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
20 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 20
- Th17/Treg-Related Intracellular Signaling in Patients with Chronic Obstructive Pulmonary Disease: Comparison between Local and Systemic Responses(2021) LOURENCO, Juliana D.; TEODORO, Walcy R.; BARBEIRO, Denise F.; VELOSA, Ana Paula P.; SILVA, Larissa E. F.; KOHLER, Julia B.; MOREIRA, Alyne R.; V, Marcelo Aun; SILVA, Isadora C. da; FERNANDES, Frederico L. A.; NEGRI, Elnara M.; GROSS, Jefferson L.; TIBERIO, Iolanda F. L. C.; ITO, Juliana T.; LOPES, Fernanda D. T. Q. S.Th17/Treg imbalance plays a pivotal role in COPD development and progression. We aimed to assess Th17/Treg-related intracellular signaling at different COPD stages in local and systemic responses. Lung tissue and/or peripheral blood samples were collected and divided into non-obstructed (NOS), COPD stages I and II, and COPD stages III and IV groups. Gene expression of STAT3 and -5, ROR gamma t, Foxp3, interleukin (IL)-6, -17, -10, and TGF-beta was assessed by RT-qPCR. IL-6, -17, -10, and TGF-beta levels were determined by ELISA. We observed increased STAT3, ROR gamma t, Foxp3, IL-6, and TGF-beta gene expression and IL-6 levels in the lungs of COPD I and II patients compared to those of NOS patients. Regarding the systemic response, we observed increased STAT3, ROR gamma t, IL-6, and TGF-beta gene expression in the COPD III and IV group and increased IL-6 levels in the COPD I and II group. STAT5 was increased in COPD III and IV patients, although there was a decrease in Foxp3 expression and IL-10 levels in the COPD I and II and COPD III and IV groups, respectively. We demonstrated that an increase in Th17 intracellular signaling in the lungs precedes this increase in the systemic response, whereas Treg intracellular signaling varies between the compartments analyzed in different COPD stages.
- The tick-derived rBmTI-A protease inhibitor attenuates the histological and functional changes induced by cigarette smoke exposure(2018) LOURENCO, Juliana D.; ITO, Juliana T.; CERVILHA, Daniela A. B.; SALES, Davi S.; RIANI, Alyne; SUEHIRO, Camila L.; GENARO, Isabella S.; DURAN, Adriana; PUZER, Luciano; MARTINS, Milton A.; SASAKI, Sergio D.; LOPES, Fernanda D. T. Q. S.Introduction. Smoking is the main risk factor for chronic obstructive pulmonary disease development and cigarette smoke (CS) exposure is considered an important approach to reproduce in rodents this human disease. We have previously shown that in an elastase induced model of emphysema, the administration of a protease inhibitor (rBmTI-A) prevented and attenuated tissue destruction in mice. Thus, in this study we aimed to verify the effects of rBmTI-A administration on the physiopathological mechanisms of CS induced emphysema. Methods. Mice (C57BL/6) were exposed to CS or room air for 12 weeks. In this period, 3 nasal instillations of rBmTI-A inhibitor or its vehicle were performed. After euthanasia, respiratory mechanics were evaluated and lungs removed for analysis of mean linear intercept, volume proportion of collagen and elastic fibers, density of polymorphonuclear cells, macrophages, and density of positive cells for MMP-12, MMP-9, TIMP-1 and gp91phox. Results. The rBmTI-A administration improved tissue elastance, decreased alveolar enlargement and collagen fibers accumulation to control levels and attenuated elastic fibers accumulation in animals exposed to CS. There was an increase of MMP-12, MMP-9 and macrophages in CS groups and the rBmTIA only decreased the number of MMP-12 positive cells. Also, we demonstrated an increase in gp91phox in CS treated group and in TIMP-1 levels in both rBmTI-A treated groups. Conclusion. In summary, the rBmTI-A administration attenuated emphysema development by an increase of gp91phox and TIMP-1, accompanied by a decrease in MMP-12 levels.
- Extracellular Matrix Component Remodeling in Respiratory Diseases: What Has Been Found in Clinical and Experimental Studies?(2019) ITO, Juliana T.; LOURENCO, Juliana D.; RIGHETTI, Renato F.; TIBERIO, Iolanda F. L. C.; PRADO, Carla M.; LOPES, Fernanda D. T. Q. S.Changes in extracellular matrix (ECM) components in the lungs are associated with the progression of respiratory diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome (ARDS). Experimental and clinical studies have revealed that structural changes in ECM components occur under chronic inflammatory conditions, and these changes are associated with impaired lung function. In bronchial asthma, elastic and collagen fiber remodeling, mostly in the airway walls, is associated with an increase in mucus secretion, leading to airway hyperreactivity. In COPD, changes in collagen subtypes I and III and elastin, interfere with the mechanical properties of the lungs, and are believed to play a pivotal role in decreased lung elasticity, during emphysema progression. In ARDS, interstitial edema is often accompanied by excessive deposition of fibronectin and collagen subtypes I and III, which can lead to respiratory failure in the intensive care unit. This review uses experimental models and human studies to describe how inflammatory conditions and ECM remodeling contribute to the loss of lung function in these respiratory diseases.
