MARIANA MATERA VERAS
Projetos de Pesquisa
Unidades Organizacionais
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder
26 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 26
- Assessing socioeconomic bias of exposure to urban air pollution: an autopsy-based study in Sao Paulo, Brazil(2023) SINGER, Julio da Motta; ANDRE, Carmen Diva Saldiva de; ANDRE, Paulo Afonso de; ROCHA, Francisco Marcelo Monteiro; WAKED, Dunia; VAZ, Aline Macedo; GOIS, Gustavo Ferreira; ANDRADE, Maria de Fatima; VERAS, Mariana Matera; SALDIVA, Paulo Hilario Nascimento; BARROZO, Ligia VizeuBackground The characterisation of individual exposure to air pollution in urban scenarios is a challenge in environmental epidemiological studies. We investigated if the city's pollution monitoring stations over or underes-timate the exposure of individuals depending on their socioeconomic conditions and daily commuting times. Methods The amount of black carbon accumulated in the lungs of 604 deceased who underwent autopsy in Sao Paulo was considered as a proxy for PM10. The concentrations of PM10 in the residence of the deceased were estimated by interpolating an ordinary kriging model. These two-exposure metrics allowed us to construct an environmental exposure misclassification index ranging from -1 to 1. The association between the index and daily commuting, socioeconomic context index (GeoSES), and street density as predictors was assessed by means of a multilevel linear regression model. Findings With a decrease of 0.1 units in GeoSES, the index increases, on average, by 0.028 units and with an increase of 1 h in daily commuting, the index increases, on average, by 0.022 units indicating that individual exposure to air pollution is underestimated in the lower GeoSES and in people with many hours spent in daily commuting. Interpretation Reduction of health consequences of air pollution demands not only alternative fuel and more efficient mobility strategies, but also should include profound rethink of cities.
- Early and late pulmonary effects of nebulized LPS in mice: An acute lung injury model(2017) COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; ALEMANY, Adair Aparecida dos Santos; BELOTTI, Luciano; ZATI, Douglas Hidalgo; CAVALCANTE, Marcela Frota; VERAS, Mariana Matera; RIBEIRO, Susan; KALLAS, Esper Georges; SALDIVA, Paulo Hilario Nascimento; DOLHNIKOTT, Marisa; SILVA, Luiz Fernando Ferraz daBackground and objective Acute respiratory distress syndrome (ARDS) has a high mortality rate of 35 - 46% depending on its severity. Animal models are crucial to better understand the pathophysiology of diseases, including ARDS. This study presents a feasible animal model of acute lung injury (ALI) using nebulized lipopolysaccharide (LPS) in a non-invasive approach, focusing on its short and long-term effects. Methods Mice received nebulized LPS or vehicle only (control group). Blood, BALF and lung tissue were collected 24 hours (LPS 24h) or 5 weeks (LPS 5w) after the nebulized LPS-induced lung injury. Inflammatory cytokines were assessed in the blood serum, BALF and lung tissue. Stereological analyses and remodeling changes were assessed by histology and immunohistochemistry at the specified time points. Results The LPS 24h group showed increased pro-inflammatory cytokine levels, intense cell influx, increased total septal volume, septal thickening and decreased surface density of the alveolar septa. The LPS 5w group showed persistent lung inflammation, septal thickening, increased total lung volume, accentuated collagen deposition, especially of collagen type I, and decreased MMP-2 protein expression. Conclusion We present a feasible, reproducible and non-invasive nebulized-LPS animal model that allows the assessment of both the acute and late phases of acute lung injury. The presence of lung remodeling with collagen deposition after 5 weeks makes it useful to study the pathophysiology, complications, and possible therapeutic intervention studies that aim to understand and reduce pulmonary fibrosis in the late phases of ALI.
