Browsing by Author "Vieira, Etel Rocha"
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Item Avaliação do estresse oxidativo e defesas antioxidantes na infecção pelo vírus Oropouche em modelo animal.(2023) Menegatto, Marília Bueno da Silva; Magalhães, Cíntia Lopes de Brito; Magalhães, Cíntia Lopes de Brito; Ferreira, Jaqueline Maria Siqueira; Vieira, Etel Rocha; Silva, André Talvani Pedrosa da; Bezerra, Frank SilvaO Oropouche orthobunyavirus (OROV) é o arbovírus causador da Febre Oropouche, cujos sintomas são febre alta, cefaléia, mialgia, artralgia, fotofobia, tontura, náuseas e vômito. Mais de meio milhão de pessoas já foram infectadas com o OROV desde seu isolamento em 1955, sendo a Febre Oropouche uma doença negligenciada de caráter emergente. Até o momento não há medicamentos antivirais ou vacinas disponíveis contra a infecção e ainda, pouco se sabe sobre os mecanismos envolvidos em sua patogenicidade. Assim, estudos que busquem entender os mecanismos envolvidos na patogênese do OROV são de extrema importância. Nesse sentido, dados da literatura vêm demonstrando que o estresse oxidativo pode estar envolvido na patogênese de vários agentes virais, dentre alguns arbovírus como Dengue, Zika, Chikungunya e Mayaro. O estresse oxidativo é a condição que se estabelece quando há um desequilíbrio entre os oxidantes, como as “Espécies Reativas de Oxigênio” (ERO), e os antioxidantes, como as enzimas Superóxido Dismutase (SOD) e Catalase (CAT), a favor dos oxidantes. Sendo assim, este estudo teve como objetivo investigar em modelo animal, a homeostase redox em órgãos alvos da infecção. Primeiramente camundongos BALB/c de 21 dias de vida foram infectados via subcutânea com 6x106 Unidades Formadoras de Placas (UFP) do OROV e monitorados por 21 dias quanto ao desenvolvimento da doença e sobrevida. Os animais desenvolveram doença aguda autolimitada, com menor ganho de peso entre os dias 2 e 5, sem mortalidade. Para os próximos experimentos, os animais foram infectados da mesma forma e eutanasiados no 4o dia pós infecção (dpi). Ao final desse período, os animais infectados apresentaram aumento significativo do baço, leucopenia, anemia e trombocitopenia. Ainda, desenvolveram anticorpos neutralizantes anti-OROV, aumento dos níveis séricos das transaminases hepáticas (AST/ALT) e das citocinas pró-inflamatórias Fator de Necrose Tumoral alfa (TNF-α) e Interferon-γ (IFN-γ). O genoma do OROV e partículas virais infecciosas foram detectados no fígado e baço dos animais. A histopatologia revelou inflamação hepática e aumento do número e área total de nódulos linfóides no baço. No que diz respeito à homeostase redox, a infecção pelo OROV levou a um aumento dos níveis de ERO e dos biomarcadores de estresse oxidativo malondialdeído (MDA) e proteína carbonilada no fígado e baço. Ainda, nesses mesmos órgãos, a infecção pelo OROV levou a uma diminuição nas atividades das enzimas SOD e CAT. Juntos, estes resultados mostram que a infecção pelo OROV culmina com desequilíbrio na homeostase redox e consequente estresse oxidativo em órgãos alvos da infecção, ajudando a elucidar alguns aspectos importantes que podem contribuir na patogênese da Febre Oropouche.Item Divergent cytokine response following maximum progressive swimming in hot water.(2011) Azevedo, Ana Carolina Campi; Cleto, Lorena Sabino; Silva, Renata Sabino da; Franco, Junia de Sousa; Magalhães, José Carlos de; Penaforte, Claudia Lopes; Pinto, Kelerson Mauro de Castro; Vieira, Etel RochaExercise promotes transitory alterations in cytokine secretion, and these changes are affected by exercise duration and intensity. Consideringthat exercise responses also are affected by environmental factors, the goal of the present study was to investigate the effect of watertemperature on the cytokine response to maximum swimming. Swiss mice performed a maximum progressive swimming exercise at 31 or38C, and plasma cytokine levels were evaluated immediately or 1, 6 or 24 h after exercise. The cytokine profile after swimming at 31Cwas characterized by increased interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1) levels, which peaked 1 h after exercise, sug-gesting an adequate inflammatory milieu to induce muscle regeneration. Transitory reductions in IL-10 and IL-12 levels also were observedafter swimming at 31C. The cytokine response to swimming was modified when the water temperature was increased to 38C. Althoughexercise at 38C also led to IL-6 secretion, the peak in IL-6 production occurred 6 h after exercise, and IL-6 levels were significantly lowerthan those observed after maximum swimming at 31C(p =0030). Furthermore, MCP-1 levels were lower and tumour necrosis factor-alevels were higher immediately after swimming at 38C, suggesting a dysregulated pro-inflammatory milieu. These alterations in the cyto-kine profile can be attributed in part to reduced exercise total work because exhaustion occurred sooner in mice swimming at 38C than inthose swimming at 31oC.Item Germ-free mice produce high levels of interferon-gamma in response to infection with Leishmania major but fail to heal lesions.