NILSA REGINA DAMACENO RODRIGUES
Projetos de Pesquisa
Unidades Organizacionais
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina
33 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 33
- Aerobic Exercise Improves Asthma Phenotype in a Model of Severe Asthma: Involvement of Kinins(2021) BRANDAO-RANGEL, Maysa A. R.; MORAES-FERREIRA, Renilson; SILVA-REIS, Anamei; HUGO, Victor; PALMEIRA, Souza; ALMEIDA, Francine Maria; OLIMPIO, Fabiana Regina Da Silva; AIMBIRE, Flavio; ZAMARIOLI, Lucas Santos; OLIVEIRA, Carlos Rocha; DAMACENO-RODRIGUES, Nilsa Regina; PESQUERO, Joao Bosco; VIEIRA, Rodolfo P.
- A model for preservation of thymocyte-depleted thymus(2023) DIAS, A. S.; DAMACENO-RODRIGUES, N. R.; GIMENEZ, T. M.; OLIVEIRA, P. M.; ZERBINI, M. C.; CARNEIRO-SAMPAIO, M.; FILHO, V. Odone; JATENE, M. B.; VASCONCELOS, D. M.; ROCHA, V.; NOVAK, E. M.DiGeorge syndrome is a disorder caused by a microdeletion on the long arm of chromosome 22. Approximately 1% of patients diagnosed with DiGeorge syndrome may have an absence of a functional thymus, which characterizes the complete form of the syndrome. These patients require urgent treatment to reconstitute T cell immunity. Thymus transplantation is a promising investigational procedure for reconstitution of thymic function in infants with congenital athymia. Here, we demonstrate a possible optimization of the preparation of thymus slices for transplantation through prior depletion of thymocytes and leukocyte cell lineages followed by cryopreservation with cryoprotective media (5% dextran FP 40, 5% Me2SO, and 5% FBS) while preserving tissue architecture. Thymus fragments were stored in liquid nitrogen at -196 & DEG;C for 30 days or one year. The tissue architecture of the fragments was preserved, including the distinction between medullary thymic epithelial cells (TECs), cortical TECs, and Hassall bodies. Moreover, depleted thymus fragments cryopreserved for one year were recolonized by intrathymic injections of 3 x 106 thymocytes per mL, demonstrating the capability of these fragments to support T cell development. Thus, this technique opens up the possibility of freezing and storing large volumes of thymus tissue for immediate transplantation into patients with DiGeorge syndrome or atypical (Omenn-like) phenotype.
- Dietary interesterified fat enriched with palmitic acid induces atherosclerosis by impairing macrophage cholesterol efflux and eliciting inflammation(2016) AFONSO, Milessa Silva; LAVRADOR, Maria Silvia Ferrari; KOIKE, Marcia Kiyomi; CINTRA, Dennys Esper; FERREIRA, Fabiana Dias; NUNES, Valeria Sutti; CASTILHO, Gabriela; GIOIELLI, Luiz Antonio; BOMBO, Renata Paula; CATANOZI, Sergio; CALDINI, Elia Garcia; DAMACENO-RODRIGUES, Nilsa Regina; PASSARELLI, Marisa; NAKANDAKARE, Edna Regina; LOTTENBERG, Ana MariaInteresterified fats are currently being used to replace trans fatty acids. However, their impact on biological pathways involved in the atherosclerosis development was not investigated. Weaning male LDLr-KO mice were fed for 16 weeks on a high-fat diet (40% energy as fat) containing polyunsaturated (PUFA), TRANS, palmitic (PALM), palmitic interesterified (PALM INTER), stearic (STEAR) or stearic interesterified (STEAR INTER). Plasma lipids, lipoprotein profile, arterial lesion area, macrophage infiltration, collagen content and inflammatory response modulation were determined. Macrophage cholesterol efflux and the arterial expression of cholesterol uptake and efflux receptors were also performed. The interesterification process did not alter plasma lipid concentrations. Although PALM INTER did not increase plasma cholesterol concentration as much as TRANS, the cholesterol enrichment in the LDL particle was similar in both groups. Moreover, PALM INTER induced the highest IL-1 beta, MCP-1 and IL-6 secretion from peritoneal macrophages as compared to others. This inflammatory response elicited by PALM INTER was confirmed in arterial wall, as compared to PALM. These deleterious effects of PALM INTER culminate in higher atherosclerotic lesion, macrophage infiltration and collagen content than PALM, STEAR, STEAR INTER and PUFA. These events can partially be attributed to a macrophage cholesterol accumulation, promoted by apoAl and HDL2-mediated cholesterol efflux impairment and increased Olr-1 and decreased Abca1 and Nr1h3 expressions in the arterial wall. Interesterified fats containing palmitic acid induce atherosclerosis development by promoting cholesterol accumulation in LDL particles and macrophagic cells, activating the inflammatory process in LDLr-KO mice.
