Navegando por Autor "Azevedo, Maíra Araújo"

Agora exibindo 1 - 5 de 5

Avaliação da resposta inflamatória cardiovascular em ratos com hipertensão renovascular (2R1C) infectados pelo Trypanosoma cruzi.
(2012) Azevedo, Maíra Araújo; Silva, André Talvani Pedrosa da; Rezende, Simone Aparecida; Silva, André Talvani Pedrosa da; Leite, Romulo
A Hipertensão Arterial Sistêmica (HAS), caracterizada pelo aumento de Angiotensina II plasmática/tecidual, é uma das doenças com maior prevalência no mundo moderno. Evidencias apontam para o envolvimento da inflamação vascular no processo inicial da HAS. A cardiopatia chagásica é causada pelo protozoário Trypanosoma cruzi, capaz de desencadear uma resposta inflamatória progressiva gerando importantes alterações elétricas e morfo-funcionais ao coração. Nosso objetivo neste estudo foi avaliar a associação da HAS e os aspectos inflamatórios cardiovasculares em animais infectados pela cepa Y do T. cruzi. Ratos Wistars machos foram submetidos à cirurgia renovascular (modelo Goldblatt – 2Rins/1CLIP) ou à cirurgia fictícia (SHAM) e divididos e agrupados de acordo com a infecção ou não pelo T. cruzi. Foram realizados três experimentos em diferentes momentos da “infecção e cirurgia” para avaliação da HAS e do patológico induzido pelo parasito sendo (I) indução da HAS + infecção pelo T.cruzi (ao mesmo tempo), experimento teve duração de 1 semana; (II) indução da HAS + infecção com o T. cruzi 3 semanas após a cirurgia e (III) indução da HAS + infecção pelo T.cruzi (ao mesmo tempo) e experimento teve duração de 8 semanas. Nesse estudo, avaliou-se parâmetros fisiológicos e inflamatórios como pletismografia, Ang II e mediadores inflamatórios plasmáticos, parasitemia e achados histopatológicos no tecido cardíaco. Após a 3ª semana de cirurgia os animais apresentaram picos pressóricos havendo concordância com a produção de Angio II plasmática nas primeiras semanas, mas não se observando relação direta entre o aumento da pressão arterial e o numero de parasitos circulantes. No entanto, o T. cruzi exerceu papel definidor na alta produção de TNF-alfa e da CX3CL1/Fractalkine e, em associação com a cirurgia renovascular, observou-se maior elevação nesses mediadores inflamatórios em diferentes etapas do estudo. Por outro lado, o aumento da pressão arterial não exerceu interferência no processo inflamatório tecidual nem na invasão tecidual pelo parasito, mas contribuiu para a manutenção do número de vasos sanguíneos após 8 semanas de experimento, quando houve diminuição no grupo de animais normotensos. Com este estudo conclui-se que o tempo de infecção pelo T. cruzi e o tempo de desenvolvimento da hipertensão interferem, mutualmente, no perfil inflamatório induzido pelo hospedeiro mamífero. No entanto, acredita-se também, que esse estudo fosse reproduzido em outro modelo experimental mais susceptível à infecção pelo T. cruzi, as lesões cardiovasculares seriam mais evidenciadas principalmente numa etapa crônica de ambas as doenças.
Low doses of Simvastatin therapy ameliorate cardiac inflammatory remodeling in Trypanosoma cruzi-Infected dogs.
(2011) Melo, Lilian; Caldas, Ivo Santana; Azevedo, Maíra Araújo; Gonçalves, Karolina Ribeiro; Nascimento, Alvaro Fernando da Silva do; Figueiredo, Vivian Paulino; Diniz, Lívia de Figueiredo; Lima, Wanderson Geraldo de; Torres, Rosália Morais; Bahia, Maria Terezinha; Silva, André Talvani Pedrosa da
Chagas cardiomyopathy remodeling is based on the presence of Trypanosoma cruzi in heart tissue and on the complex inflammatory response leading to a myocardium fibrosis and alterations in conductive and functional heart parameters. This study aims to evaluate Simvastatin on the inflammatory response and heart functionality using dogs infected with Y strain of T. cruzi . Animals were treated daily with Simvastatin (20 mg) for 6 months and submitted to clinical and immunopathological evaluations. Simvastatin reduced heart expression and serum levels of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) but not interleukin-10 (IL-10), possibly favoring blood parasitism but reducing inflammation and fibrosis in the left ventricle and right atrium. Simvastatin also ameliorated ejection fraction, diastolic diameter, and mass index of the left ventricle 6 months after infection. This study suggests that more investigation should be performed on the use of statins as a prophylactic therapy against cardiac remodeling because of their effects on modifying immune response and benefiting functional parameters in dogs with T. cruzi -induced ventricular dysfunctions.
Myocardial scars correlate with eletrocardiographic changes in chronic Trypanosoma cruzi infection for dogs treated with Benznidazole.
