DOLORES HELENA RODRIGUEZ FERREIRA RIVERO
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, 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
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article 31 Citação(ões) na Scopus Short-term exposure of mice to cigarette smoke and/or residual oil fly ash produces proximal airspace enlargements and airway epithelium remodeling(2011) BISELLI, P. J. C.; LOPES, F. D. T. Q. S.; MORIYA, H. T.; RIVERO, D. H. R. F.; TOLEDO, A. C.; SALDIVA, P. H. N.; MAUAD, T.; MARTINS, A.Chronic obstructive pulmonary disease (COPD) is associated with inflammatory cell reactions, tissue destruction and lung remodeling. Many signaling pathways for these phenomena are still to be identified. We developed a mouse model of COPD to evaluate some pathophysiological mechanisms acting during the initial stage of the disease. Forty-seven 6- to 8-week-old female C57/BL6 mice (approximately 22 g) were exposed for 2 months to cigarette smoke and/or residual oil fly ash (ROFA), a concentrate of air pollution. We measured lung mechanics, airspace enlargement, airway wall thickness, epithelial cell profile, elastic and collagen fiber deposition, and by immunohistochemistry transforming growth factor-beta 1 (TGF-beta 1), macrophage elastase (MMP12), neutrophils and macrophages. We observed regional airspace enlargements near terminal bronchioles associated with the exposure to smoke or ROFA. There were also increases in airway resistance and thickening of airway walls in animals exposed to smoke. In the epithelium, we noted a decrease in the ciliated cell area of animals exposed to smoke and an increase in the total cell area associated with exposure to both smoke and ROFA. There was also an increase in the expression of TGF-beta 1 both in the airways and parenchyma of animals exposed to smoke. However, we could not detect inflammatory cell recruitment, increases in MMP12 or elastic and collagen fiber deposition. After 2 months of exposure to cigarette smoke and/or ROFA, mice developed regional airspace enlargements and airway epithelium remodeling, although no inflammation or increases in fiber deposition were detected. Some of these phenomena may have been mediated by TGF-beta 1.- Air Pollution's Impact on Cardiac Remodeling in an Experimental Model of Chagas Cardiomyopathy(2022) FONSECA, Keila Cardoso Barbosa; PESSOA, Fernanda Gallinaro; RIBEIRO, Orlando do Nascimento; HOTTA, Viviane Tiemi; IANNI, Barbara Maria; FERNANDES, Fabio; RIVERO, Dolores Helena Rodriguez Ferreira; SALDIVA, Paulo Hilario Nascimento; MADY, Charles; RAMIRES, Felix Jose AlvarezBackgroundChagas disease is characterized by intense myocardial fibrosis stimulated by the exacerbated production of inflammatory cytokines, oxidative stress, and apoptosis. Air pollution is a serious public health problem and also follows this same path. Therefore, air pollution might amplify the inflammatory response of Chagas disease and increase myocardial fibrosis. MethodsWe studied groups of Trypanosoma cruzi infected Sirius hamsters (Chagas=CH and Chagas exposed to pollution=CH+P) and 2 control groups (control healthy animals=CT and control exposed to pollution=CT+P). We evaluated acute phase (60 days post infection) and chronic phase (10 months). Echocardiograms were performed to assess left ventricular systolic and diastolic diameter, in addition to ejection fraction. Interstitial collagen was measured by morphometry in picrosirius red staining tissue. The evaluation of inflammation was performed by gene and protein expression of cytokines IL10, IFN-gamma, and TNF; oxidative stress was quantified by gene expression of NOX1, MnSOD, and iNOS and by analysis of reactive oxygen species; and apoptosis was performed by gene expression of BCL2 and Capsase3, in addition to TUNEL analysis. ResultsChagas groups had increased collagen deposition mainly in the acute phase, but air pollution did not increase this deposition. Also, Chagas groups had lower ejection fraction in the acute phase (p = 0.002) and again air pollution did not worsen ventricular function or dilation. The analysis of the inflammation and oxidative stress pathways were also not amplified by air pollution. Apoptosis analysis showed increased expression of BCL2 and Caspase3 genes in chagasic groups in the acute phase, with a marginal p of 0.054 in BCL2 expression among infected groups, and TUNEL technique showed amplified of apoptotic cells by pollution among infected groups. ConclusionsA possible modulation of the apoptotic pathway was observed, inferring interference from air pollution in this pathway. However, it was not enough to promote a greater collagen deposition, or worsening ventricular function or dilation caused by air pollution in this model of Chagas cardiomyopathy.
- 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.
- Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution(2012) VIEIRA, Rodolfo de Paula; TOLEDO, Alessandra Choqueta; SILVA, Lucas Bogaz; ALMEIDA, Francine Maria; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; SANTOS, Angela Batista Gomes; RIVERO, Dolores Helena; HIZUME, Deborah Camargo; LOPES, Fernanda Degobbi Tenorio Quirino Santos; OLIVO, Clarice Rosa; CASTRO-FARIA-NETO, Hugo Caire; MARTINS, Milton Arruda; SALDIVA, Paulo Hilario Nascimento; DOLHNIKOFF, MarisaPurpose: Exposure to diesel exhaust particles (DEP) results in lung inflammation. Regular aerobic exercise improves the inflammatory status in different pulmonary diseases. However, the effects of long-term aerobic exercise on the pulmonary response to DEP have not been investigated. The present study evaluated the effect of aerobic conditioning on the pulmonary inflammatory and oxidative responses of mice exposed to DEP. Methods: BALB/c mice were subjected to aerobic exercise five times per week for 5 wk, concomitantly with exposure to DEP (3 mg.mL (1); 10 mu L per mouse). The levels of exhaled nitric oxide, reactive oxygen species, cellularity, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were analyzed in bronchoalveolar lavage fluid, and the density of neutrophils and the volume proportion of collagen fibers were measured in the lung parenchyma. The cellular density of leukocytes expressing IL-1 beta, keratinocyte chemoattractant (KC), and TNF-alpha in lung parenchyma was evaluated with immunohistochemistry. The levels of IL-1 beta, KC, and TNF-alpha were also evaluated in the serum. Results: Aerobic exercise inhibited the DEP-induced increase in the levels of reactive oxygen species (P < 0.05); exhaled nitric oxide (P < 0.01); total (P < 0.01) and differential cells (P < 0.01); IL-6 and TNF-alpha levels in bronchoalveolar lavage fluid (P < 0.05); the level of neutrophils (P < 0.001); collagen density in the lung parenchyma (P < 0.05); the levels of IL-6, KC, and TNF-alpha in plasma (P < 0.05); and the expression of IL-1 beta, KC, and TNF-alpha by leukocytes in the lung parenchyma (P < 0.01). Conclusions: We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.
- In vivo assessment of antiretroviral therapy-associated side effects(2014) RAMOS-SANCHEZ, Eduardo Milton; GOTO, Hiro; RIVERO, Dolores Helena Rodriguez Ferreira; MAUAD, Thais; SOUZA, Fernando Nogueira de; MONTEIRO, Andrea Moreira; GIDLUND, MagnusAntiretroviral therapy has been associated with side effects, either from the drug itself or in conjunction with the effects of human immunodeficiency virus infection. Here, we evaluated the side effects of the protease inhibitor (PI) indinavir in hamsters consuming a normal or high-fat diet. Indinavir treatment increased the hamster death rate and resulted in an increase in triglyceride, cholesterol and glucose serum levels and a reduction in anti-oxLDL auto-antibodies. The treatment led to histopathological alterations of the kidney and the heart. These results suggest that hamsters are an interesting model for the study of the side effects of antiretroviral drugs, such as PIs.
- Acute exposure to diesel and sewage biodiesel exhaust causes pulmonary and systemic inflammation in mice(2018) BRITO, Jose Mara de; MAUAD, Thais; CAVALHEIRO, Guilherme Franco; YOSHIZAKI, Kelly; ANDRE, Paulo Afonso de; LICHTENFELS, Ana Julia F. C.; GUIMARAES, Eliane Tigre; RIVERO, Dolores Helena Rodriguez Ferreira; ANTONANGELO, Leila; OLIVEIRA, Luciano Basto; PEDROSO, Luiz Roberto Martins; MACCHIONE, Mariangela; SALDIVA, Paulo Hilario NascimentoBiodiesel is a renewable energy source that reduces particle emission, but few studies have assessed its effects. To assess the effects of acute inhalation of two doses (600 and 1200 mu g/m(3)) of diesel (DE) and biodiesel (BD) fuels on the inflammatory pulmonary and systemic profile of mice. Animals were exposed for 2 h in an inhalation chamber inside the Container Laboratory for Fuels. Heart rate, heart rate variability (HRV) and blood pressure were determined 30 min after exposure. After 24 h. we analyzed the lung inflammation using bronchoalveolar lavage fluid (BALF); neutrophil and macrophage quantification in the lung parenchyma was performed, and blood and bone marrow biomarkers as well as receptor of endothelin-A (ET-Ar), receptor of endothelin-B (ET-Br), vascular cell adhesion molecule 1 (VCAM-1), inducible nitric oxide synthase (iNOs) and isoprostane (ISO) levels in the pulmonary vessels and bronchial epithelium were evaluated. HRV increased for BD600, D600 and D1200 compared to filtered air (FA). Both fuels (DE and BD) produced alterations in red blood cells independent of the dose. BALI from the BD600 and BD1200 groups showed an increase in neutrophils compared to those of the FA group. Numeric density of the polyrnorphonuclear and mononudear cells was elevated with BD600 compared to FA. In the peribronchiolar vessels, there was an increase in ET-Ar and ET-Br expression following BD600 compared to IA; and there was a reduction in the iNOs expression for BD1200 and the VCAM-1 for D1200 compared to FA. In the bronchial epithelium, there was an increase in ETAr at BD600, ET-Br at two doses (600 and 1200 mu g/m(3)) of DE and BD, iNOs at D600 and VCAM-1 at BD1200 and D600; all groups were compared to the FA group. Acute exposure to DE and BD derived from sewage methyl esters triggered pulmonary and cardiovascular inflammatory alterations in mice.