- Air pollution impairs recovery and tissue remodeling in a murine model of acute lung injury(2020) COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; ALEMANY, Adair Aparecida dos Santos; BELOTTI, Luciano; SCHALCH, Alexandre Santos; CAVALCANTE, Marcela Frota; RIBEIRO, Susan; VERAS, Mariana Matera; KALLAS, Esper Georges; SALDIVA, Paulo Hilario Nascimento; DOLHNIKOFF, Marisa; SILVA, Luiz Fernando Ferraz daEvidence regarding the impact of air pollution on acute respiratory distress syndrome (ARDS) is limited, and most studies focus on ARDS onset. Our study aimed to evaluate whether exposure to fine particulate matter interferes with lung recovery and remodeling in a murine model of acute lung injury. Forty-eight mice received nebulized LPS or the vehicle (controls). Blood, BALF, lungs and spleen were collected after 5 weeks of exposure to either PM2.5 (PM and LPS+PM group) or filtered air (control and LPS5w groups). Inflammatory cells and cytokines were assessed in the blood, BALF, lungs and spleen. Stereological analyses and remodeling assessments were performed by histology. The LPS+PM group showed increased BALF leukocytes, characterized by increased macrophages, increased IL-1 beta and IL-6 levels, anemia and thrombocytopenia. Moreover, we also observed septal thickening, decreased alveolar air space total volume and, septa surface density. Finally, regarding tissue remodeling, we observed elastosis of the lung parenchyma, and unlike in the LPS5w group, we did not observe fibrosis in the LPS+PM group. In conclusion, the delayed inflammation resolution due to subchronic exposure to PM2.5 could be influenced by low systemic and local lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.
- Concentrated ambient fine particulate matter (PM2.5) exposure induce brain damage in pre and postnatal exposed mice(2020) DOMENICO, Marlise Di; BENEVENUTO, Sarah Gomes de Menezes; TOMASINI, Paula Pellenz; YARIWAKE, Victor Yuji; ALVES, Nilmara de Oliveira; RAHMEIER, Francine Luciano; FERNANDES, Marilda da Cruz; MOURA, Dinara Jaqueline; SALDIVA, Paulo Hilario Nascimento; VERAS, Mariana MateraAir pollution is a public health concern that has been associated with adverse effects on the development and functions of the central nervous system (CNS). However, studies on the effects of exposure to pollutants on the CNS across the entire developmental period still remain scarce. In this study, we investigated the impacts of prenatal and/or postnatal exposure to fine particulate matter (PM2.5) from Sao Paulo city, on the brain structure and behavior of juvenile male mice. BALB/c mice were exposed to PM2.5 concentrated ambient particles (CAP) at a daily concentration of 600 mu g/m(3) during the gestational [gestational day (GD) 1.5-18.5] and the postnatal periods [postnatal day (PND) 22-90] to filtered air (FA) in both periods (FA/FA), to CAP only in the postnatal period (FA/CAP), to CAP only in the gestational period (CAP/FA), and to CAP in both periods (CAP/CAP). Behavioral tests were performed when animals were at PND 30 and PND 90. Glial activation, brain volume, cortical neuron number, serotonergic and GABAergic receptors, as well as oxidative stress, were measured. Mice at PND 90 presented greater behavioral changes in the form of greater locomotor activity in the FA-CAP and CAP-CAP groups. In general, these same groups explored objects longer and the CAP-FA group presented anxiolytic behavior. There was no difference in total brain volume among groups, but a lower corpus callosum (CC) volume was observed in the CAP-FA group. Also, the CAP-CAP group presented an increase in microglia in the cortex and an increased in astrocytes in the cortex, CC, and C1A and dentate gyrus of hippocampus regions. Gene expression analysis showed a decrease in BDNF in the hippocampus of CAP-CAP group. Treatment of immortalized glial cells with non-cytotoxic doses of ambient PM2.5 increased micronuclei frequencies, indicating genomic instability. These findings highlight the potential for negative neurodevelopmental outcomes induced by exposure to moderate levels of PM2.5 in Sao Paulo city.
