Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response

dc.creatorMalvezi, Aparecida Donizette
dc.creatorPanis, Carolina
dc.creatorSilva, Rosiane Valeriano da
dc.creatorFreitas, Rafael Carvalho
dc.creatorLovo-Martins, Maria Isabel
dc.creatorTatakihara, Vera Lúcia Hideko
dc.creatorZanluqui, Nágela Ghabdan
dc.creatorGoldenberg, Samuel
dc.creatorBordignon, Juliano
dc.creatorYamada-Ogatta, Sueli Fumie
dc.creatorMartins-Pinge, Marli Cardoso
dc.creatorCecchini, Rubens
dc.creatorPinge-Filho, Phileno
dc.date2014-11-24T17:06:59Z
dc.date2014-11-24T17:06:59Z
dc.date2014
dc.date.accessioned2023-09-26T21:01:01Z
dc.date.available2023-09-26T21:01:01Z
dc.identifierMALVEZI, A. et al. Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response. Antimicrobial Agents and Chemotherapy, v. 58, p. 6157-6164, 2014. 
dc.identifier0066-4804
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/8946
dc.identifier10.1128/AAC.02752-14
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8867779
dc.descriptionThis work was supported by the Conselho Nacional de Desenvolvimento Científico e Tecnológico, Brasil (CNPq; 302097/2010-474792/2011-0), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), and by the Fundação Araucaria (Convênio 419/2009).
dc.descriptionThe intracellular protozoan parasite Trypanosoma cruzi is the etiologic agent of 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) enzymes during T. cruzi invasion. Pharmacological antagonists for COX-1 (aspirin) and COX-2 (celecoxib) caused marked inhibition of T. cruzi infection when rat cardiac cells were pretreated with these nonsteroidal anti-inflammatory drugs (NSAIDs) for 60 min at 37°C before inoculation. This inhibition was associated with an increase in the production of NO and interleukin-1 and decreased production of transforming growth factor (TGF- ) by cells. Taken together, these results indicate that COX-1 more than COX-2 is involved in the regulation of anti-T. cruzi activity in cardiac cells, and they provide a better understanding of the influence of TGF- -interfering therapies on the innate inflammatory response to T. cruzi infection and may represent a very pertinent target for new therapeutic treatments of Chagas disease.
dc.formatapplication/pdf
dc.languageeng
dc.publisherJournal.ASM.org
dc.rightsopen access
dc.subjectCyclooxygenase 1
dc.subjectCyclooxygenase 2
dc.subjectMyocytes
dc.subjectInflammation
dc.subjectCiclooxigenasa 1
dc.subjectCiclooxigenasa 2
dc.subjectMiocitos Cardíacos
dc.subjectInflamación
dc.subjectCiclo-Oxigenase 1
dc.subjectCiclo-Oxigenase 2
dc.subjectMiócitos Cardíacos
dc.subjectInflamação
dc.subjectTrypanosoma Cruzi
dc.titleInhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response
dc.typeArticle


Este ítem pertenece a la siguiente institución