FERNANDA DEGOBBI TENORIO QUIRINO DOS SANTOS LOPES
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
15 resultados
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- Green Areas and PM2,5 exposure could be associated with Asthma and COPD?(2023) ALMEIDA, Francine Maria; MOREIRA, Tiana Carla Lopes; OLIVEIRA, Lucas Miranda; RIGHETTI, Renato Fraga; LOPES, Fernanda Degobbi Tenorio Quirino Santos; ALENCAR, Airlane P.; GOUVEIA, Nelson; MAUAD, Thais; LOTUFO, Paulo A.; BENSENOR, Isabela; SANTOS, Itamar Souza; TIBERIO, Iolanda Fatima Lopes Calvo
- Respiratory mechanics do not always mirror pulmonary histological changes in emphysema(2011) ANCIAES, Adriana Martins; OLIVO, Clarice Rosa; PRADO, Carla Maximo; KAGOHARA, Keila H.; PINTO, Tatiana da Silva; MORIYA, Henrique T.; MAUAD, Thais; MARTINS, Milton de Arruda; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosOBJECTIVE : To verify the accordance of functional and morphometric parameters during the development of emphysema. METHODS : BALB/c mice received a nasal drop of either papain or saline solution and were studied after 1, 3, 15, 28, and 40 days. Functional parameters, such as airway resistance, tissue damping, and tissue elastance, were analyzed. To evaluate the structural changes and possible mechanisms involved in this disease, we measured the mean linear intercept, the volume proportions of elastic and collagen fibers, the number of macrophages, the numbers of cells expressing metalloprotease 12 and 8-isoprostane in lung parenchyma. RESULTS : We only observed decreases in tissue elastance and tissue damping on the 28(th) day, with a concomitant increase in the mean linear intercept, indicating the presence of emphysema. However, only the mean linear intercept values remained increased until the 40(th) day. The volume proportion of collagen fibers was increased from the 15(th) day to the 40(th) day, whereas the volume proportion of elastic fibers was only increased on the 40(th) day. The number of macrophages increased beginning on the 1(st) day. The expression of metalloproteinase 12 was increased from the 3(rd) day until the 40(th) day. However, 8-isoprostane expression was only increased on the 1(st) and 3(rd) days. CONCLUSIONS : In this study, morphometric parameters were found to be more reliable for detecting the presence of emphysema than the functional parameters measured by respiratory mechanics. Further investigations are necessary to understand how the extracellular matrix remodeling observed in the lung parenchyma could be involved in this process.
- 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.
- Anacardic Acids from Cashew Nuts Ameliorate Lung Damage Induced by Exposure to Diesel Exhaust Particles in Mice(2013) CARVALHO, Ana Laura Nicoletti; ANNONI, Raquel; TORRES, Larissa Helena Lobo; DURAO, Ana Carolina Cardoso Santos; SHIMADA, Ana Lucia Borges; ALMEIDA, Francine Maria; HEBEDA, Cristina Bichels; LOPES, Fernanda Degobbi Tenorio Quirino Santos; DOLHNIKOFF, Marisa; MARTINS, Milton Arruda; SILVA, Luiz Fernando Ferraz; FARSKY, Sandra Helena Poliselli; SALDIVA, Paulo Hilario Nascimento; ULRICH, Cornelia M.; OWEN, Robert W.; MARCOURAKIS, Tania; TREVISAN, Maria Teresa Salles; MAUAD, ThaisAnacardic acids from cashew nut shell liquid, a Brazilian natural substance, have antimicrobial and antioxidant activities and modulate immune responses and angiogenesis. As inflammatory lung diseases have been correlated to environmental pollutants exposure and no reports addressing the effects of dietary supplementation with anacardic acids on lung inflammation in vivo have been evidenced, we investigated the effects of supplementation with anacardic acids in a model of diesel exhaust particle-(DEP-) induced lung inflammation. BALB/c mice received an intranasal instillation of 50 mu g of DEP for 20 days. Ten days prior to DEP instillation, animals were pretreated orally with 50, 150, or 250mg/kg of anacardic acids or vehicle (100 mu L of cashew nut oil) for 30 days. The biomarkers of inflammatory and antioxidant responses in the alveolar parenchyma, bronchoalveolar lavage fluid (BALF), and pulmonary vessels were investigated. All doses of anacardic acids ameliorated antioxidant enzyme activities and decreased vascular adhesion molecule in vessels. Animals that received 50mg/kg of anacardic acids showed decreased levels of neutrophils and tumor necrosis factor in the lungs and BALF, respectively. In summary, we demonstrated that AAs supplementation has a potential protective role on oxidative and inflammatory mechanisms in the lungs.