(2013) Caldas, Ivo Santana; Guedes, Paulo Marcos da Matta; Santos, Fabiane Matos dos; Diniz, Lívia de Figueiredo; Martins, Tassiane Assíria Fontes; Nascimento, Alvaro Fernando da Silva do; Azevedo, Maíra Araújo; Lima, Wanderson Geraldo de; Nascimento Neto, Raimundo Marques do; Torres, Rosália Morais; Silva, André Talvani Pedrosa da; Bahia, Maria Terezinha
objectives The cardiac form of Chagas disease is evidenced by a progressive cardiac inflammation that leads to myocarditis, fibrosis and electrocardiographic (ECG) conduction abnormalities. Considering these characteristics, the aim of this study was to prospectively evaluate the early ECG changes in dogs that were experimentally inoculated with Benznidazole (Bz)-susceptibly (Berenice-78) and Bz-resistant (VL-10, and AAS) Trypanosoma cruzi strains and, later, evaluate the efficacy of Bz treatment for preventing these ECG alterations. methods Electrocardiographic changes of treated and untreated animals were prospectively evaluated for up to 270 days after infection, at which point collagen (right atrium) quantification was performed. results All infected dogs had a high intensity of heart fibrosis (4616.00 ± 1715.82 collagen ⁄ 74931 lm2 in dogs infected with Berenice-78 strain, 5839.2 ± 1423.49 collagen ⁄ 74931 lm2 in infected by AAS and 6294.40 ± 896.04 collagen ⁄ 74931 lm2 in animals infected with VL-10 strain), while 78.57% of all infected dogs showed ECG alterations. Bz Therapy reduced or prevented fibrosis in Bz-susceptible Berenice-78 (2813.00 ± 607.13 collagen ⁄ 74931 lm2) and Bz-resistant AAS strains (4024 ± 1272.44 collagen ⁄ 74931 lm2), coincident with only 10% de ECG alterations at 270 days. However, in those animals infected with a Bz-resistant VL-10 strain, specific treatment did not alter collagen deposition (6749.5 ± 1596.35 collagen ⁄ 74931 lm2) and there was first atrioventricular block and chamber overload at 120 and 270 days after infection, with 75% abnormal ECG exams. conclusions These findings indicate that an effective antiparasitic treatment in the early stage of Chagas disease can lead to a significant reduction in the frequency and severity of the parasite-induced cardiac disease, even if parasites are not completely eliminated.
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection.
(2018) Silva, M. C.; Azevedo, Maíra Araújo; Figueiredo, Vivian Paulino; Moura Junior, Manoel Ramos de; Coelho Junior, Diógenes; Martinelli, Patrícia Massara; Machado, Raquel do Pilar; Alzamora, Andréia Carvalho; Silva, André Talvani Pedrosa da
Trypanosoma cruzi triggers a progressive inflammatory response affecting cardiovascular functions in humans and experimental models. Angiotensin II, a key effector of the renin-angiotensin system, plays roles in mediating hypertension, heart failure, and inflammatory responses. T. cruzi and AngII can induce inflammatory responses by releasing inflammatory mediators. The aim of this study was to evaluate systemic AngII, tumor necrosis factor (TNF), and CX3CL1 mediators in a two-kidney one-clip (2K1C) renovascular hypertension model using Wistar rats infected with T. cruzi. Our data showed an increase in serum AngII in uninfected and T. cruzi-infected rats 1 week after 2K1C surgery compared to non-2K1C (Sham) animals. The baseline systolic blood pressure was higher in both uninfected and infected 2K1C rats. Despite no difference in circulating parasites in the acute phase of infection, elevated serum TNF and CX3CL1 were observed at 8 weeks post-infection in 2K1C rats in association with higher cardiac inflammatory infiltration. In summary, AngII-induced hypertension associated with T. cruzi infection may act synergistically to increase TNF and CX3CL1 in the 2K1C rat model, thereby intensifying cardiac inflammatory infiltration and worsening the underlying inflammation triggered by this protozoan.
Trypanosoma cruzi infection increases atherosclerotic lesion in ApoE-deficient mice.
(2022) Figueiredo, Vivian Paulino; Silva, Maria Cláudia; Souza, Débora Maria Soares de; Coelho Junior, Diógenes; Lopes, Laís Roquete; Azevedo, Maíra Araújo; Menezes, Ana Paula de Jesus; Lima, Wanderson Geraldo de; Peluzio, Maria do Carmo Gouveia; Silva, André Talvani Pedrosa da
Apolipoprotein E (ApoE) is the major ligand for the transporting and removal of chylomicrons and lipoproteins by the liver. Since the creation of the ApoE-knockout mice, it is well established that ApoE deficiency results in spontaneous atherosclerosis in aged animals. Atherosclerosis is also observed in animals infected with Trypa- nosoma cruzi, a protozoan that elicits a systemic inflammatory response in mammalian hosts, culminating in damage to cardiac, neuronal, and endothelial cells. Pro-atherogenic effects related to the experimental infection with T. cruzi may be induced by inflammatory components affecting the vascular wall. Herein, we evaluated whether infection with different strains of T. cruzi worsened the atherogenic lesions observed in aged ApoE− /− mice. After four weeks of infection with Berenice-78 (Be-78) or Colombian (Col) strains of the parasite, mice presented increased CCL2 and CCL5 production and high migration of inflammatory cells to cardiac tissue. Although the infection with either strain did not affect the survival rate, only the infection with Col strain caused abundant parasite growth in blood and heart and increased aortic root lesions in ApoE− /− mice. Our findings show, for the first time that ApoE exerts a protective anti-atherosclerotic role in the aortic root of mice in the acute phase of experimental infection with the Col strain of T. cruzi. Further studies should target ApoE and nutritional interventions to modulate susceptibility to cardiovascular disabilities after T. cruzi infection, mini- mizing the risk of death in both experimental animals and humans.