EDNA APARECIDA LEICK
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, 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
- 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.
- 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.
- Inflammation and remodeling modulated by anti IL17 in model of lung injury induced by elastase in mice(2019) LEICK, Edna A.; FUKUZAKI, Silvia; RIGHETTI, Renato F.; SANTOS, Tabata M.; CAMARGO, Leandro N.; GARRIDO, Aurelio C.; ARISTOTELES, Luciana R. C. R. B.; SOUZA, Flavia C. R.; SARAIVA-ROMANHOLO, Beatriz M.; PRADO, Carla M.; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.
- Effects of the serine protease inhibitor rBmTI-A in an experimental mouse model of chronic allergic pulmonary inflammation (vol 9, 12624, 2019)(2019) FLORENCIO, Ariana Correa; ALMEIDA, Robson S. de; ARANTES-COSTA, Fernanda M.; SARAIVA-ROMANHOLO, Beatriz M.; DURAN, Adriana F.; SASAKI, Sergio D.; MARTINS, Milton A.; LOPES, Fernanda D. T. Q. S.; TIBERIO, Iolanda F. L. C.; LEICK, Edna A.
- Effects of the serine protease inhibitor rBmTI-A in an experimental mouse model of chronic allergic pulmonary inflammation(2019) FLORENCIO, Adana Correa; ALMEIDA, Robson S. de; ARANTES-COSTA, Fernanda M.; SARAIVA-ROMANHOLO, Beatriz M.; DURAN, Adriana F.; SASAKI, Sergio D.; MARTINS, Milton A.; LOPES, Fernanda D. T. Q. S.; TIBERIO, Iolanda F. L. C.; LEICK, Edna A.To evaluate whether a recombinant serine protease inhibitor (rBmTI-A) modulates inflammation in an experimental model of chronic allergic lung inflammation. Balb/c mice were divided into four groups: SAL (saline), OVA (sensitized with ovalbumin), SAL + rBmTI-A (control treated with rBmTI-A) and OVA + rBmTI-A (sensitized with ovalbumin and treated with rBmTI-A). The animals received an intraperitoneal injection of saline or ovalbumin, according to the group. The groups received inhalation with saline or ovalbumin and were treated with rBmTI-A or saline by nasal instillation. After 29 days, we evaluated the respiratory mechanics; bronchoalveolar lavage fluid (BALF); cytokines; MMP-9, TIMP-1; eosinophils; collagen and elastic fibre expression in the airways; and the trypsin-like, MMP-1, and MMP-9 lung tissue proteolytic activity. Treatment with rBmTI-A reduced the trypsin-like proteolytic activity, the elastance and resistance maximum response, the polymorphonuclear cells, IL-5, IL-10, IL-13 and IL-17A in the BALF, the expression of IL-5, IL-13, IL-17, CD4+, MMP-9, TIM P-1, eosinophils, collagen and elastic fibres in the airways of the OVA + rBmTI-A group compared to the OVA group (p < 0.05). rBmTI-A attenuated bronchial hyperresponsiveness, inflammation and remodelling in this experimental model of chronic allergic pulmonary inflammation. This inhibitor may serve as a potential therapeutic tool for asthma treatment.
- Bronchial vascular remodeling is attenuated by anti-IL17 in asthmatic responses exacerbated by LPS(2019) CAMARGO, Leandro; ANDRADE, Felipp Costa Pinto De; SANTOS, Tabata M.; FUKUZAKI, Silvia; PRADO, Carla Maximo; MARTINS, Milton Arruda; LEICK, Edna Aparecida; RIGHETTI, Renato Fraga; TIBERIO, Iolanda De Fatima Lopes Calvo
- Effect of anti-IL17 and/or Rho-kinase inhibitor treatments on vascular remodelling in an asthma model in mice(2019) SANTOS, Tabata M.; CAMPOS, Elaine C.; RIGUETTI, Renato F.; CAMARGO, Leandro N.; FUKUZAKI, Silvia; REZENDE, Bianca G.; SARAIVA-ROMANHOLO, Beatriz M.; PRADO, Carla M.; LEICK, Edna A.; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.