Navegando por Autor "Moraes, Michele Macedo"
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Item Acute exercise modulates the inflammatory response in adipose tissue of lean and obese mice.(2023) Lacerda, Débora Romualdo; Silva, Albená Nunes da; Silveira, Ana Letícia Malheiros; Costa, Kátia Anunciação; Rodrigues, Débora Fernandes; Moraes, Michele Macedo; Pinho, Vanessa; Menezes, Gustavo Batista; Teixeira, Mauro Martins; Wanner, Samuel Penna; Soares, Danusa Dias; Ferreira, Adaliene Versiani MatosAcute physical exercise act as a metabolic stressor, promoting activation of the immune system, and this response could be relevant in the adipose tissue remodelling process. In addition, some cytokines have important functions in lipolysis. Since chronic exercise improves obesity-related metabolic and inflammatory dysfunction, herein, we investigated the effect of acute exercise on the inflammatory responses in the adipose tissues of lean and obese mice. Lean mice were fed a standard chow diet, whereas obese mice were fed a high- refined carbohydrate (HC) diet for 8 weeks. Both groups were subjected to 60 min of moderately-intensity exercise. In the epididymal adipose tissue (EAT) of lean mice, exercise enhanced IL-6 and TNF-α levels, which correlated positively with increased serum free fatty acid concentrations. In vivo confocal imaging of EAT vessels revealed higher recruitment of neutrophils following exercise. Also, the number of leucocytes expressing CD11b+F480– was elevated 6 h after exercise. Similarly, the CXCL-1 level increased at 6 h and remained high until 24 h after exercise. Myeloperoxidase activity were increased at 6, 12, and 24 h after exercise. Surprisingly, however, no changes were observed in EAT from obese mice considering pro-inflammatory cytokines (IL-6 and TNF-). On the other hand, IL-13, IL-4, and IL-10 levels were higher in obese mice after exercise. These data suggest that acute exercise promotes an inflammatory response in the adipose tissue of lean mice that is observed as part of its role in adipose tissue remodelling. In contrast, acute exercise promotes an anti-inflammatory response in adipose tissue from obese mice, likely as an important tool for restoring homeostatic.Item Aerobic training reduces immune cell recruitment and cytokine levels in adipose tissue in obese mice.(2018) Lacerda, Débora Romualdo; Moraes, Michele Macedo; Silva, Albená Nunes da; Costa, Kátia Anunciação; Rodrigues, Débora Fernandes; Sabino, Josiana Lopes; Cordeiro, Letícia Maria de Souza; Pinho, Vanessa; Teixeira, Mauro Martins; Wanner, Samuel Penna; Soares, Danusa Dias; Ferreira, Adaliene Versiani MatosObesity is associated with an energy imbalance that results from excessive energy intake, low diet quality and a sedentary lifestyle. In this regard, the increased consumption of a high-refined carbohydrate diet (HC) is strongly related to higher adiposity and low-grade inflammation. Aerobic training is a well-known non-pharmacological intervention to treat obesity and metabolic disturbances. However, the mechanisms through which aerobic training ameliorates the low-grade inflammation induced by the HC diet need to be further investigated. Herein, our hypothesis was that aerobic training would decrease the recruitment of leukocytes in the adipose tissue thereby reducing the levels of cytokines and improving metabolism in mice fed the HC diet. Male Balb/c were assigned to the following groups: control non-trained (C-NT), control trained (C-T), HC-NT and HC-T. Mice were submitted to moderate-intensity training sessions that consisted of running 60 min/day for 8 weeks. The intravital microscopy technique was performed in vivo in anesthetized mice to visualize the microvasculature of the adipose tissue. The HC diet induced obesity and increased the influx of immune cells into the adipose tissue. In contrast, HC-T mice presented a lower adiposity and adipocyte area. Furthermore, HC-T mice showed an increased resting energy expenditure, a decreased recruitment of immune cells in the adipose tissue, reduced cytokine levels, and ameliorated hyperglycemia and fatty liver deposition relative to HC-NT mice. Collectively, our data enhance the understanding about the antiinflammatory effect of aerobic training and shed light on the adipose tissue-mediated mechanisms by which training promotes a healthier metabolic profile.Item Neuronal parasitism, early myenteric neurons depopulation and continuous axonal networking damage as underlying mechanisms of the experimental intestinal Chagas' disease.(2020) Ricci, Mayra Fernanda; Béla, Samantha Ribeiro; Moraes, Michele Macedo; Bahia, Maria Terezinha; Mazzeti, Ana Lia; Oliveira, Anny Carolline Silva; Oliveira, Luciana Souza de; Radi, Rafael; Piacenza, Lucía; Arantes, Rosa Maria EstevesThere is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite’s DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.Item A potential role of cholinergic dysfunction on Impaired Colon Motility in experimental intestinal Chagas disease.(2022) Ricci, Mayra Fernanda; Béla, Samantha Ribeiro; Barbosa, Joana Lobato; Moraes, Michele Macedo; Mazzeti, Ana Lia; Bahia, Maria Terezinha; Horta, Laila Sampaio; Santiago, Helton da Costa; Cruz, Jader dos Santos; Capettini, Luciano dos Santos Aggum; Arantes, Rosa Maria EstevesBackground/Aims Chagasic megacolon is caused by Trypanosoma cruzi, which promotes in several cases, irreversible segmental colonic dilation. This alteration is the major anatomic-clinical disorder, characterized by the enteric nervous system and muscle wall structural damage. Herein, we investigate how T. cruzi-induced progressive colonic structural changes modulate the colonic contractile pattern activity. Methods We developed a murine model of T. cruzi-infection that reproduced long-term modifications of the enlarged colon. We evaluated colonic and total intestinal transit time in animals. The patterns of motor response at several time intervals between the acute and chronic phases were evaluated using the organ bath assays. Enteric motor neurons were stimulated by electric field stimulation. The responses were analyzed in the presence of the nicotinic and muscarinic acetylcholine receptor antagonists. Western blot was performed to evaluate the expression of nicotinic and muscarinic receptors. The neurotransmitter expression was analyzed by real-time polymerase chain reaction. Results In the chronic phase of infection, there was decreased intestinal motility associated with decreased amplitude and rhythmicity of intestinal contractility. Pharmacological tests suggested a defective response mediated by acetylcholine receptors. The contractile response induced by acetylcholine was decreased by atropine in the acute phase while the lack of its action in the chronic phase was associated with tissue damage, and decreased expression of choline acetyltransferase, nicotinic subunits of acetylcholine receptors, and neurotransmitters. Conclusions T. cruzi-induced damage of smooth muscles was accompanied by motility disorders such as decreased intestinal peristalsis and cholinergic system response impairment. This study allows integration of the natural history of Chagasic megacolon motility disorders and opens new perspectives for the design of effective therapeutic.