(2005) Oliveira, Marcia Rosa de; Tafuri, Wagner Luiz; Afonso, Luís Carlos Crocco; Oliveira, Milton Adriano Pelli de; Nicoli, Jacques Robert; Vieira, Etel Rocha; Scott, Phillip; Melo, Maria Norma; Vieira, Leda QuerciaIn order to investigate the importance of the host microbiota on differentiation of T cell subsets in response to infection, Swiss/NIH germ-free mice and conventional (microbiota-bearing) mice were infected with Leishmania major, and lesion development, parasite loads, and cytokine production were assessed. Germ-free mice failed to heal lesions and presented a higher number of parasites at the site of infection than their conventional counterparts. In addition, histopathological analysis indicated a higher density of parasitized macrophages in lesions from germ-free mice than in conventional mice. The initial production of interleukin (IL)-12 and interferon-gamma (IFN-c) in germ-free mice was comparable to the conventional controls. Also, germ-free mice produced elevated levels of IFN-c and lower levels of IL-4 throughout the course of infection, suggesting the development of a Th1 response. Macrophages from germ-free mice exposed to IFN-c and infected with amastigotes in vitro were not as efficient at killing parasites as macrophages from conventional animals. These observations indicate that the microbiota is not essential for the development of Th1 immune responses, but seems to be important for macrophage activation.Item IL-33 in obesity : where do we go from here?(2019) Oliveira, Marcos Felipe Andrade de; Silva, André Talvani Pedrosa da; Vieira, Etel RochaIL-33 is a cytokine that belongs to the IL-1 family and is classically associated with type 2-like immune responses. In the adipose tissue, IL-33 is related to the beiging of adipocytes and to the maintenance of adipose tissue-resident immune cells, such as innate lymphoid cells 2, alternatively activated macrophages and regulatory T cells, which contribute to the maintenance of adipose tissue homeostasis. In the obese adipose tissue, the number of these cells is diminished, unlike the expression of IL-33, which is up-regulated. However, despite its increased expression, IL-33 is not able to maintain the homeostasis of the obese adipose tissue. IL-33 treatment, on the other hand, highly improves obesity-related inflammatory and metabolic alterations. The evidence that exogenous IL-33, but not adipose tissue-driven IL-33, regulates the inflammatory process in obesity leaves a gap in the understanding of IL-33 biology. Thus, in this review we discuss the potential mechanisms associated with the impaired action of IL-33 in obesity.Item Plasma cytokine response, lipid peroxidation and NF-κB activation in skeletal muscle following maximum progressive swimming.(2011) Cleto, Lorena Sabino; Oleto, A. F.; Sousa, L. P.; Barreto, Tatiane Oliveira; Cruz, Jader dos Santos; Penaforte, Claudia Lopes; Magalhães, José Carlos de; Franco, Junia de Sousa; Pinto, Kelerson Mauro de Castro; Azevedo, Ana Carolina Campi; Vieira, Etel RochaOur objective was to determine lipid peroxidation and nuclear factor-κB (NF-κB) activation in skeletal muscle and the plasma cytokine profile following maximum progressive swimming. Adult male Swiss mice (N = 15) adapted to the aquatic environment were randomly divided into three groups: immediately after exercise (EX1), 3 h after exercise (EX2) and control. Animals from the exercising groups swam until exhaustion, with an initial workload of 2% of body mass attached to the tail. Control mice did not perform any exercise but were kept immersed in water for 20 min. Maximum swimming led to reactive oxygen species (ROS) generation in skeletal muscle, as indicated by increased thiobarbituric acid reactive species (TBARS) levels (4062.67 ± 1487.10 vs 19,072.48 ± 8738.16 nmol malondialdehyde (MDA)/mg protein, control vs EX1). Exercise also promoted NF-κB activation in soleus muscle. Cytokine secretion following exercise was marked by increased plasma