- Maternal exposure to air pollution alters energy balance transiently according to gender and changes gut microbiota(2023) ZORDAO, Olivia Pizetta; CAMPOLIM, Clara Machado; YARIWAKE, Victor Yuji; CASTRO, Gisele; FERREIRA, Clilton Krauess de Oliveira; SANTOS, Andrey; NORBERTO, Sonia; VERAS, Mariana Matera; SAAD, Mario Jose Abdalla; SALDIVA, Paulo Hilario Nascimento; KIM, Young-Bum; PRADA, Patricia OliveiraIntroductionThe timing of maternal exposure to air pollution is crucial to define metabolic changes in the offspring. Here we aimed to determine the most critical period of maternal exposure to particulate matter (PM2.5) that impairs offspring's energy metabolism and gut microbiota composition. MethodsUnexposed female and male C57BL/6J mice were mated. PM2.5 or filtered air (FA) exposure occurred only in gestation (PM2.5/FA) or lactation (FA/PM2.5). We studied the offspring of both genders. ResultsPM(2.5) exposure during gestation increased body weight (BW) at birth and from weaning to young in male adulthood. Leptin levels, food intake, Agrp, and Npy levels in the hypothalamus were also increased in young male offspring. Ikbke, Tnf increased in male PM2.5/FA. Males from FA/PM2.5 group were protected from these phenotypes showing higher O-2 consumption and Ucp1 in the brown adipose tissue. In female offspring, we did not see changes in BW at weaning. However, adult females from PM2.5/FA displayed higher BW and leptin levels, despite increased energy expenditure and thermogenesis. This group showed a slight increase in food intake. In female offspring from FA/PM2.5, BW, and leptin levels were elevated. This group displayed higher energy expenditure and a mild increase in food intake. To determine if maternal exposure to PM2.5 could affect the offspring's gut microbiota, we analyzed alpha diversity by Shannon and Simpson indexes and beta diversity by the Linear Discriminant Analysis (LDA) in offspring at 30 weeks. Unlike males, exposure during gestation led to higher adiposity and leptin maintenance in female offspring at this age. Gestation exposure was associated with decreased alpha diversity in the gut microbiota in both genders. DiscussionOur data support that exposure to air pollution during gestation is more harmful to metabolism than exposure during lactation. Male offspring had an unfavorable metabolic phenotype at a young age. However, at an older age, only females kept more adiposity. Ultimately, our data highlight the importance of controlling air pollution, especially during gestation.
- Pleural anthracosis as an indicator of lifetime exposure to urban air pollution: An autopsy-based study in Sao Paulo(2019) TAKANO, Ana Paula Cremasco; JUSTO, Lisie Tocci; SANTOS, Nathalia Villa dos; MARQUEZINI, Monica Valeria; ANDRE, Paulo Afonso de; ROCHA, Francisco Marcelo Monteiro da; PASQUALUCCI, Carlos Augusto; BARROZO, Ligia Vizeu; SINGER, Julio M.; ANDRE, Carmen Diva Saldiva De; SALDIVA, Paulo Hilario Nascimento; VERAS, Mariana MateraMany studies have been conducted to evaluate the association between air pollution and adverse health effects using a wide variety of methods to assess exposure. However, the assessment of individual long-term exposure to ambient air pollution is a challenging task and has not been evaluated in a large autopsy study. Our goal was to investigate whether exposure to urban air pollution is associated to the degree of lung anthracosis, considering modifying factors such as personal habits, mobility patterns and occupational activities. We conducted a study in Sao Paulo, Brazil from February 2017 to June 2018, combining epidemiological, spatial analysis and autopsybased approaches. Information about residential address, socio-demographic details, occupation, smoking status, time of residence in the city and time spent commuting was collected via questionnaires applied to the next-ofkin. Images of the pleura surface from upper and lower lobes were used to quantify anthracosis in the lungs. We used multiple regression models to assess the association between the amount of carbon deposits in human lungs, measured by the fraction of pleural anthracosis (FA), and potential explanatory variables. We analyzed 413 cases and our data showed that for each additional hour spent in daily commuting, the ratio FA/(1-FA) is multiplied by 1.05 (95% confidence interval: [1.02; 1.08]). The estimated coefficient for daily hours spent in traffic was not considerably affected by the inclusion of socio-demographic variables and smoking habits. We estimate a tobacco equivalent dose of 5 cigarettes per day in a city where annual PM2.5 concentration oscillates around 25 mu g/m(3). Pleural anthracosis is a potential index of lifetime exposure to traffic-derived air pollution.
