Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/24927
Title: Response to Trypanosoma cruzi by human blood cells enriched with Dentritic Cells is controlled by Cyclooxygenase-2 Pathway
Authors: Lonien, Sandra C. H.
Malvezi, Aparecida D.
Suzukawa, Helena T.
Yamauchi, Lucy M.
Yamada-Ogatta, Sueli F.
Rizzo, Luiz V.
Bordignon, Juliano
Pinge-Filho, Phileno
Affilliation: Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunologia. Londrina, PR, Brasil.
Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunologia. Londrina, PR, Brasil.
Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunologia. Londrina, PR, Brasil.
Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Microbiologia. Laboratório de Biologia Molecular de Microrganismos, Londrina, PR, Brasil.
Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Microbiologia. Laboratório de Biologia Molecular de Microrganismos, Londrina, PR, Brasil.
Hospital Israelita Albert Einstein, São Paulo, SP, Brasil.
Fundação Oswaldo Cruz. Instituto Carlos Chagas. Laboratório de Virologia Molecular. Curitiba, PR, Brasil.
Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunologia. Londrina, PR, Brasil.
Abstract: Chagas disease (Cd) or American human trypanosomiasis is caused by Trypanosoma cruzi and affects ~7 million people, mostly in Latin America. The infective trypomastigote forms of the parasite can invade several human blood cell populations, including monocytes and dendritic cells (DC). Although these cells display a wide functional diversity, their interactions with T. cruzi via cyclooxygenase (COX) and cyclic adenosine monophosphate (cAMP) dependent pathways have not been analyzed. To exploiting this mechanism, DC-enriched peripheral human blood mononuclear cell populations (DC-PBMC) were used as our model. Our results showed that the treatment of these cell populations with celecoxib (CEL), a cyclooxygenase-2 selective inhibitor or SQ 22,536, an adenilate cyclase inhibitor, significantly caused marked inhibition of T. cruzi infection. In contrast, aspirin (ASA, a non-selective COX-1 and COX-2 inhibitor) treatment did not inhibit the infection of the cells by the parasite and was independent of nitric oxide (NO) production. The expression of co-stimulatory molecules CD80 and CD86 were similar on cells treated or not with both COX-inhibitors. The infection stimulated the release of TNF-α, IL-1β, IL-6, IL-8, and IL-10 production by infected cells. Treatment with ASA or CEL did not affect TNF-α, IL-6, IL-8, IL-10, and NO production by infected cells, but increased IL-1β production by them. Our results suggest a key role of COX-2 and cAMP pathways in T. cruzi invasion process of human blood cells and these pathways may represent targets of new therapeutic options for Cd.
Keywords: Dendritic Cells
Aspirin
Celecoxib
Keywords in spanish: Células Dendríticas
Aspirin
Celecoxib
keywords: Trypanosoma cruzi
DeCS: Células Dendríticas
Aspirina
Celecoxib
Issue Date: 2017
Publisher: Frontiers Media
Citation: LONIEN, SCH. et al. Response to Trypanosoma cruzi by human blood cells enriched with Dentritic Cells is controlled by Cyclooxygenase-2 Pathway. Front. Microbiol. v.8, n.2020, p. 1-11, 2017.
ISSN: 1664-302X
Copyright: open access
Appears in Collections:PR - ICC - Artigos de Periódicos

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