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Journal of Immunology Research
Volume 2019, Article ID 5836476, 14 pages
https://doi.org/10.1155/2019/5836476
Research Article

Altered Metabolism of Phospholipases, Diacylglycerols, Endocannabinoids, and N-Acylethanolamines in Patients with Mastocytosis

1Department of Translational Medical Sciences and Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, WAO Center of Excellence, Naples, Italy
2Endocannabinoid Research Group, Istituto di Chimica Biomolecolare-Consiglio Nazionale delle Ricerche (ICB-CNR), Pozzuoli, Italy
3Division of Allergy and Clinical Immunology, University of Salerno, Italy
4Department of Public Health, University of Naples Federico II, Italy
5Monaldi Hospital Pharmacy, Naples, Italy
6Canada Excellence Research Chair on the Microbiome-Endocannabinoidome Axis in Metabolic Health, Université Laval, Centre de Recherche de l’Institut Universitaire de Cardiologie et Pneumologie de Quèbec, and Institut sur la Nutrition et les Aliments Fonctionnels, Québec City, Canada

Correspondence should be addressed to Maria Rosaria Galdiero; ti.aninu@oreidlag.airasorairam

Received 30 October 2018; Revised 2 April 2019; Accepted 14 May 2019; Published 1 July 2019

Academic Editor: Enrique Ortega

Copyright © 2019 Anne Lise Ferrara et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Mastocytosis is a condition characterized by the expansion and accumulation of mast cells (MCs) in various organs. The symptoms are related to the increased release of MC-derived mediators that exert local and distant effects. MCs are a source and target of phospholipase enzymes (PLs), which catalyze the cleavage of membrane phospholipids releasing lipid mediators (e.g., diacylglycerols (DAGs) and the endocannabinoid (EC) 2-arachidonoylglycerol (2-AG)). To date, there are no data on the role of these lipid mediators in mastocytosis. Here, we analyzed plasma levels of PLA2, PLC, DAG, ECs, and EC-related N-acylethanolamines in patients with mastocytosis. Methods. In 23 patients with mastocytosis and 23 healthy individuals, we measured plasma PLA2 and PLC activities, DAG, 2-AG, anandamide (AEA), palmitoylethanolamide (PEA), and oleoylethanolamide (OEA). Results. Plasma PLA2 and PLC activities were increased in mastocytosis patients compared to controls. Concentrations of DAG (18:1 20:4 and 18:0 20:4), two second messengers produced by PLC, were higher in mastocytosis compared to controls, whereas the concentrations of their metabolite, 2-AG, were not altered. AEA was decreased in mastocytosis patients compared to controls; by contrast, AEA congener, PEA, was increased. PLA2 and PLC activities were increased only in patients with mediator-related symptoms. Moreover, PLC activity was positively correlated with disease severity and tryptase concentrations. By contrast, AEA was negatively correlated with tryptase concentrations. Conclusions. PLs and some lipid mediators are altered in patients with mastocytosis. Our results may pave the way for investigating the functions of these mediators in the pathophysiology of mastocytosis and provide new potential biomarkers and therapeutic targets.