- Exposure to fine particulate matter in the air alters placental structure and the renin-angiotensin system(2017) SOTO, Sonia de Fatima; MELO, Juliana Oliveira de; MARCHESI, Guilherme D'Aprile; LOPES, Karen Lucasechi; VERAS, Mariana Matera; OLIVEIRA, Ivone Braga de; SOUZA, Regiane Machado de; CASTRO, Isac de; FURUKAWA, Luzia Naoko Shinohara; SALDIVA, Paulo Hilario Nascimento; HEIMANN, Joel C.Transforming growth factor beta 1 (TGF beta 1), the uteroplacental renin-angiotensin system (RAS) and vascular endothelial growth factor A (VEGF-A) participate in the placentation process. The aim of this study was to investigate the effects of exposure to pollutants on the placenta. Methods Female Wistar rats were exposed to filtered air (F) or to concentrated fine particulate matter (P) for 15 days. After mating, the rats were divided into four groups and again exposed to F or P (FF, FP, PF, PP) beginning on day 6 of pregnancy. At embryonic day 19, the placenta was collected. The placental structure, the protein and gene expression of TGF beta 1, VEGF-A, and its receptor Flk-1 and RAS were evaluated by indirect ELISA and quantitative real-time PCR. Results Exposure to P decreased the placental mass, size, and surface area as well as the TGF beta 1, VEGF-A and Flk-1 content. In the maternal portion of the placenta, angiotensin II (AngII) and its receptors AT(1) (AT(1)R) and AT(2) (AT(2)R) were decreased in the PF and PP groups. In the fetal portion of the placenta, AngII in the FP, PF and PP groups and AT(2)R in the PF and PP groups were decreased, but AT(1)R was increased in the FP group. VEGF-A gene expression was lower in the PP group than in the FF group. Conclusions Exposure to pollutants before and/or during pregnancy alters some characteristics of the placenta, indicating a possible impairment of trophoblast invasion and placental angiogenesis with possible consequences for the maternal-fetal interaction, such as a limitation of fetal nutrition and growth.
- The impact of chronic exposure to air pollution over oxidative stress parameters and brain histology(2021) BERNARDI, Rosane Bossle; ZANCHI, Ana Claudia Tedesco; DAMACENO-RODRIGUES, Nilsa Regina; VERAS, Mariana Matera; SALDIVA, Paulo Hilario Nascimento; BARROS, Helena Maria Tannhauser; RHODEN, Claudia RamosAir pollution (AP) triggers neuroinflammation and lipoperoxidation involved in physiopathology of several neurodegenerative diseases. Our study aims to investigate the effect of chronic exposure to ambient AP in oxidative stress (OS) parameters and number of neurons and microglial cells of the cortex and striatum. Seventy-two male Wistar rats were distributed in four groups of exposure: control group (FA), exposed throughout life to filtered air; group PA-FA, pre-natal exposed to polluted air until weaning and then to filtered air; group FA-PA, pre-natal exposed to filtered air until weaning and then to polluted air; and group PA, exposed throughout life to polluted air. After 150 days of exposure, the rats were euthanized for biochemical and histological determinations. The malondialdehyde concentration in the cortex and striatum was significantly higher in the PA group. The activity of superoxide dismutase was significantly decreased in the cortex of all groups exposed to AP while activity of catalase was not modified in the cortex or striatum. The total glutathione concentration was lower in the cortex and higher in the striatum of the FA-PA group. The number of neurons or microglia in the striatum did not differ between FA and PA. On the other hand, neurons and microglia cell numbers were significantly higher in the cortex of the FA-PA group. Our findings suggest that the striatum and cortex have dissimilar thresholds to react to AP exposure and different adaptable responses to chronically AP-induced OS. At least for the cortex, changing to a non-polluted ambient early in life was able to avoid and/or reverse the OS, although some alterations in enzymatic antioxidant system may be permanent. As a result, it is important to clarify the effects of AP in the cortical organization and function because of limited capacity of brain tissue to deal with threatening environments.
