Profiling unique eosinophile-generated eicosanoid metabolites in eosinophilic esophagitis using a liquid chromatography tandem mass spectrometry (LC-MS/MS)-based metabolomics approach

Overall objective of this study is to determine the ω-3 an ω-6 polyunsaturated fatty acids (PUFAs) metabolites/eicosanoids profile in eosinophilic esophagitis using a liquid chromatography tandem mass spectrometry (LC-MS/MS)-based metabolomics approach and to identify the unique eicosanoids or biomarker/s for diagnosis, prognosis and monitoring therapeutic effect of EoE. There are only two fatty acids known to be essential for humans: alpha-linolenic acid (an omega-3 fatty acid) and linoleic acid (an omega-6 fatty acid), also known as polyunsaturated fatty acid (PUFAs). Eicosanoids are signaling molecules derived from the essential fatty acids (EFA), which are oxygenated via the metabolism by oxygenases including cyclooxygenases (COX), lipoxygenases (LOX), and cytochromes P450 oxy/epoxygenases (CYP). Eicosanoids function in diverse physiological systems and pathological processes such as: mounting or inhibiting inflammation, allergy, fever and other immune responses; regulating the abortion of pregnancy and normal childbirth; contributing to the perception of pain; regulating cell growth; controlling blood pressure; and modulating the regional flow of blood to tissues. Aberrant polyunsaturated fatty acid (PUFAs) metabolism, particularly arachidonic acid (ARA), is believed to be the key mediators contributing to inflammatory process. In the "arachidonic acid cascade" – more than 20 different signaling paths that control a wide array of bodily functions, especially those functions involving inflammation. In the inflammatory response, two other groups of dietary essential fatty acids including Eicosapentaenoic acid (EPA, 20:5 ω-3) and Docosahexaenoic acid (DHA, 22:6 ω-3) form cascades that parallel and compete with the arachidonic acid cascade. However, there is no study on PUFAs metabolism and the role of these PUFAs metabolites in the pathogenesis of eosinophilic esophagitis.