Research Article Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages Aparecida Donizette Malvezi, 1 Rosiane Valeriano da Silva, 1 Carolina Panis, 1 Lucy Megumi Yamauchi, 2 Maria Isabel Lovo-Martins, 1 Nagela Ghabdan Zanluqui, 1 Vera Lúcia Hideko Tatakihara, 1 Luiz Vicente Rizzo, 3 Waldiceu A. Verri Jr., 4 Marli Cardoso Martins-Pinge, 5 Sueli Fumie Yamada-Ogatta, 2 and Phileno Pinge-Filho 1 1 Laborat´ orio de Imunopatologia Experimental, Departamento de Ciˆ encias Patol´ ogicas, Centro de Ciˆ encias Biol´ ogicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, Brazil 2 Laborat´ orio de Biologia Molecular de Microrganismos, Departamento de Microbiologia, Centro de Ciˆ encias Biol´ ogicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, Brazil 3 Instituto Israelita de Ensino e Pesquisa Albert Einstein, 056510-901 S˜ ao Paulo, SP, Brazil 4 Departamento de Ciˆ encias Patol´ ogicas, Centro de Ciˆ encias Biol´ ogicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, Brazil 5 Departamento de Ciˆ encias Fisiol´ ogicas, Centro de Ciˆ encias Biol´ ogicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, Brazil Correspondence should be addressed to Phileno Pinge-Filho; pingeilho@uel.br Received 3 March 2014; Revised 13 May 2014; Accepted 20 May 2014; Published 19 June 2014 Academic Editor: Marcelo T. Bozza Copyright © 2014 Aparecida Donizette Malvezi et al. his 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. he intracellular protozoan parasite Trypanosoma cruzi causes Chagas disease, a serious disorder that afects millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite’s life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host’s cyclooxygenase (COX) enzyme during T. cruzi invasion. Pharmacological antagonist for COX-1, aspirin (ASA), caused marked inhibition of T. cruzi infection when peritoneal macrophages were pretreated with ASA for 30 min at 37 ∘ C before inoculation. his inhibition was associated with increased production of IL-1 and nitric oxide (NO ∙ ) by macrophages. he treatment of macrophages with either NOS inhibitors or prostaglandin E 2 (PGE 2 ) restored the invasive action of T. cruzi in macrophages previously treated with ASA. Lipoxin ALX- receptor antagonist Boc2 reversed the inhibitory efect of ASA on trypomastigote invasion. Our results indicate that PGE 2 , NO ∙ , and lipoxins are involved in the regulation of anti-T. cruzi activity by macrophages, providing a better understanding of the role of prostaglandins in innate inlammatory response to T. cruzi infection as well as adding a new perspective to speciic immune interventions. 1. Introduction Trypanosoma cruzi is an intracellular protozoan parasite causing Chagas disease, which afects millions of people in Latin America. During the acute inlammatory phase of the T. cruzi infection, high-level expression of inducible nitric oxide synthase (iNOS) [1], proinlammatory cytokines [2], and arachidonic acid- (AA-) derived lipids such as leukotrienes, lipoxins (LXs), H (P) ETEs, prostaglandins, and thromboxane is prevalent [3, 4]. In the early T. cruzi infection, nitric oxide (NO ∙ ) and arachidonic acid metabolites could be attributed to resistance, but later on to tissue damage [4]. Prostaglandins (PGs) are oxygenated lipid mediators formed from the 6 essential fatty acid, arachidonic acid Hindawi Publishing Corporation Mediators of Inflammation Volume 2014, Article ID 580919, 9 pages http://dx.doi.org/10.1155/2014/580919