JULIANA DIAS LOURENCO
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
32 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 32
- 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.
- Increased bone resorption by long-term cigarette smoke exposure in animal model(2021) JUNQUEIRA, Jader Joel Machado; LOURENCO, Juliana Dias; SILVA, Kaique Rodrigues da; JORGETTI, Vanda; VIEIRA, Rodolfo P.; ARAUJO, Amanda Aparecida de; ANGELIS, Katia De; CORREIA, Aristides Tadeu; ALVES, Luan Henrique Vasconcelos; TIBERIO, Iolanda de Fatima Lopes Calvo; BARBOSA, Alexandre Povoa; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosIntroduction: Clinical and experimental studies have been attesting the deleterious effects of smoking mainly due to the stimulation of osteoclastogenesis and inhibition of osteoblastogenesis. However the physiological mechanisms that can explain these changes are not fully understood. Aims: To evaluate the trabecular bone resorption effect caused by long-term exposure to cigarette smoke and the action of cytokines and reactive oxygen species involved in this process. Methods: Sixty young adult C57BL/6 mice were allocated to two groups: control, 30 animals exposed to filtered air for 1, 3 and 6 months; and smoke, 30 animals exposed to cigarette smoke for 1, 3 and 6 months. Femoral and tibial extraction was performed to evaluate the bone mineral matrix, bone cytokines (Receptor activator of nuclear factor-kappa B ligand -RANKL and Osteoprotegerin -OPG) and oxidative stress markers (Thiobarbituric acid reactive substances -Tbars). Results: Exposure to cigarette smoke (CS) generated changes in bone structural parameters in the 6th month of follow-up, demonstrating an evident bone loss; reduction in OPG/RANKL ratio from the 3rd month on and increase in Tbars in the first month, both closely related to the increase in osteoclastogenic activity and bone resorption. Conclusion: These findings reinforce the importance of CS-induced oxidative stress in bone compromising the bone cellular activities with a consequent impairment in bone turn over and changes in bone structure.
- Smoking induces increased apoptosis in osteoblasts: changes in bone matrix organic components(2023) KOHLER, Julia Benini; SILVA, Alex Ferreira da; FARIAS, Walleson Alves; SAMPAIO, Barbara Fialho Carvalho; NEVES, Marco Aurelio Silveiro; LIMA, Leandro Gregorut; LOURENCO, Juliana Dias; MOREIRA, Alyne Riani; BARBOSA, Alexandre Povoa; TIBERIO, Iolanda de Fatima Lopes Calvo; TEODORO, Walcy Rosolia; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosClinical studies demonstrate the impact of smoking on bone tissue fragility and higher incidence of fractures. However, it is not totally understood which physiological mechanisms could be involved in these events. Previously, we showed important changes in bone tissue components in experimental model of cigarette smoke (CS) exposure. CS exposure induces worsening in bone mineralization and a decrease in collagen type I deposition, leading to bone fragility. Considering that the majority of clinical studies described bone structural changes by radiographic images, in this study we performed analyses ""in situ"" using tissue samples from smokers, former smokers and non-smokers to better understand how the increase in inflammatory mediators induced by smoking exposure could interfere in bone cells activity leading bone structural changes. We observed increased levels of IL-1 beta, IL-6 and TNF-alpha in bone tissue homogenates with a concomitant increase in osteoblast apoptosis in smokers and former smokers compared with non-smokers. Histological changes in both smokers and former smokers were characterized by reduction in collagen type I. Only in smokers, it was observed decrease in trabecular area, suggesting increased bone resorption and increase in collagen type V. These results showed that osteoblasts apoptosis in association with increased bone resorption leads bone structural changes in smokers.
conferenceObject Cigarette smoke exposure leads to bone resorption, matrix remodeling and a worsening in bone mineralization(2016) TEODORO, W. Rosolia; BARHOSA, A. Povoa; LOURENCO, J. Dias; VELOSA, A. P. Pereira; MARTINS, J.; OLIVO, C. Rosa; JORGETTI, V.; LOPES, F. D. T. Q. S.- Effects of anti-IL 17 on inflammation in Asthma, COPD and Asthma-COPD models(2022) ALMEIDA, F. M.; CAMARGO, L. N.; MARTINS, N.; LOURENCO, J. D.; BEZERRA, S. K. M.; SARAIVA-ROMANHOLO, B.; LEICK, E. A.; LOPES, F. D. Q. S.; PRADO, C. M.; RIGHETTI, R. F.; TIBERIO, I. F. L. C.
- 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.
- Time-dependent effects of diesel exhaust exposure on worsening of emphysema(2017) MOREIRA, Alyne Riani; LOURENCO, Juliana D.; KOHLER, Julia B.; EMIDIO, Larissa; CASTRO, Thamyres; DELESPOSTE, Luciano; SARAIVA, Beatriz M.; BRITO, Jose Mara; OLIVO, Clarice; PRADO, Carla M.; MARTINS, Milton; LOPES, Fernanda D. T. Q. S.; RIVERO, Dolores
conferenceObject Metalloproteases gene expression and remodeling of lung parenchyma fibers during the progression of elastase induced emphysema(2014) ROBERTONI, Fabiola Santos Zambon; OLIVO, Clarice Rosa; LOURENCO, Juliana Dias; GONCALVES, Natalia Comes; VELOSA, Ana Paula Pereira; TEODORO, Walcy Rosolia; LIN, Chin Jia; MARTINS, Milton De Arruda; LOPES, Fernanda D. T. Q. dos SantosconferenceObject 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.