IOLANDA DE FATIMA LOPES CALVO TIBERIO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
20 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 20
- Alpha-7 nicotinic receptor stimulation reduces airway inflammation in a murine model of asthma(2016) SANTANA, Fernanda Paula Roncon; MIRANDA, Claudia Jeane Claudino de Pontes; PINHEIRO, Nathalia Montouro; PERINI, Adenir; CAPERUTO, Luciana Chagas; TIBERIO, Iolanda de Fatima Lopes Calvo; PRADO, Marco Antonio Maximo; MARTINS, Milton de Arruda; PRADO, Vania Ferreira; PRADO, Carla Maximo
- Nicotinic alpha-7 receptor stimulation (alpha 7nAChR) inhibited NF-kB/STAT3/SOCS3 pathways in a murine model of asthma(2017) SANTANA, Fernanda Paula Roncon; TOMARI, Sergio Festa; MIRANDA, Claudia Jeane Claudino de Pontes; PINHEIRO, Nathalia Montouro; CAPERUTO, Luciana Chagas; TIBERIO, Iolanda de Fatima Lopes Calvo; PRADO, Marco Antonio Maximo; MARTINS, Milton de Arruda; PRADO, Vania Ferreira; PRADO, Carla Maximo
- Low-dose chlorine exposure impairs lung function, inflammation and oxidative stress in mice(2021) GENARO, Isabella Santos de; ALMEIDA, Francine Maria de; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; KUNZLER, Deborah De Camargo Hizume; TRIPODE, Bruna Gabryela Busoletto; KURDEJAK, Adriana; CORDEIRO, Bruna Nakamura; PANDOLPHO, Renata; MACCHIONE, Mariangela; BRUGGEMANN, Thayse Regina; VIEIRA, Rodolfo Paula; MARTINS, Milton Arruda; TIBERIO, Iolanda de Fatima Lopes Calvo; SARAIVA-ROMANHOLO, Beatriz MangueiraAim: To explore the different consequences of acute and chronic exposure to chlorine gas (Cl-2) on the functional and histological parameters of health mice. Main methods: Firstly, male BALB/c mice were acute exposed to 3.3 or 33.3 or 70.5 mg/m(3) Cl-2. We analyzed the lung function, the inflammatory cells in the bronchoalveolar lavage, cell influx in the peribrochoalveolar space and mucus production. In a second phase, mice were chronic exposed to 70.5 mg/m(3) Cl-2. Besides the first phase analyses, we also evaluated the epithelial cells thickness, collagen deposition in the airways, immunohisto-chemistry stain for IL-1 beta, iNOS, IL-17 and ROCK-2 and the levels of IL-5, IL-13, IL-17, IL-1 beta and TNF-alpha in lung homogenate. Key findings: Acute exposure to chlorine impaired the lung function, increased the number of inflammatory cells in the BALF and in the airways, also increased the mucus production. Furthermore, when chlorine was exposed chronically, increased the airway remodeling with collagen deposition and epithelial cells thickness, positive cells for IL-1 beta, iNOS, IL-17 in the airways and in the alveolar walls and ROCK-2 in the alveolar walls, lung inflammation with increased levels of IL-5, IL-13, IL-1 beta and TNF-alpha in the lung homogenate, and also, induced the acid mucus production by the nasal epithelium. Significance: Acute and chronic exposure to low dose of chlorine gas worsens lung function, induces oxidative stress activation and mucus production and contributes to augmenting inflammation in health mice.