- The effects of exercise training on the lungs and cardiovascular function of animals exposed to diesel exhaust particles and gases(2022) OLIVO, C. R.; CASTRO, T. B. P.; RIANE, A.; REGONHA, T.; RIVERO, D. H. R. F.; VIEIRA, R. P.; SARAIVA-ROMANHOLO, B. M.; LOPES, F. D. T. Q. S.; TIBERIO, I. F. L. C.; MARTINS, M. A.; PRADO, C. M.Air pollution has been identified as one of the main environmental risks to health. Since exercise training seems to act as an anti-inflammatory modulator, our hypothesis is that exercise training prevents damage to respiratory and cardiovascular function caused by diesel exhaust particle (DEP) exposure. This study aimed to evaluate whether aerobic exercise training prior to DEP exposure prevents inflammatory processes in the pulmonary and cardiovascular systems. Therefore, BALB/C male mice were or were not submitted to a 10-week exercise training protocol (5x/week, 1 h/d), and after four weeks, they were exposed to DEP in a chamber with 24 mu g/m3 PM2.5 or filtered air. Heart rate variability, lung mechanics and bronchoalveolar lavage fluid, cytokines and polymorphonuclear cells in the lung parenchyma were evaluated. Exposure to DEPs reduced heart rate variability and the elastance of the respiratory system and increased the number of cells in bronchoalveolar lavage fluid, as well as macrophages, neutrophils and lymphocytes, the density of polymorphonuclear cells and the proportion of collagen fibres in the lung parenchyma. Additionally, DEP-exposed animals showed increased expression of IL-23 and IL-12p40 (proinflammatory cytokines) and inducible nitric oxide synthase. Exercise training avoided the increases in all these inflammatory parameters, except the elastance of the respiratory system, the amount of collagen fibres and the expression of inducible nitric oxide synthase. Additionally, trained animals showed increased expression of the anti-inflammatory cytokine IL-1ra. Although our data showed a reduction in proinflammatory markers and an increase in markers of the anti-inflammatory pathway, these changes were not sufficient to prevent damage to the lung and cardiovascular function induced by DEPs. Based on these data, we propose that aerobic exercise training prevents the lung inflammatory process induced by DEPs, although it was not sufficient to avoid chronic damage, such as a loss of lung function or cardiovascular events.
- Acute cardiopulmonary effects induced by the inhalation of concentrated ambient particles during seasonal variation in the city of Sao Paulo(2014) BRITO, Jose Mara de; MACCHIONE, Mariangela; YOSHIZAKI, Kelly; TOLEDO-ARRUDA, Alessandra Choqueta; SARAIVA-ROMANHOLO, Beatriz Mangueira; ANDRADE, Maria de Fatima; MAUAD, Thais; RIVERO, Dolores Helena Rodriguez Ferreira; SALDIVA, Paulo Hilario NascimentoAmbient particles may undergo modifications to their chemical composition as a consequence of climatic variability. The determination of whether these changes modify the toxicity of the particles is important for the understanding of the health effects associated with particle exposure. The objectives were to determine whether low levels of particles promote cardiopulmonary effects, and to assess if the observed alterations are influenced by season. Mice were exposed to 200 mu g/m(3) concentrated ambient particles (CAPs) and filtered air (FA) in cold/dry and warm/humid periods. Lung hyperresponsiveness, heart rate, heart rate variability, and blood pressure were evaluated 30 min after each exposure. After 24 h, blood and tissue samples were collected. During both periods (warm/humid and cold/dry), CAPs induced alterations in red blood cells and lung inflammation. During the cold/dry period, CAPs reduced the mean corpuscular volume levels and increased erythrocytes, hemoglobin, mean corpuscular hemoglobin concentration, and red cell distribution width coefficient variation levels compared with the FA group. Similarly, CAPs during the warm/humid period decreased mean corpuscular volume levels and increased erythrocytes, hemoglobin, hematocrit, and red cell distribution width coefficient variation levels compared with the FA group. CAPs during the cold/dry period increased the influx of neutrophils in the alveolar parenchyma. Short-term exposure to low concentrations of CAPs elicited modest but significant pulmonary inflammation and, to a lesser extent, changes in blood parameters. In addition, our data support the concept that changes in climate conditions slightly modify particle toxicity because equivalent doses of CAPs in the cold/dry period produced a more exacerbated response.