interleukin-6 (IL-6) levels 3 h post-exercise (P < 0.05). Interleukin-10 (IL-10) levels were reduced following exercise and remained reduced 3 h post-exercise (P < 0.05). Plasma levels of other cytokines investigated, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-12 (IL-12), were not altered by exercise. The present findings showed that maximum swimming, as well as other exercise models, led to lipid peroxidation and NF-κB activation in skeletal muscle and increased plasma IL-6 levels. The plasma cytokine response was also marked by reduced IL-10 levels. These results were attributed to exercise type and intensity.Item Similar inflammatory adaptation in women following 10 weeks of two equalized resistance training with different muscle action duration.(2022) Pinto, Kelerson Mauro de Castro; Diniz, Rodrigo César Ribeiro; Tourino, Frank Douglas; Lacerda, Lucas Túlio de; Bearzoti, Eduardo; Costa, Karine Beatriz; Souza, Débora Maria Soares de; Lima, Fernando Vitor; Vieira, Etel Rocha; Chagas, Mauro Heleno; Silva, André Talvani Pedrosa daThis study is aimed at evaluating the profile of inflammatory markers and components of redox regulation in untrained women after 10 weeks of resistance training using equalized protocols but different muscle action duration (MAD). Twenty-two women underwent progressive resistance training exercising the knee extensor muscles for 10 weeks—3x/week, with 3-5 sets of 6 repetitions at 50% of the 1 repetition maximum strength test (1RM), with a rest of 180 s between the series, following the training protocol (i) 5 s of concentric muscle action for 1 s of eccentric muscle action (5C-1E) and (ii) 1 s of concentric muscle action for 5 s of eccentric muscle action (1C-5E). Quadriceps muscle hypertrophy maximum strength (1RM) and redox regulation/muscle damage/inflammatory markers (CAT, SOD, TBARS, FRAP, CH, LDH, CXCL8, and CCL2) were evaluated. Plasma markers were evaluated before and 30 minutes after the first and last training sessions. A similar gain in hypertrophy and maximum strength was observed in both groups. However, in the 5C-1E, a significant major effect was observed for SOD (F1:19 = 10:480, p = 0:004) and a significant major time effect, with a reduction in the last training session, was observed for CXCL8 (F1:37 = 27:440, p < 0:001). In conclusion, similar protocols of resistance training, with different MAD, produced similar inflammatory and adaptive responses to strength training. As the training load is progressive, the maintenance of this inflammatory and redox regulation profile suggests an adaptive response to the proposed strength training.Item Swim training does not protect mice from skeletal muscle oxidative damage following a maximum exercise test.(2011) Barreto, Tatiane Oliveira; Cleto, Lorena Sabino; Gioda, Carolina Rosa; Silva, Renata Sabino da; Azevedo, Ana Carolina Campi; Franco, Junia de Sousa; Magalhães, José Carlos de; Penaforte, Claudia Lopes; Pinto, Kelerson Mauro de Castro; Cruz, Jader dos Santos; Vieira, Etel RochaWe investigated whether swim training protects skeletal muscle from oxidative damage in response to a maximum progressive exercise. First, we investigated the effect of swim training on the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the gastrocnemius muscle of C57Bl/6 mice, 48 h after the last training session. Mice swam for 90 min, twice a day, for 5 weeks at 31C (±1C). The activities of SOD and CAT were increased in trained mice (P\0.05) compared to untrained group. However, no effect of training was observed in the activity of GPx. In a second experiment, trained and untrained mice were submitted to a maximum progressive swim test. Compared to control mice (untrained, not acutely exercised), malondialdehyde (MDA) levels were increased in the skeletal muscle of both trained and untrained mice after maximum swim. The activity of GPx was increased in the skeletal muscle of both trained and untrained mice, while SOD activity was increased only in trained mice after maximum swimming. CAT activity was increased only in the untrained compared to the control group. Although the trained mice showed increased activity of citrate synthase in skeletal muscle, swim performance was not different compared to untrained mice. Our results show an imbalance in the activities of SOD, CAT and GPx in response to swim training, which could account for the oxidative damage observed in the skeletal muscle of trained mice in response to maximum swim, resulting in the absence of improved exercise performance.