- A plant proteinase inhibitor from Enterolobium contortisiliquum attenuates airway hyperresponsiveness, inflammation and remodeling in a mouse model of asthma(2019) RODRIGUES, Adriana Palmeira Dias; BORTOLOZZO, Anelize Sartori Santos; ARANTES-COSTA, Fernanda Magalhaes; SARAIVA-ROMANHOLO, Beatriz Mangueira; SOUZA, Flavia Castro Ribas de; BRUGGEMANNI, Thayse Regina; SANTANA, Fernanda Paula Roncon; BRITO, Marlon Vilela de; BONTURI, Camila Ramalho; NUNES, Natalia Neto dos Santos; PRADO, Carla Maximo; LEICK, Edna Aparecida; OLIVA, Maria Luiza Vilela; MARTINS, Milton de Arruda; RIGHETTI, Renato Fraga; TIBERIO, Iolanda de Fatima Lopes CalvoIntroduction. Proteinase inhibitors have been associated with anti-inflammatory and antioxidant activities and may represent a potential therapeutic treatment for asthma. Purpose. The aim of the present study was to evaluate the effects of Enterolobium contortisiliquum trypsin inhibitor (EcTI) on pulmonary mechanical function, eosinophilic recruitment, inflammatory cytokines, remodeling and oxidative stress in an experimental model of chronic allergic pulmonary inflammation. Methods. BALB/c mice were divided into 4 groups: C (saline i.p and inhalations with saline), OVA (ovalbumin i.p and inhalations with ovalbumin); C+EC (saline i.p, inhalations with s aline and treatment with EcTI); OVA+EC (ovalbumin i.p, inhalations with ovalbumin and treatment with EcTI). On day 29, we performed the following tests: resistance (Rrs) and elastance (Ers) of the respiratory system; (b) quantify eosinophils, 8-ISO-PGF2 alpha, collagen and elastic fiber volume fractions; (c) IFN-gamma, IL-4, IL-5, IL-13, MMP-9, TIMP-1,TGF-beta, iNOS and p65-NF kappa B-positive cells in the airway and alveolar walls. Results. In OVA+EC group, there was an attenuation of the Rrs and Ers, reduction of eosinophils, IL-4, IL-5, IL-13, IFN-gamma, iNOS and p65-NF kappa B-positive cells compared to OVA group. The 8-ISO-PGF2 alpha, elastic and collagen fibers volume fractions as well as the positive cells for MMP-9, TIMP-1 and TGF-beta positive cells were decreased in OVA+EC compared to the OVA group. Conclusion. EcTI attenuates bronchial hyperresponsiveness, inflammation, remodeling and oxidative stress activation in this experimental mouse model of asthma.
- Resilience and its impact on the mental health of physiotherapists during the COVID-19 pandemic in Sa?o Paulo, Brazil(2022) PIGATI, Patricia Angeli da Silva; RIGHETTI, Renato Fraga; NISIAYMAMOTO, Bruna Tiemi Cunha; SARAIVA-ROMANHOLO, Beatriz Mangueira; TIBERIO, Iolanda de Fatima Lopes CalvoObjective: To analyze whether resilience modulates the levels of depression, anxiety, stress and the impact of events in physiotherapists who work with COVID-19 patients with those who do not.Methods: A cross-sectional study was conducted from August 2020 up to October 2020. A total of 519 physiotherapists were enrolled and divided according to resilience and whether they worked with COVID-19 patients. Volunteers answered sociodemographic questionnaires, rating their depression, anxiety, and stress on a scale (DASS-21). The impact of event scale revised (IES-R) and 14-item resilience scale (14-RS) were also used.Results: Physiotherapists with low resilience present scores significantly high of depression, anxiety, stress and impact of event compared to the high resilience group (P < .001). Additionally, working with COVID-19 patients also resulted in increased levels of depression, anxiety, stress, and impact of event compared with the NO COVID19 group (P < .001). These responses were modulated by age, sex, number of absences from work, whether or not personal protective equipment was received, host leadership, and the practice and maintenance of regular physical activity.Limitations: The responses to the questionnaires were anonymous and self-administered. We cannot assess whether these people had a previous diagnosis of depression, anxiety and stress.Conclusions: Low resilience and work with COVID-19 patients were associated with high levels of depression, anxiety, and stress and worse psychological impacts of events. Several aspects modulate these responses and can contribute to improving the resilience and mental health of physiotherapists who are responsible for the care of COVID-19 patients.