- Mucociliary transport, differential white blood cells, and cyto-genotoxicity in peripheral erythrocytes in fish from a polluted urban pond(2018) SILVA, Edison Bezerra da; CORREA, Sandra Aparecida da Silva; ABESSA, Denis Moledo de Souza; SILVA, Bruno Ferreira Xavier da; RIVERO, Dolores Helena Rodriguez Ferreira; SERIANI, RobsonThe present study evaluated the water quality of a polluted pond through the analysis of in vitro mucociliary transport, hematological parameters, and biomarkers of cyto-genotoxicity in the Nile tilapia (Oreochromis niloticus). Blood and mucus samples were collected from ten specimens from the polluted pond and from ten specimens from a control area. The fish were anesthetized with 3% benzocaine, mucus was collected directly from the gills, and blood was drawn from the caudal artery. Blood smears were stained using the May-Grunwald Giemsa process for the differential leukocyte counts and to determine the frequency of leukocytes, thrombocytes, erythroblasts, micronuclei, and nuclear abnormalities. The results revealed low transportability in vitro, a high percentage of monocytes and eosinophils, and increased frequency of leukocytes and nuclear abnormalities in fish from the polluted pond. However, the frequency of thrombocytes and erythroblasts and the percentage of lymphocytes and neutrophils were significantly lower. It is possible to conclude that changes in fish are due to poor water quality and that these non-destructive biomarkers can be used for the biomonitoring of aquatic environments vulnerable to contamination.
- Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model(2020) MOREIRA, Alyne Riani; CASTRO, Thamyres Barros Pereira de; KOHLER, Julia Benini; ITO, Juliana Tiyaki; SILVA, Larissa Emidio de Franca; LOURENCO, Juliana Dias; ALMEIDA, Rafael Ribeiro; SANTANA, Fernanda Roncon; BRITO, Jose Mara; RIVERO, Dolores Helena Rodriguez Ferreira; VALE, Maria Isabel Cardoso Alonso; PRADO, Carla Maximo; CAMARA, Niels Olsen Saraiva; SALDIVA, Paulo Hilario Nascimento; OLIVO, Clarice Rosa; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosChronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions. M1 macrophages are recognized by their proinflammatory activity, whereas M2 macrophages play pivotal roles in responding to microorganisms and in efferocytosis to avoid the progression of inflammatory conditions. To verify how exposure to air pollutants interferes with macrophage polarization in emphysema development, we evaluated the different macrophage phenotypes in a PPE-induced model with the exposure to diesel exhaust particles. C57BL/6 mice received intranasal instillation of porcine pancreatic elastase (PPE) to induce emphysema, and the control groups received saline. Both groups were exposed to diesel exhaust particles or filtered air for 60 days according to the groups. We observed that both the diesel and PPE groups had an increase in alveolar enlargement, collagen and elastic fibers in the parenchyma and the number of macrophages, lymphocytes and epithelial cells in BAL, and these responses were exacerbated in animals that received PPE instillation prior to exposure to diesel exhaust particles. The same response pattern was found inCaspase-3 positive cell analysis, attesting to an increase in cell apoptosis, which is in agreement with the increase in M2 phenotype markers, measured by RT-PCR and flow cytometry analysis. We did not verify differences among the groups for the M1 phenotype. In conclusion, our results showed that both chronic exposure to diesel exhaust particles and PPE instillation induced inflammatory conditions, cell apoptosis and emphysema development, as well as an increase in M2 phenotype macrophages, and the combination of these two factors exacerbated these responses. The predominance of the M2-like phenotype likely occurred due to the increased demand for efferocytosis. However, M2 macrophage activity was ineffective, resulting in emphysema development and worsening of symptoms.