FRANCINE MARIA DE ALMEIDA
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
7 resultados
Resultados de Busca
Agora exibindo 1 - 7 de 7
- Creatine supplementation attenuates inflammation in collateral lung after left lung transplantation(2019) ALMEIDA, Francine Maria de; BATTOCHIO, Angela Silva; NAPOLI, Joao Pithon; ALVES, Katiusa Abreu; BALBIN, Grace Susana; OLIVEIRA-JUNIOR, Manoel; MORIYA, Henrique Takachi; PEGO-FERNANDES, Paulo; VIEIRA, Rodolfo Paula; PAZETTI, Rogerio
- iNOS Inhibition Reduces Lung Mechanical Alterations and Remodeling Induced by Particulate Matter in Mice(2019) PRADO, Carla Maximo; RIGHETTI, Renato Fraga; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; LEICK, Edna Aparecida; ARANTES-COSTA, Fernanda Magalhaes; ALMEIDA, Francine Maria de; SALDIVA, Paulo Hilario Nascimento; MAUAD, Thais; TIBERIO, Iolanda de Fatima Lopes Calvo; MARTINS, Milton de ArrudaBackground. The epidemiologic association between pulmonary exposure to ambient particulate matter (PM) and acute lung damage is well known. However, the mechanism involved in the effects of repeated exposures of PM in the lung injury is poorly documented. This study tested the hypotheses that chronic nasal instillation of residual oil fly ash (ROFA) induced not only distal lung and airway inflammation but also remodeling. In addition, we evaluated the effects of inducible nitric oxide inhibition in these responses. For this purpose, airway and lung parenchyma were evaluated by quantitative analysis of collagen and elastic fibers, immunohistochemistry for macrophages, neutrophils, inducible nitric oxide synthase (iNOS), neuronal nitric oxide synthase (nNOS), and alveolar septa 8-iso prostaglandin F2 (8-iso-PGF-2) detection. Anesthetized in vivo (airway resistance, elastance, H, G, and Raw) respiratory mechanics were also analyzed. C57BL6 mice received daily 60ul of ROFA (intranasal) for five (ROFA-5d) or fifteen days (ROFA-15d). Controls have received saline (SAL). Part of the animals has received 1400W (SAL+1400W and ROFA-15d+1400W), an iNOS inhibitor, for four days before the end of the protocol. A marked neutrophil and macrophage infiltration and an increase in the iNOS, nNOS, and 8-iso-PGF2 expression was observed in peribronchiolar and alveolar wall both in ROFA-5d and in ROFA-15d groups. There was an increment of the collagen and elastic fibers in alveolar and airway walls in ROFA-15d group. The iNOS inhibition reduced all alterations induced by ROFA, except for the 8-iso-PGF2 expression. In conclusion, repeated particulate matter exposures induce extracellular matrix remodeling of airway and alveolar walls, which could contribute to the pulmonary mechanical changes observed. The mechanism involved is, at least, dependent on the inducible nitric oxide activation.