- VAChT reduction increased mortality probably due to alveolar edema in a model of lung injury induced by intestinal isquemia/reperfusion in female mice(2017) SANTANA, Fernanda Paula Roncon; FANTOZZI, Evelyn; SILVA, Fernanda Yamamoto Ricardo da; PINHEIRO, Nathalia Montouro; TIBERIO, Iolanda de Fatima Lopes Calvo; MARTINS, Milton de Arruda; PRADO, Vania Ferreira; PRADO, Marco Antonio Maximo; LIMA, Wothan Tavares de; FALOPPA, Ana Cristina Breithaupt; PRADO, Carla Maximo
- Decreased Bone Type I Collagen in the Early Stages of Chronic Obstructive Pulmonary Disease (COPD)(2020) JUNQUEIRA, Jader Joel Machado; LOURENCO, Juliana Dias; SILVA, Kaique Rodrigues da; CERVILHA, Daniela Aparecida de Brito; SILVEIRA, Lizandre Keren Ramos da; CORREIA, Aristides Tadeu; SILVA, Larissa Emidio de Franca; TEODORO, Walcy Rosolia; TIBERIO, Iolanda de Fatima Lopes Calvo; BARBOSA, Alexandre Povoa; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosSmoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) and is known to have deleterious effects on bone metabolism. However, the effects on bone collagen matrix during the development of COPD are unclear. The aim of this study was to evaluate the temporal effect of cigarette smoke exposure on bone type I collagen during COPD development in a cigarette smoke-induced model. C57BL/6 mice were allocated to three groups: control (C), animals exposed to filtered air for 1, 3 and 6 months; cigarette smoke (S), animals exposed to cigarette smoke for 1, 3 and 6 months; provisional smoking (PS), animals exposed to cigarette smoke for 3 months, followed by another 3 months of filtered air exposure. Evaluation of the respiratory mechanics and alveolar enlargement were performed. Femoral and tibial extraction was also performed to evaluate the type I collagen by immunofluorescence andCOL1A1gene expression. Exposure to cigarette smoke led to an alveolar enlargement and progressive reduction in lung tissue resistance and elastance, progressive reduction of type I collagen and reduction inCOL1A1gene expression. Although we did not observe any improvement in the functional and histological parameters in the provisional smoking group, we detected an increase inCOL1A1gene expression. A worsening in bone collagen matrix is part of the initial physiopathological events during COPD development and the smoking cessation induced an evident recovery ofCOL1A1expression, possibly to attempt at tissue repair.
- Effects of Rho-kinase inhibition in lung tissue with chronic inflammation(2014) I, Renato Fraga Righett; PIGATI, Patricia Angeli da Silva; POSSA, Samantha Souza; HABRUM, Fabio Cetinic; XISTO, Debora Goncalves; ANTUNES, Mariana Alves; LEICK, Edna Aparecida; PRADO, Carla Maximo; MARTINS, Milton de Arruda; ROCCO, Patricia Rieken Macedo; TIBERIO, Iolanda de Fatima Lopes CalvoWe evaluated whether Rho-kinase inhibition (Y-27632) modulated distal lung responsiveness, inflammation, extracellular matrix remodeling and oxidative stress activation in guinea pigs (GPs) with chronic allergic inflammation. GPs were submitted to inhalation of ovalbumin (OVA-2x/week/4 weeks). From the 5th inhalation on, the Rho-kinase inhibitor group animals were submitted to Y-27632 inhalation 10 min before each inhalation of OVA. Seventy-two hours after the seventh inhalation, the oscillatory mechanics of the distal lung strips were assessed under the baseline condition and after the ovalbumin challenge. Subsequently, the lung slices were submitted to morphometry. Rho-kinase inhibition in the ovalbumin-exposed animals attenuated distal lung elastance and resistance, eosinophils, IL-2, IL-4, IL-5, IL-13, TIMP-1, MMP-9, TGF-beta, IFN-gamma, NF-kappa B and iNOS-positive cells and the volume fraction of 8-iso-PGF2 alpha, elastic, collagen and actin in alveolar walls compared with the OVA group (P < 0.05). Rho-kinase inhibition contributed to the control of distal lung responsiveness, eosinophilic and Th1/Th2 responses and extracellular matrix remodeling in an animal model of chronic allergic inflammation.