- A nanoformulation containing a scFv reactive to electronegative LDL inhibits atherosclerosis in LDL receptor knockout mice(2016) CAVALCANTE, Marcela Frota; KAZUMA, Soraya Megumi; BENDER, Eduardo Andre; ADORNE, Marcia Duarte; ULLIAN, Mayara; VERAS, Mariana Matera; SALDIVA, Paulo Hilario Nascimento; MARANHAO, Andrea Queiroz; GUTERRES, Silvia Staniscuaski; POHLMANN, Adriana Raffin; ABDALLA, Dulcineia Saes ParraAtherosclerosis is a chronic inflammatory disease responsible for the majority of cases of myocardial infarction and ischemic stroke. The electronegative low-density lipoprotein, a modified subfraction of native LDL, is pro-inflammatory and plays an important role in atherogenesis. To investigate the effects of a nanoformulation (scFv anti-LDL(-)-MCMN-Zn) containing a scFv reactive to LDL(-) on the inhibition of atherosclerosis, its toxicity was evaluated in vitro and in vivo and further it was also administered weekly to LDL receptor knockout mice. The scFv anti-LDL(-)-MCMN-Zn nanoformulation did not induce cell death in RAW 264.7 macrophages and HUVECs. The 5 mg/kg dose of scFv anti-LDL(-)-MCMN-Zn did not cause any typical signs of toxicity and it was chosen for the evaluation of its atheroprotective effect in LdIr(-/-) mice. This nanoformulation significantly decreased the atherosclerotic lesion area at the aortic sinus, compared with that in untreated mice. In addition, the Il1b mRNA expression and CD14 protein expression were downregulated in the atherosclerotic lesions at the aortic arch of LdIr(-/-) mice treated with scFv anti-LDL(-)-MCMN-Zn. Thus, the scFv anti-LDL(-)-MCMN-Zn nanoformulation inhibited the progression of atherosclerotic lesions, indicating its potential use in a future therapeutic strategy for atherosclerosis.
- Ambient levels of concentrated PM2.5 affects cell kinetics in adrenal glands: an experimental study in mice(2017) FUCHS, Luiz Fernando Portugal; VERAS, Mariana Matera; SALDIVA, Paulo Hilario Nascimento; SASSO, Gisela Rodrigues da Silva; CARVALHO, Katia Candido; SIMOES, Manuel de Jesus; SOARES JR., Jose Maria; BARACAT, Edmund ChadaWe evaluated the effects of air pollution on the adrenal cortex using 30 female mice divided into two groups of fifteen animals each. One group was conditioned daily in a chamber with exposure to particulate matter (PM) 2.5 mu m (GExp). Animals were exposed on daily basis in an ambient particles concentrator during the period of time enough to reach an accumulated dose of 600 mu g/m(3), which corresponds to a 24-h exposure of 25 mu g/m(3) that approximates to the annual mean of PM2.5 in Sao Paulo. The other group was allocated to another chamber with filtered air (GCrt). After euthanasia, the adrenals underwent histological processing and immunohistochemistry staining for Ki-67 and cleaved caspase-3. Histomorphometry of the adrenal glands in GExp showed increased thickness of the zona glomerulosa, while in GCrt; the adrenal glands from GExp had higher Ki-67 immunostaining scores in the zona reticularis than those from GCrt. The adrenal from GExp showed higher cleaved caspase-3 immunoreactivity in the zona fasciculata than the unexposed group (GCrt). The homeostasis index indicated higher cell proliferation in the zona glomerulosa and zona reticularis in GExp than in GCrt. Our data indicate that PM2.5 air pollution induces alterations on cell kinetics in mouse adrenal glands.
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