- Impairment on Cardiopulmonary Function after Marathon: Role of Exhaled Nitric Oxide(2019) SIERRA, Ana Paula; OLIVEIRA-JUNIOR, Manoel Carneiro; ALMEIDA, Francine Maria; BENETTI, Marino; OLIVEIRA, Rodrigo; FELIX, Soraia Nogueira; GENARO, Isabella Santos; ROMANHOLO, Beatriz Mangueira Saraiva; GHORAYEB, Nabil; KISS, Maria Augusta Peduti Dal Molin; CURY-BOAVENTURA, Maria Fernanda; PESQUERO, Joao Bosco; VIEIRA, Rodolfo PaulaBackground. The endurance exercise is capable of inducing skeletal muscle, heart, and respiratory fatigue, evidenced by morphofunctional cardiac changes, release of myocardial injury biomarkers, and reduction of maximal voluntary ventilation and oxygen consumption (VO2) at peak exercise. Purpose. The aim of this study was to investigate whether marathoners present cardiac fatigue after marathon and whether it correlates with pulmonary levels of exhaled nitric oxide (eNO) and pulmonary inflammation. Methods. 31 male marathoners, age 39 +/- 9 years, were evaluated by cardiopulmonary exercise test three weeks before and between three and 15 days after a marathon; eNO analysis and spirometry were evaluated before, immediately after, and 24 and 72 hours after the marathon, and sputum cellularity and cytokine level were assessed before and after the marathon. Results. Marathon induced an increase in the percentage of macrophages, neutrophils (from 0.65% to 4.28% and 6.79% to 14.11%, respectively), and epithelial cells and a decrease in cytokines in induced sputum, followed by an increase in eNO concentration (20 +/- 11 to 35 +/- 19 ppb), which presented a significant reduction 24 and 72 hours after marathon (9 +/- 12 e 12 +/- 9 ppb, p < 0.05). We observed a decrease in the spirometry parameters in all time points assessed after the marathon (p < 0.05) as well as in cardiopulmonary capacity, evidenced by a reduction in VO2 and ventilation peaks (57 +/- 6 to 55 +/- 6 mL.min(-1).Kg(-1 )and 134 +/- 19 to 132 +/- 18 Lpm, respectively, p < 0.05). Finally, we observed a negative correlation between the decrease in forced expiratory volume and decrease in eNO 24 and 72 hours after marathon (r = -0.4, p = 0.05). Conclusion. Reduction in eNO bioavailability after marathon prevents the reduction in cardiopulmonary capacity induced by acute inflammatory pattern after marathon.
- Inflammatory and functional responses after (bio)diesel exhaust exposure in allergic sensitized mice. A comparison between diesel and biodiesel(2019) TIMMERMAN, Tirza; BRITO, Jose Mara de; ALMEIDA, Natalia Madureira de; ALMEIDA, Francine Maria de; ARANTES-COSTA, Fernanda Magalhaes; GUIMARAES, Eliane Tigre; LICHTENFELS, Ana Julia Faria Coimbra; RIVERO, Dolores Helena Rodriguez Ferreira; OLIVEIRA, Regiani Carvalho de; LACERDA, Joao Paulo Amorim de; MORAES, Jamille Moreira; PIMENTAL, Danilo Augusto; SARAIVA-ROMANHOLO, Beatriz Mangueira; SALDIVA, Paulo Hilario Nascimento; VIEIRA, Rodolfo de Paula; MAUAD, ThaisMany cities fail to meet air quality standards, which results in increased risk for pulmonary disorders, including asthma. Human and experimental studies have shown that diesel exhaust (DE) particles are associated with worsening of allergic asthma. Biodiesel (BD), a cleaner fuel from renewable sources, was introduced in the eighties. Because of the reduction in particulate matter (PM) emissions, BD was expected to cause fewer adverse pulmonary effects. However, only limited data on the effect of BD emissions in asthma are available. Objective: Determine whether BD exhaust exposure in allergic sensitized mice leads to different effects on inflammatory and functional responses compared to DE exposure. Methods: Balb/C mice were orotracheally sensitized with House Dust Mite (HDM) or a saline solution with 3 weekly instillations. From day 9 until day 17 after sensitization, they were exposed daily to filtered air (FA), DE and BD exhaust (concentration: 600 mu g/m(3) PM2.5). Lung function, bronchoalveolar lavage fluid (BALF) cell counts, cytokine levels (IL-2, IL-4, IL-5, IL-17, TNF-alpha, TSLP) in the BALF, peribronchiolar eosinophils and parenchymal macrophages were measured. Results: HDM-sensitized animals presented increased lung elastance (p = 0.046), IgG1 serum levels (p = 0.029), peribronchiolar eosinophils (p = 0.028), BALF levels of total cells (p = 0.020), eosinophils (p = 0.028), IL-5 levels (p = 0.002) and TSLP levels (p = 0.046) in BALF. DE exposure alone increased lung elastance (p = 0.000) and BALF IL-4 levels (p = 0.045), whereas BD exposure alone increased BALF TSLP levels (p = 0.004). BD exposure did not influence any parameters after HDM challenge, while DE exposed animals presented increased BALF levels of total cells (p = 0.019), lymphocytes (p = 0.000), neutrophils (p = 0.040), macrophages (p = 0.034), BALF IL-4 levels (p = 0.028), and macrophagic inflammation in the lung tissue (p = 0.037), as well as decreased IgG1 (p = 0.046) and lgG2 (p = 0.043) levels when compared to the HDM group. Conclusion: The results indicate more adverse pulmonary effects of DE compared to BD exposure in allergic sensitized animals.