- Exercise Reduces Lung Fibrosis Involving Serotonin/Akt Signaling(2016) PEREIRA, Paulo Rogerio; OLIVEIRA-JUNIOR, Manoel Carneiro; MACKENZIE, Breanne; CHIOVATTO, Jaime Eduardo Davino; MATOS, Yves; GREIFFO, Flavia Regina; RIGONATO-OLIVEIRA, Nicole Cristine; BRUGEMMAN, Thayse Regina; DELLE, Humberto; IDZKO, Marco; ALBERTINI, Regiane; OLIVEIRA, Ana Paula Ligeiro; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; FERNANDEZ, Isis Ensil; CASTRO-FARIA-NETO, Hugo Caire; DOLHNIKOFF, Marisa; EICKELBERG, Oliver; VIEIRA, Rodolfo PaulaPurpose: Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneumonia, which involves aberrant serotonin (5-hydroxytryptamine [5-HT]) and Akt signaling. As protective effects of chronic aerobic training (AT) have been demonstrated in the context of lung injury, this study investigated whether AT attenuates bleomycin-induced lung fibrosis partly via a reduction of 5-HT and AKT signaling. Methods: Seventy-two C57BL/6 male mice were distributed in Control (Co), Exercise (Ex), Fibrosis (Fi), and Fibrosis + Exercise (Fi + Ex) groups. Bleomycin (1.5 UI.kg(-1)) was administered on day 1 and treadmill AT began on day 15 and continued for 60 min.d(-1), 5 d.wk(-1) for 4 wk. We evaluated total and differential cell counts in bronchoalveolar lavage (BAL), interleukin (IL)-1A, IL-6, CXCL1/KC, IL-10, tumor necrosis factor alpha, and transforming growth factor A levels in BAL, collagen content in lung parenchyma, 5-HT levels in BAL fluid and in serum, the expression of 5-HT2B receptor, and Akt phosphorylation in lung tissue. Results: AT reduced bleomycin-increased number of total cells (P < 0.001), neutrophils (P < 0.01), macrophages (P < 0.01), and lymphocytes (P < 0.05) in BAL. It also reduced the levels of IL-1A (P < 0.01), IL-6 (P < 0.05), CXCL1/KC (P < 0.001), tumor necrosis factor > (P < 0.001), and transforming growth factor A (P < 0.001). It increased expression of ant-inflammatory cytokine IL-10 (P < 0.001). It reduced bleomycin-increased 5-HT levels in BAL (P < 0.001) and in serum (P < 0.05). Reductions in collagen fiber deposition (P < 0.01), 5-HT2B receptor expression (P < 0.01), and Akt phosphorylation in lung tissue were observed. Conclusions: AT accelerates the resolution of lung inflammation and fibrosis in a model of bleomycin-induced lung fibrosis partly via attenuation of 5-HT/Akt signaling.
article 23 Citação(ões) na Scopus Effects of Aerobic Exercise on Molecular Aspects of Asthma: Involvement of SOCS-JAK-STAT(2019) ALMEIDA-OLIVEIRA, A. R.; AQUINO JR., J. C. J.; ABBASI, A.; SANTOS-DIAS, A.; OLIVEIRA JR., M. C.; ALBERCA-CUSTODIO, R. W.; RIGONATO-OLIVEIRA, N. C.; SALLEY-DIAS, L. P.; DAMACENO-RODRIGUES, N. R.; CALDINI, E. G.; ARANTES-COSTA, F. M.; LIGEIRO-OLIVEIRA, A. P.; BELVISI, M. G.; VIEIRA, R. P.Background: Aerobic training (AT) decreases airway inflammation in asthma, but the underlying cellular and molecular mechanisms are not completely understood. Thus, this study evaluated the participation of SOCS-JAK-STAT signaling in the effects of AT on airway inflammation, remodeling and hyperresponsiveness in a model of allergic airway inflammation. Methods: C57Bl/6 mice were divided into Control (Co), Exercise (Ex), HDM (HDM), and HDM+ Exercise (HDM+ Ex). Dermatophagoides