Captopril increases the intensity of monocyte infection by Trypanosoma cruzi and induces human T helper type 17 cells.

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dc.contributor.authorSantos, Janete Soares Coelho dos
dc.contributor.authorMenezes, Cristiane Alves da Silva
dc.contributor.authorVillani, Fernanda Nobre Amaral
dc.contributor.authorMagalhães, Luísa Mourão Dias
dc.contributor.authorScharfstein, Julio
dc.contributor.authorGollob, Kenneth John
dc.contributor.authorDutra, Walderez Ornelas
dc.date.accessioned2017-06-05T16:47:28Z
dc.date.available2017-06-05T16:47:28Z
dc.date.issued2010
dc.description.abstractThe anti-hypertensive drug captopril is used commonly to reduce blood pressure of patients with severe forms of Chagas disease, a cardiomyopathy caused by chronic infection with the intracellular protozoan Trypanosoma cruzi. Captopril acts by inhibiting angiotensin-converting enzyme (ACE), the vasopressor metallopeptidase that generates angiotensin II and promotes the degradation of bradykinin (BK). Recent studies in micemodels of Chagas disease indicated that captopril can potentiate the T helper type 1 (Th1)-directing natural adjuvant property of BK. Equipped with kinin-releasing cysteine proteases, T. cruzi trypomastigotes were shown previously to invade nonprofessional phagocytic cells, such as human endothelial cells and murine cardiomyocytes, through the signalling of G protein-coupled bradykinin receptors (B2KR). Monocytes are also parasitized by T. cruzi and these cells are known to be important for the host immune response during infection. Here we showed that captopril increases the intensity of T. cruzi infection of human monocytes in vitro. The increased parasitism was accompanied by up-regulated expression of ACE in human monocytes.While T. cruzi infection increased the expression of interleukin (IL)-10 by monocytes significantly, compared to uninfected cells, T. cruzi infection in association with captopril down-modulated IL-10 expression by the monocytes. Surprisingly, studies with peripheral blood mononuclear cells revealed that addition of the ACE inhibitor in association with T. cruzi increased expression of IL-17 by CD4+ T cells in a B2KR-dependent manner. Collectively, our results suggest that captopril might interfere with host–parasite equilibrium by enhancing infection of monocytes, decreasing the expression of the modulatory cytokine IL-10, while guiding development of the proinflammatory Th17 subset.pt_BR
dc.identifier.citationSANTOS. J. S. C. dos et al. Captopril increases the intensity of monocyte infection by Trypanosoma cruzi and induces human T helper type 17 cells. Clinical and Experimental Immunology, v. 162, p. 528-536, 2010. Disponível em: <http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2249.2010.04270.x/abstract>. Acesso em: 19 fev. 2017.pt_BR
dc.identifier.doihttps://doi.org/10.1111/j.1365-2249.2010.04270.x
dc.identifier.issn1365-2249
dc.identifier.urihttp://www.repositorio.ufop.br/handle/123456789/7883
dc.identifier.uri2http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2249.2010.04270.x/abstractpt_BR
dc.language.isoen_USpt_BR
dc.rightsrestritopt_BR
dc.titleCaptopril increases the intensity of monocyte infection by Trypanosoma cruzi and induces human T helper type 17 cells.pt_BR
dc.typeArtigo publicado em periodicopt_BR
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