- Outdoor Endurance Training with Air Pollutant Exposure Versus Sedentary Lifestyle: A Comparison of Airway Immune Responses(2019) SANTOS, Juliana de Melo Batista dos; FOSTER, Roberta; JONCKHEERE, Anne-Charlotte; ROSSI, Marcelo; LUNA JUNIOR, Luiz Antonio; KATEKARU, Catherine Machado; SA, Matheus Cavalcante de; PAGANI, Lucas Guimaraes; ALMEIDA, Francine Maria de; AMARAL, Jonatas do Bussador; VIEIRA, Rodolfo de Paula; BACHI, Andre Luis Lacerda; BULLENS, Dominique Magdalena A.; VAISBERG, MauroAlthough regular exercise-training improves immune/inflammatory status, the influence of air pollutants exposure during outdoor endurance training compared to a sedentary lifestyle has not yet been clarified. This study aimed to compare the immune/inflammatory responses in the airways of street runners and sedentary people after acute and chronic particulate matter (PM) exposure. Forty volunteers (street runners (RUN, n = 20); sedentary people (SED, n = 20)) were evaluated 1 (acute) and 10 (chronic) weeks after PM exposure. Cytokines [interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, IL-13, and IL-17A] in nasal lavage fluid, salivary antibacterial peptides (lactoferrin (LTF), cathelicidin (LL-37), defensin-alpha 1-3), and secretory immunoglobulin A (SIgA), plasma club cell protein (CC16), and fractional exhaled nitric oxide (FeNO) were analyzed. After acute exposure, the RUN group showed lower levels of IL-13, IL-10, and FeNO, but higher defensin-alpha than the SED group. After chronic exposure, the RUN group showed elevation of IFN-gamma, IL-10, IL-17A, and a decrease of FeNO levels, whereas the SED group showed elevation of TNF-alpha, IL-6, IL-10, and a decrease of IL-13 levels. Comparing these groups, the RUN group showed higher levels of SIgA and LTF, and lower FeNO levels than the SED group. In relation to the Th immune response analysis after acute and chronic PM exposure, the RUN group showed a pattern associated with Th1, while in the SED group, a Th2 pattern was found. Both groups showed also a Th17 immune response pattern. Our results allow us to suggest that the immune/inflammatory status of the respiratory tract after acute and chronic PM exposure was improved by the long-standing regular practice of outdoor endurance exercise compared to a sedentary lifestyle.
- Low dose of sodium hypochlorite impair lung function, inflammation and oxidative stress of naive mice(2019) GENARO, Isabella Santos De; SILVA, Stefani Cristina Da; NANNI, Gabriela Delourence; ARAUJO, Lethicia Cristinne Silva; MEDEIROS, Rebeca Roberta Campos; LIEVORE, Giovanna Del Vecchi; ALMEIDA, Francine Maria De; BEZERRA, Suellen Karoline Moreira; KUNZLER, Deborah De Camargo Hizume; LOPES, Fernanda Degobbi Tenorio Quirino Dos Santos; VIEIRA, Rodolfo De Paula; MARTINS, Milton De Arruda; TIBERIO, Iolanda De Fatima Lopes Calvo; SARAIVA-ROMANHOLO, Beatriz Mangueira
- A possible association between fructose consumption and pulmonary emphysema(2019) SUEHIRO, Camila Liyoko; TOLEDO-ARRUDA, Alessandra Choqueta de; VIEIRA, Rodolfo de Paula; ALMEIDA, Francine Maria de; OLIVO, Clarice Rosa; MARTINS, Milton de Arruda; LIN, Chin JiaChronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu.