Abstract
Event Abstract Back to Event Role of arachidonic acid metabolites in Trypanosoma cruzi infection Néstor A. Guerrero1, Manuel Fresno1 and Núria Gironès1* 1 Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Spain Cardiac inflammation plays an important role in the pathophysiology of Chagas disease, caused by Trypanosoma cruzi. Lipid mediators derived from arachidonic acid (AA), like prostaglandins and leukotrienes, are considered regulators of homeostasis and inflammation. These molecules are produced by a biosynthetic pathway controlled by enzymes as cyclooxygenases and lipoxygenases. The role of cyclooxygenase-2 (COX-2) in immunosuppression during the acute phase of T. cruzi infection has been described using non-steroidal anti-inflammatory drugs, which are inhibitors of this enzyme. In this study, we first investigated the expression of enzymes involved in AA metabolism during T. cruzi infection. Susceptible and non-susceptible mouse models of infection were used to further analyze the role of lipid mediators in T. cruzi infection. Our results confirm the expression of several of these enzymes in T. cruzi-infected heart, in particular COX-2. CD68+ heart-infiltrating macrophages were the major cell type expressing COX-2. CD11b+ heart-infiltrating myeloid cells were purified and they were able to produce prostaglandins PGE2 and PGF2α. Studies using gene-deficient mouse models indicated that regulation of COX-2 and PGE2, through PGE2 receptor 2 signaling, was in part responsible of cardiac inflammation in T. cruzi infection. The key role of lipid mediators in Chagas disease inflammation and the availability of drugs that inhibit their synthesis and their receptors could be useful for the treatment of this neglected disease. Acknowledgements This work was supported by grants: SAF2007-61716, SAF2005-02220, PS09/00538, RECAVA RD06/0014/1013, RICET RD06/0021/0016, HEALTH-FE-2008-22303,ChagasEpiNet, CC08-UAM/SAL-4440/08, AECID A/025417/09 and ‘‘Fundacion Ramon Areces". M. Fresno and N. Girones are professors at the UAM. N.A.G. was a recipient of a fellowship from ISCIII and RICET. We thank Beatriz Barrocal, Maria A. Chorro, M.C. Maza and Carlos Chillon for their technical assistance. Keywords: Trypanosoma cruzi, Cyclooxigenase-2, Prostaglandin E2 receptor 2, Cardiac inflammation, in vivo infection Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Host-pathogen interactions Citation: Guerrero NA, Fresno M and Gironès N (2013). Role of arachidonic acid metabolites in Trypanosoma cruzi infection. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.01131 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 12 Jul 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Núria Gironès, Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Madrid, 28049, Spain, ngirones@cbm.csic.es Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Néstor A Guerrero Manuel Fresno Núria Gironès Google Néstor A Guerrero Manuel Fresno Núria Gironès Google Scholar Néstor A Guerrero Manuel Fresno Núria Gironès PubMed Néstor A Guerrero Manuel Fresno Núria Gironès Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
Highlights
We already know that human and mouse immune system differ in some important aspects (Mestas and Hughes, 2004), experimental infections of murine models have provided a big amount of important data regarding Chagas disease
BALB/c mice are susceptible to infection, C57BL/6 mice are resistant to T. cruzi infection with the Y parasite strain
COX-2 deficiency produces no changes in parasite burden but reduces cardiac inflammation induced by Trypanosoma cruzi infection and this acute inflammation seems to be longer
Summary
Chagas diseaseChagas disease is a multisystemic disorder that due to the scarcity of preventive and therapeutic tools and population at risk is considered as a neglected tropical disease (Hotez et al, 2007; Morillo, 2013). Chronic cardiomyopathy is the most common and severe manifestation of human Chagas’ disease, causing congestive heart failure, arrhythmias and conduction abnormalities, which often lead to stroke and sudden death. This type of dilated cardiomyopathy is associated with chronic inflammation and fibrosis, cardiac hypertrophy and thrombo-embolic events [2]. The main goal of this work is to establish an easier and cheaper tool of choice for real-time monitoring of the establishment and progression of this pathology either in BALB/c mice or in vitro assays To validate this new technique we vaccinated mice with an attenuated Dhsp70-II strain of Leishmania to assess protection against this disease
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