conferenceObject Cigarette Smoke Exposure Combined To LPS Instillation: A New Experimental Model Of Exacerbation In Chronic Obstructive Pulmonary Disease In Mice(2016) CERVILHA, D. A. B.; ITO, J. T.; LOURENCO, J. D.; OLIVO, C. R.; SALES, D. S.; SARAIVA, B. M.; OLIVEIRA-JUNIOR, M. C.; MARTINS, M. A.; VIEIRA, R. P.; LOPES, F. D. T. Q. S.conferenceObject Autonomic modulation's recovery after acute smoking in adults(2014) XAVIER, Rafaella Fagundes; ITO, Juliana Tiyaki; RAMOS, Dionei; LIMA, Fabiano Francisco; MANZANO, Beatriz Martins; RODRIGUES, Fernanda Maria Machado; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; VANDERLEI, Luiz Carlos Marques; RAMOS, Ercy Mara Cipulo- Effect of exercise training on Treg cell response in severe COPD individuals: a randomized and controlled trial(2022) ITO, J. T.; OLIVEIRA, L. M.; V, L. Alves; XAVIER, R. F.; SATO, M. N.; CARVALHO, C. R. F.; TIBERIO, I. F. L. C.; LOPES, F. D. T. Q. S.
- Temporal analysis of the intracellular signaling pathways involved in Th17/Treg response in COPD development(2019) SILVA, Larissa Emidio de Franca; LOURENCO, Juliana Dias; SILVA, Kaique Rodrigues Da; KOHLER, Julia Benini; SANTANA, Fernanda Paula Roncon; MOREIRA, Alyne Riani; CERVILHA, Daniela Aparecida De Brito; HAMAGUCHI, Sara Sumie Sobral; PRADO, Carla Maximo; VIEIRA, Rodolfo De Paula; VELOSA, Ana Paula Pereira; ITO, Juliana Tiyaki; LOPES, Fernanda Degobbi Tenorio Quirino Dos Santos
- The imbalance between subpopulations of regulatory T (TREG) Cells at different stages of chronic obstructive pulmonary disease (COPD)(2023) ALVES, Luan Henrique Vasconcelos; A, Juliana Tiyaki Ito; OLIVEIRA, Luana Mendonca De; TIBERIO, Iolanda Lopes Calvo; STELMACH, Rafael; SATO, Maria Notomi; ALMEIDA, Francine Maria; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos
- Intracellular mechanisms of Th17/Treg differentiation in mild and moderate COPD patients(2019) LOURENCO, Juliana Dias; SILVA, Larissa Emidio De Franca; GENARO, Isabella Santos De; ITO, Juliana Tiyaki; PIETROBON, Anna Julia; SATO, Maria Notomi; GROSS, Jefferson Luiz; NEGRI, Elnara Marcia; BARBEIRO, Denise Frediani; TEODORO, Walcy Paganelli Rosolia; MIRANDA, Jurandir Tomaz De; SARAIVA-ROMANHOLO, Beatriz Mangueira; VIEIRA, Rodolfo De Paula; LOPES, Fernanda Degobbi Tenorio Quirino Dos Santos
- Microenvironmental stimuli induce different macrophage polarizations in experimental models of emphysema(2019) KOHLER, Julia Benini; CERVILHA, Daniela Aparecida de Brito; MOREIRA, Alyne Riani; SANTANA, Fernanda Roncon; FARIAS, Talita M.; VALE, Maria Isabel Cardoso Alonso; MARTINS, Milton de Arruda; PRADO, Carla Maximo; TIBERIO, Iolanda Calvo; ITO, Juliana Tiyaki; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosMacrophages play a pivotal role in the development of emphysema and depending on the microenvironment stimuli can be polarized into M1- or M2-like macrophage phenotypes. We compared macrophage polarizations in cigarette smoke (CS)- and porcine pancreatic elastase (PPE)-induced emphysema models. C57BL/6 mice were subdivided into four experimental groups. In the PPE group, animals received an intranasal instillation of PPE (0.677 IU); in the saline group, animals received an intranasal instillation of saline (0.9%). Animals from both groups were euthanized on day 28. In the CS group, animals were exposed to CS for 30 min, twice a day, 5 days per week for 12 weeks. In the control group, animals received filtered air. We observed an increase in total macrophages for both experimental models. For M1-like macrophage markers, we observed an increase in TNF-alpha(+) and IFN-gamma(+) cells, Cxcl-9 and Cxcl-10 expressions in PPE and CS groups. Only in the CS group, we detected an increased expression of IL-12b. For M2-like macrophages markers we observed a down regulation in IL-10, IL-4, IL-13, Arg1 and Fizz1 and an increase of TGF-beta(+) cells in the PPE group, while for the CS group there was an increase in TGF-beta(+) cells and IL-10 expression. All exposure groups were compared to their respective controls. In summary, we demonstrated that CS- and PPE-induced models resulted in different microenvironmental stimuli. CS exposure induced an environmental stimulus related to M1- and M2-like macrophage phenotypes similar to previous results described in COPD patients, whereas the elastase-induced model provided an environmental stimulus related only to the M1 phenotype.