pteronyssinus (100ug/mouse) were administered oro-tracheally on days 0, 7, 14, 21, 28, 35, 42 and 49. AT was performed in a treadmill during 4 weeks in moderate intensity, from day 24 until day 52. Results: AT inhibited HDM-induced total cells (p<0.001), eosinophils (p<0.01), neutrophils (p<0.01) and lymphocytes (p<0.01) in BAL, and eosinophils (p<0.01), neutrophils (p<0.01) and lymphocytes (p<0.01) in peribronchial space. AT also reduced BAL levels of IL-4 (p<0.001), IL-5 (p<0.001), IL-13 (p<0.001), CXCL1 (p<0.01), IL-17 (p<0.01), IL-23 (p<0.05), IL-33 (p<0.05), while increased IL-10 (p<0.05). Airway collagen fibers (p<0.01), elastic fibers p<0.01) and mucin (p<0.01) were also reduced by AT. AT also inhibited HDM-induced airway hyperresponsiveness (AHR) to methacholine 6,25mg/ml (p<0.01), 12,5mg/mL (p<0.01), 25mg/mL (p<0.01) and 50mg/mL (p<0.01). Mechanistically, AT reduced the expression of STAT6 (p<0.05), STAT3 (p<0.001), STAT5 (p<0.01) and JAK2 (p<0.001), similarly by peribronchial leukocytes and by airway epithelial cells. SOCS1 expression (p<0.001) was upregulated in leukocytes and in epithelial cells, SOCS2 (p<0.01) was upregulated in leukocytes and SOCS3 down-regulated in leukocytes (p<0.05) and in epithelial cells (p<0.001). Conclusions: AT reduces asthma phenotype involving SOCS-JAK-STAT signaling.- Low level laser therapy reduces acute lung inflammation in a model of pulmonary and extrapulmonary LPS-induced ARDS(2014) OLIVEIRA JR., Manoel Carneiro; GREIFFO, Flavia Regina; RIGONATO-OLIVEIRA, Nicole Cristine; CUSTODIO, Ricardo Wesley Alberca; SILVA, Vanessa Roza; DAMACENO-RODRIGUES, Nilsa Regina; ALMEIDA, Francine Maria; ALBERTINI, Regiane; LOPES-MARTINS, Rodrigo Alvaro B.; OLIVEIRA, Luis Vicente Franco de; CARVALHO, Paulo de Tarso Camillo de; OLIVEIRA, Ana Paula Ligeiro de; LEAL JR., Ernesto Cesar P.; VIEIRA, Rodolfo P.The present study aimed to investigate the effects low level laser therapy (LLLT) in a LPS-induced pulmonary and extrapulmonary acute respiratory distress syndrome (ARDS) in BALB/c mice. Laser (830 nm laser, 9 J/cm(2), 35 mW, 80 s per point, 3 points per application) was applied in direct contact with skin, 1 h after LPS administration. Mice were distributed in control (n = 6; PBS), ARDS IT (n = 7; LPS orotracheally 10 mu g/mouse), ARDS IP (n = 7; LPS intra-peritoneally 100 mu g/mouse), ARDS IT + Laser (n = 9; LPS intra-tracheally 10 mu g/mouse), ARDS IP + Laser (n = 9; LPS intra-peritoneally 100 mu g/mouse). Twenty-four hours after last LPS administration, mice were studied for pulmonary inflammation by total and differential cell count in bronchoalveolar lavage (BAL), cytokines (IL-1 beta, IL-6, KC and TNF-alpha) levels in BAL fluid and also by quantitative analysis of neutrophils number in the lung parenchyma. LLLT significantly reduced pulmonary and extrapulmonary inflammation in LPS-induced ARDS, as demonstrated by reduced number of total cells (p < 0.001) and neutrophils (p < 0.001) in BAL, reduced levels of IL-1 beta, IL-6, KC and TNF-alpha in BAL fluid and in serum (p < 0.001), as well as the number of neutrophils in lung parenchyma (p < 0.001). LLLT is effective to reduce pulmonary inflammation in both pulmonary and extrapulmonary model of LPS-induced ARDS.
