also contributes to the activation of fibroblasts in the lamina propria, collagen deposition, and tissue stiffness.
doi:10.1001/jama.2021.14920.
Eosinophilic esophagitis (EOE)
● Symptoms and Causes
Early-life exposures, genetic factors, and an atopic state likely increase disease susceptibility in eosinophilic esophagitis. Exposure to antigens causes the esophageal epithelium to release alarmins, IL-33, and thymic stromal lymphopoietin (TSLP). These cytokines in turn stimulate T-helper type 2 (Th2) cells’ secretion of IL-13, IL-4, and IL-5. IL-13 and IL-4 stimulate the changes seen in the esophageal epithelium, including basal cell hyperplasia and dilated intracellular spaces. Chemotaxins, eotaxin-3 and IL-5, lead to granulocyte infiltration. The mixed cytokine milieu also contributes to the activation of fibroblasts in the lamina propria, collagen deposition, and tissue stiffness.
doi:10.1001/jama.2021.14920.