Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages
The intracellular protozoan parasite Trypanosoma cruzi causes Chagas disease, a serious disorder that affects 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, w...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/580919 |
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| author | Aparecida Donizette Malvezi Rosiane Valeriano da Silva Carolina Panis Lucy Megumi Yamauchi Maria Isabel Lovo-Martins Nagela Ghabdan Zanluqui Vera Lúcia Hideko Tatakihara Luiz Vicente Rizzo Waldiceu A. Verri Marli Cardoso Martins-Pinge Sueli Fumie Yamada-Ogatta Phileno Pinge-Filho |
| author_facet | Aparecida Donizette Malvezi Rosiane Valeriano da Silva Carolina Panis Lucy Megumi Yamauchi Maria Isabel Lovo-Martins Nagela Ghabdan Zanluqui Vera Lúcia Hideko Tatakihara Luiz Vicente Rizzo Waldiceu A. Verri Marli Cardoso Martins-Pinge Sueli Fumie Yamada-Ogatta Phileno Pinge-Filho |
| author_sort | Aparecida Donizette Malvezi |
| collection | DOAJ |
| description | The intracellular protozoan parasite Trypanosoma cruzi causes Chagas disease, a serious disorder that affects 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. This inhibition was associated with increased production of IL-1β and nitric oxide (NO∙) by macrophages. The treatment of macrophages with either NOS inhibitors or prostaglandin E2 (PGE2) restored the invasive action of T. cruzi in macrophages previously treated with ASA. Lipoxin ALX-receptor antagonist Boc2 reversed the inhibitory effect of ASA on trypomastigote invasion. Our results indicate that PGE2, 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 inflammatory response to T. cruzi infection as well as adding a new perspective to specific immune interventions. |
| format | Article |
| id | doaj-art-288f87023662449b9bf00e030cac5303 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-288f87023662449b9bf00e030cac53032025-02-03T01:04:46ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/580919580919Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal MacrophagesAparecida Donizette Malvezi0Rosiane Valeriano da Silva1Carolina Panis2Lucy Megumi Yamauchi3Maria Isabel Lovo-Martins4Nagela Ghabdan Zanluqui5Vera Lúcia Hideko Tatakihara6Luiz Vicente Rizzo7Waldiceu A. Verri8Marli Cardoso Martins-Pinge9Sueli Fumie Yamada-Ogatta10Phileno Pinge-Filho11Laboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Biologia Molecular de Microrganismos, Departamento de Microbiologia, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilInstituto Israelita de Ensino e Pesquisa Albert Einstein, 056510-901 São Paulo, SP, BrazilDepartamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilDepartamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Biologia Molecular de Microrganismos, Departamento de Microbiologia, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, PR, BrazilThe intracellular protozoan parasite Trypanosoma cruzi causes Chagas disease, a serious disorder that affects 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. This inhibition was associated with increased production of IL-1β and nitric oxide (NO∙) by macrophages. The treatment of macrophages with either NOS inhibitors or prostaglandin E2 (PGE2) restored the invasive action of T. cruzi in macrophages previously treated with ASA. Lipoxin ALX-receptor antagonist Boc2 reversed the inhibitory effect of ASA on trypomastigote invasion. Our results indicate that PGE2, 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 inflammatory response to T. cruzi infection as well as adding a new perspective to specific immune interventions.http://dx.doi.org/10.1155/2014/580919 |
| spellingShingle | Aparecida Donizette Malvezi Rosiane Valeriano da Silva Carolina Panis Lucy Megumi Yamauchi Maria Isabel Lovo-Martins Nagela Ghabdan Zanluqui Vera Lúcia Hideko Tatakihara Luiz Vicente Rizzo Waldiceu A. Verri Marli Cardoso Martins-Pinge Sueli Fumie Yamada-Ogatta Phileno Pinge-Filho Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages Mediators of Inflammation |
| title | Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages |
| title_full | Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages |
| title_fullStr | Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages |
| title_full_unstemmed | Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages |
| title_short | Aspirin Modulates Innate Inflammatory Response and Inhibits the Entry of Trypanosoma cruzi in Mouse Peritoneal Macrophages |
| title_sort | aspirin modulates innate inflammatory response and inhibits the entry of trypanosoma cruzi in mouse peritoneal macrophages |
| url | http://dx.doi.org/10.1155/2014/580919 |
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