- Aerobic exercise inhibits obesity-induced respiratory phenotype(2018) AQUINO-JUNIOR, Jefferson Comin Jonco; MACKENZIE, BreAnne; ALMEIDA-OLIVEIRA, Ana Roberta; MARTINS, Ana Carolina; OLIVEIRA-JUNIOR, Manoel Carneiro; BRITTO, Aurilea Aparecida; ARANTES-COSTA, Fernanda Magalhaes; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; OLIVEIRA, Ana Paula Ligeiro de; GUADAGNINI, Dioze; LEIRIA, Luiz Osorio; RICARDO, Djalma Rabelo; SAAD, Mario Jose Abdalla; VIEIRA, Rodolfo PaulaPurpose: Obesity results in decreased lung function and increased inflammation. Moderate aerobic exercise (AE) reduced lung inflammation and remodeling in a variety of respiratory disease models. Therefore, this study investigated whether AE can attenuate a diet-induced obesity respiratory phenotype; including airway hyperresponsiveness (AHR), remodeling and inflammation.& para;& para;Methods: Sixty C57B1/6 male mice were distributed into four groups: control lean (CL), exercise lean (EL), obese (O) and obese exercise (OE) groups (2 sets of 7 and 8 mice per group; n = 15). A classical model of diet-induced obesity (DIO) over 12 weeks was used. AE was performed 60 min/day, 5 days/week for 5 weeks. Airway hyperresponsiveness (AHR), lung inflammation and remodeling, adipokines and cytokines in bronchoalveolar lavage (BAL) was determined.& para;& para;Results: A high fat diet over 18 weeks significantly increased body weight (p < .0001). Five weeks of AE significantly reduced both AHR and pulmonary inflammation. AHR in obese mice that exercised was reduced at the basal level (p < .05), vehicle (PBS) (p < .05), 6.25 MCh mg/mL (p < .05), 12.5 MCh mg/mL (p < .01), 25 MCh mg/mL (p < .01) and 50 MCh mg/mL (p < .05). Collagen (p < .001) and elastic (p < .001) fiber deposition in airway wall and also smooth muscle thickness (p < .001) were reduced. The number of neutrophils (p < .001), macrophages (p < .001) and lymphocytes (p < .01) were reduced in the peribronchial space as well as in the BAL: lymphocytes (p < .01), macrophages (p < .01), neutrophils (p < .001). AE reduced obesity markers leptin (p < .001), IGF-1 (p < .01) and VEGF (p < .001), while increased adiponectin (p < .01) in BAL. AE also reduced pro-inflammatory cytokines in the SAL: IL-1 beta (p < .001), IL-12p40 (p < .001), IL-13 (p < .01), IL-17 (p < .001, IL-23 (p < .05) and TNF-alpha (p < .05), and increased antiinflammatory cytokine IL-10 (p < .05).& para;& para;Conclusions: Aerobic exercise reduces high fat diet-induced obese lung phenotype (AHR, pulmonary remodeling and inflammation), involving anti-inflammatory cytokine IL-10 and adiponectin.
- Perivascular Innervation in the Nasal Mucosa and Clinical Findings in Patients with Allergic Rhinitis and Idiopathic Rhinitis(2023) CARVALHO, Thiago; JR, Joao Ferreira de Mello; CALDINI, Elia Tamaso Espin Garcia; SALGADO, Daniel Calduro; CARVALHO, Nicole Mary Garcia de; DAMACENO-RODRIGUES, Nilsa Regina; VOEGELS, Richard LouisIntroduction The nonspecific hyperreactivity of rhinitis has been attributed to neurotrophins activating sensory nerves and inflammatory cells. The relationship between these markers and the intensity of the symptoms is not well established and few studies have evaluated individuals with idiopathic rhinitis.Objective The present study aims to evaluate whether perivascular innervation and nerve growth factor (NGF) are related to the intensity of the clinical conditions in allergic rhinitis (AR) and idiopathic rhinitis (IR).Methods A total of 15 patients with AR and 15 patients with IR with the indication for inferior turbinectomy (associated or not with septoplasty) were selected. The patients received a score according to their signs and symptoms. After the surgery, we quantified eosinophils, mast cells, NGF, and nerve fibers in the nasal turbinate.Results The score of the signs and symptoms was higher in the AR group. Nerve growth factor was found in the cytoplasm of inflammatory cells in the submucosa in greater quantity in the AR group. The nerve fibers were distributed throughout the tissue, mainly in the subepithelial, glandular, and vascular regions, and there was no difference between the groups. Greater perivascular innervation was associated with a higher signs and symptoms score.Conclusions We concluded that these findings suggest that the NGF produced by submucosal inflammatory cells stimulates increased perivascular innervation in rhinitis, thus directly reflecting in more intense clinical conditions, especially in AR.
- Anti-inflammatory effects of aerobic exercise in a murine model of asthma: Role of leukotrienes pathway(2015) ALBERCA-CUSTODIO, Ricardo Wesley; GREIFFO, Flavia Regina; OLIVEIRA-JUNIOR, Manoel Carneiro; ANDRADE-SOUSA, Adilson Santos; ARANTES-COSTA, Fernanda Magalhaes; SANTOS, Angela Batista Gomes; DAMACENO-RODRIGUES, Nilsa Regina; CASTRO-FARIA-NETO, Hugo Caire; ABBASI, Asghar; NORTHOFF, Hinnak; IDZKO, Marco; OLIVEIRA, Ana Paula Ligeiro; VIEIRA, Rodolfo P.
conferenceObject Aerobic exercise training reduces asthma phenotype via inhibition of cytokines production in lymphatic organs mediated by P2X7 receptor(2014) GREIFFO, F. R.; CUSTODIO, R. W. A.; OLIVEIRA, N. C. R.; CIPRIANI, F.; DAMACENO-RODRIGUES, N. R.; SOUSA, A. S. A.; OLIVEIRA, A. R. A.; PEREIRA, P. R.; OLIVEIRA-JUNIOR, M. C.; ALBERTINI, R.; OLIVEIRA, A. P. Ligeiro de; VIEIRA, R. P.