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Eosinophilc esophagitis (EE) is an emerging disease which is characterized by a dense infiltration of the esophagus by eosinophilic leukocytes. The main symptoms of this disease are dysphagia and frequent food impaction in esophagus, and they are due to a hypersentivity response to different foods or aeroallergens. Eosinophil accumulation in the esophageal epithelium is determined by local production of eosinophilotropic cytokines and chemokines, which have been well defined as a TH2-type hypersensitivity reaction in animal models of the disease. Esophageal epithelium, after T CD4+ lymphocytes stimulation, contains all the necessary cell types for the development of local immunoallergic responses. However, there is increasing data on the significant role that humoral immunity could play in the pathophysiology of EE, by means of the action of IgE over mast cells function. The high density of T CD8+ lymphocytes in inflammatory infiltrate suggests that a TH1-type reaction could also participate in the mechanism of the disease. Proteins contained in cytoplasmic granules of activated eosinophils and mast cells could act over neural and muscular components of the esophageal wall, triggering motor disturbances which can be measured by means of manometric recordings and justify the esophageal symptoms. This paper aims to review the newest clinical aspects of EE and the results of studies directed at investigating the pathophysiology of the disease. Furthermore, we carry out a critical review of available therapeutic options.

Over the last few years, three specific eosinophil activating peptides, eotaxin-1, -2 and -3, members of the chemokine family have been identified. These cytokines exert a number of functions on eosinophils including chemotaxis, transendothelial migration and induction of the release of reactive oxygen species. Eosinophils are considered to play an important role in allergic disease by causing tissue damage through the release of toxic proteases, lipid mediators, cytokines and oxygen free radicals. This article reviews the role of eotaxins in asthma and nasal polyps. Discussion focuses on therapeutic guidelines, particularly as it has been shown that CCR3, the major chemokine receptor in eosinophils, serves as a eotaxin receptor.