conferenceObject Histological analysis of compensatory lung growth effects in emphysematous rats after bilobectomy(2013) ALMEIDA, Francine Maria; SARAIVA-ROMANHOLO, Beatriz M.; PAULA, Rodolfo de; MORIYA, Henrique Takachi; LIGEIRO-DE-OLIVEIRA, Ana Paula; LOPES, Fernanda D. Q. S.; MAUAD, Thais; MARTINS, Milton de Arruda; PAZETTI, Rogerio- Regulatory T cells in COPD development: How the animal model resembles the human pathophysiological features(2017) ITO, Juliana Tiyaki; CERVILHA, Daniela Aparecida de Brito; SILVA, Larissa Emidio de Franca; LOURENCO, Juliana Dias; MOREIRA, Alyne Riani; KOHLER, Julia Benini; NEGRI, Elnara Marcia; MACCHIONE, Mariangela; MAUAD, Thais; MARTINS, Milton Arruda; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos
conferenceObject Compensatory lung growth effects on pulmonary mechanics of emphysematous rats after bilobectomy(2013) ALMEIDA, Francine Maria; SARAIVA-ROMANHOLO, Beatriz M.; VIEIRA, Rodolfo de Paula; MORIYA, Henrique Takachi; LIGEIRO-DE-OLIVEIRA, Ana Paula; LOPES, Fernanda D. T. Q. S.; MAUAD, Thais; MARTINS, Milton Arruda; PAZETTI, Rogerio- Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model(2019) ITO, Juliana Tiyaki; CERVILHA, Daniela Aparecida de Brito; LOURENCO, Juliana Dias; GONCALVES, Natalia Gomes; VOLPINI, Rildo Aparecido; CALDINI, Elia Garcia; LANDMAN, Gilles; LIN, Chin Jia; VELOSA, Ana Paula Pereira; TEODORO, Walcy Paganelli Rosolia; TIBERIO, Iolanda de Fatima Lopes Calvo; MAUAD, Thais; MARTINS, Milton de Arruda; MACCHIONE, Mariangela; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosBackground The imbalance between pro- and anti-inflammatory immune responses plays a pivotal role in chronic obstructive pulmonary disease (COPD) development and progression. To clarify the pathophysiological mechanisms of this disease, we performed a temporal analysis of immune response-mediated inflammatory progression in a cigarette smoke (CS)-induced mouse model with a focus on the balance between Th17 and Treg responses. Methods C57BL/6 mice were exposed to CS for 1, 3 or 6 months to induce COPD, and the control groups were maintained under filtered air conditions for the same time intervals. We then performed functional (respiratory mechanics) and structural (alveolar enlargement) analyses. We also quantified the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, or TGF-beta positive cells in peribronchovascular areas and assessed FOXP3 and IL-10 expression through double-label immunofluorescence. Additionally, we evaluated the gene expression of NF-kappa B and TNF in bronchiolar epithelial cells. Results Our CS-induced COPD model exhibited an increased proinflammatory immune response (increased expression of the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, and IL-6 markers) with a concomitantly decreased anti-inflammatory immune response (FOXP3, IL-10, and TGF-beta markers) compared with the control mice. These changes in the immune responses were associated with increased alveolar enlargement and impaired lung function starting on the first month and third month of CS exposure, respectively, compared with the control mice. Conclusion Our results showed that the microenvironmental stimuli produced by the release of cyto-kines during COPD progression lead to a Th17/Treg imbalance.
conferenceObject Effects of early life exposure to concentrated ambient particle on lung function of mice(2013) MENDES-LOPES, Thais; VERAS, Mariana; ALMEIDA, Francine; COSTA, Natalia; LOPES, Fernanda; SALDIVA, Paulo; MAUAD, Thais- Pre- and postnatal exposure of mice to concentrated urban PM2.5 decreases the number of alveoli and leads to altered lung function at an early stage of life(2018) LOPES, Thais de Barros Mendes; GROTH, Espen E.; VERAS, Mariana; FURUYA, Tatiane K.; COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; LOPES, Fernanda Degobbi; ALMEIDA, Francine M. de; CARDOSO, Wellington V.; SALDIVA, Paulo Hilario Nascimento; CHAMMAS, Roger; MAUAD, ThaisGestational exposure to air pollution is associated with negative outcomes in newborns and children. In a previous study, we demonstrated a synergistic negative effect of pre- and postnatal exposure to PM2.5 on lung development in mice. However, the means by which air pollution affects development of the lung have not yet been identified. In this study, we exposed pregnant BALB/c mice and their offspring to concentrated urban PM2.5 (from Sao Paulo, Brazil; target dose 600 mu g/m(3) for 1 h daily). Exposure was started on embryonic day 5.5 (E5.5, time of placental implantation). Lung tissue of fetuses and offspring was submitted to stereological and transcriptomic analyses at E14.5 (pseudoglandular stage of lung development), E18.5 (saccular stage) and P40 (postnatal day 40, alveolarized lung). Additionally, lung function and cellularity of bronchoalveolar lavage (BAL) fluid were studied in offspring animals at P40. Compared to control animals that were exposed to filtered air throughout gestation and postnatal life, PM-exposed mice exhibited higher lung elastance and a lower alveolar number at P40 whilst the total lung volume and cellularity of BAL fluid were not affected. Glandular and saccular structures of fetal lungs were not altered upon gestational exposure; transcriptomic signatures, however, showed changes related to DNA damage and its regulation, inflammation and regulation of cell proliferation. A differential expression was validated at E14.5 for the candidates Sox8, Angptl4 and Gas1. Our data substantiate the in utero biomolecular effect of gestational exposure to air pollution and provide first-time stereological evidence that pre- and early life-postnatal exposure compromise lung development, leading to a reduced number of alveoli and an impairment of lung function in the adult mouse.