Eosinophilic Esophagitis Research Paper

Eosinophilic esophagitis (EoE) is a chronic inflammatory [1, 2],relapsing[3] and recently recognized immune/antigen-mediated condition [4, 5] characterized by basal cell hyperplasia, microabscesses, degranulation, dilated intercellular spaces [6, 7] and predominant eosinophilic infiltration in the esophagus [8-11]. Allergists and gastroenterologists are seeing many more patients with EoE, this is due to an increase in the frequency of EoE in children and adults and greater physician awareness [1, 5, 12, 13]. In eosinophilic esophagitis, the lining of the esophagus becomes inflamed and examination of the lining shows a high cell count of the white blood cell eosinophils are builds up in the epithelial lining of the esophagus [14]. This buildup,
For some patients, it may seem like their EoE is worse during pollen seasons （spring and fall ）or living in a cold or dry climate [41].The pathogenesis of EoE is relatively poorly understood [42],Increasing evidence suggests a strong genetic [38],immunologic and environmental factors involvement ,some studies says that cesarean birth, premature delivery, antibiotic exposure during infancy, food allergy, lack of breast-feeding, and lack of early exposure to microbes are associated with EoE [14, 43, 44] .Esophageal microbiome may play vital role in EoE especially Haemophilus [45], Corynebacterium , Neisseria [46],and an inverse relationship between H.pylori and the development of EoE
The esophagus is unique from the rest of gastrointestinal tract ,normally there are no eosinophils in the esophagus[15].The mechanism of dysphagia in EoE is multifactorial ,including mucosal stickness ,esophageal fibrosis,strictures and ring formation [4].Eosinophils produce and release many proteins and mediators,particularly major basic protein(MBP),eosinophilic cationic protein(ECP),eosinophil-derived neurotoxin (EDN) and eosinophilic peroxidase play major role in tissue damage and remodling [8, 47], serum analysis of absolute eosinophil count (AEC) ECP, and EDN were higher in EoE subjects in one prospective cohort study .Moreover AEC predicted post-treatment eosinophilia, suggesting a potential role in monitoring EoE disease activity [48].Bone morphogenetic protein (BMP)[49] promotes squamous differentiation of basal progenitor calls upon their activation in adults esophagus, and basal cell hyperplasia is associated with high levels of follistatin on biopsies sample [6].The important inflammatory mediators Th2-type cytokines IL-4 , IL-5, IL-13 [1, 16, 20, 38, 39, 50-53] are involved in trafficking eosinophils into esophageal tissue[9, 30].Activation of STAT6 by IL-4 and IL13 to mediate the pathogenesis of allergic disorders [38, 54], epithelial cells have been recognized as major effectors in initiating EoE, both through their recruitment of iNKT cells towards the esophageal epithelium, the thymic stromal lymphpoeitin (TSLP) gene and its receptor appear to be a risk