- Aerobic exercise training engages cholinergic signaling to improve emphysema induced by cigarette smoke exposure in mice(2022) SUEHIRO, Camila Liyoko; SOUZA, Natalia Tiemi Simokomaki; SILVA, Emerson Batista da; CRUZ, Maysa Mariana; LAIA, Roseane Martins; SANTOS, Stheffany de Oliveira; SANTANA-NOVELLI, Fernanda Paula Roncon; CASTRO, Thamyres Barros Pereira de; LOPES, Fernanda D. T. Q. S.; PINHEIRO, Nathalia Montouro; TIBERIO, Iolanda de Fatima Lopes Calvo; OLIVO, Clarice Rosa; ALONSO-VALE, Maria Isabel; PRADO, Marco Antonio Maximo; PRADO, Vania Ferreira; TOLEDO-ARRUDA, Alessandra Choqueta de; PRADO, Carla MaximoLung inflammation is modulated by cholinergic signaling and exercise training protects mice against pulmonary emphysema development; however, whether exercise training engages cholinergic signaling is unknown. Aims: As cholinergic signaling is directly linked to the vesicular acetylcholine transporter (VAChT) levels, we evaluated whether the effects of aerobic exercise training depend on the VAChT levels in mice with pulmonary emphysema. Main methods: Wild-type (WT) and mutant (KDHOM) mice (65-70% of reduction in VAChT levels) were exposed to cigarette smoke (30 min, 2x/day, 5x/week, 12 weeks) and submitted or not to aerobic exercise training on a treadmill (60 min/day, 5x/week, 12 weeks). Lung function and inflammation were evaluated. Key findings: Cigarette smoke reduced body mass in mice (p < 0.001) and increased alveolar diameter (p < 0.001), inflammation (p < 0.001) and collagen deposition (p < 0.01) in lung tissue. Both trained groups improved their performance in the final physical test compared to the initial test (p < 0.001). In WT mice, exercise training protected against emphysema development (p < 0.05), reduced mononuclear cells infiltrate (p < 0.001) and increased MAC-2 positive cells in lung parenchyma (p < 0.05); however, these effects were not observed in KDHOM mice. The exercise training reduced iNOS-positive cells (p < 0.001) and collagen fibers deposition (p < 0.05) in lung parenchyma of WT and KDHOM mice, although KDHOM mice showed higher levels of iNOS-positive cells. Significance: Our data suggest that the protective effects of aerobic exercise training on pulmonary emphysema are, at least in part, dependent on the integrity of the lung cholinergic signaling.
- Sakuranetin reverses vascular peribronchial and lung parenchyma remodeling in a murine model of chronic allergic pulmonary inflammation(2016) SAKODA, Camila Pivari Pedroso; TOLEDO, Alessandra Choqueta de; PERINI, Adenir; PINHEIRO, Nathalia Montouro; HIYANE, Meire Ioshie; GRECCO, Simone dos Santos; TIBERIO, Iolanda de Fatima Lopes Calvo; CAMARA, Niels Olsen Saraiva; MARTINS, Milton de Arruda; LAGO, Joao Henrique Ghilardi; RIGHETTI, Renato Fraga; PRADO, Carla MaximoBackground and purpose: Asthma is a disease of high prevalence and morbidity that generates high costs in hospitalization and treatment. Although the airway is involved in the physiopathology of asthma, there is also evidence of the importance of vascular and lung parenchyma inflammation and remodeling, which can contribute to the functional pulmonary alterations observed in asthmatic patients. Our aim was to evaluate treatment using sakuranetin, a flavone isolated from the twigs of Baccharis retusa (Asteraceae), on vascular and lung parenchyma alterations in an experimental murine model of asthma. Methods: Male BALB/c mice were subjected to a sensitization protocol with ovalbumin for 30 days and were treated with or without sakuranetin (20 mg/kg/mice) or dexamethasone (5 mg/kg/mice); then, the lungs were collected for histopathological analysis. We evaluated extracellular matrix remodeling (collagen and elastic fibers), inflammation (eosinophils and NF-kB) and oxidative stress (8-isoprostane) in the pulmonary vessels and lung parenchyma. The thickness of the vascular wall was quantified, as well as the vascular endothelial growth factor (VEGF) levels. Results: We demonstrated that sakuranetin reduced the number of eosinophils and elastic fibers in both the pulmonary vessels and the lung parenchyma, probably due to a reduction of oxidative stress and of the transcription factor NF-kB and VEGF levels in the lung. In addition, it reduced the thickness of the pulmonary vascular wall. The treatment had no effect on the collagen fibers. In most of the parameters, the effect of sakuranetin was similar to the dexamethasone effect. Conclusions and implications: Sakuranetin had anti-inflammatory and antioxidant effects, preventing vascular and distal parenchyma changes in this experimental model of asthma.