ELIA TAMASO ESPIN GARCIA CALZOLARI
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina
3 resultados
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- Aerobic Exercise Attenuated Bleomycin-Induced Lung Fibrosis in Th2-Dominant Mice(2016) ANDRADE-SOUSA, Adilson Santos; PEREIRA, Paulo Rogerio; MACKENZIE, BreAnne; OLIVEIRA-JUNIOR, Manoel Carneiro; ASSUMPCAO-NETO, Erasmo; BRANDAO-RANGEL, Maysa Alves Rodrigues; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; VELOSA, Ana Paula Pereira; TEODORO, Walcy Rosolia; OLIVEIRA, Ana Paula Ligeiro de; DOLHNIKOFF, Marisa; EICKELBERG, Oliver; VIEIRA, Rodolfo PaulaIntroduction The aim of this study was to investigate the effect of aerobic exercise (AE) in reducing bleomycin- induced fibrosis in mice of a Th2-dominant immune background (BALB/c). Methods BALB/c mice were distributed into: sedentary, control (CON), Exercise-only (EX), sedentary, bleomycin-treated (BLEO) and bleomycin-treated+exercised (BLEO+EX); (n = 8/group). Following treadmill adaptation, 15 days following a single, oro-tracheal administration of bleomycin (1.5U/kg), AE was performed 5 days/week, 60min/day for 4 weeks at moderate intensity (60% of maximum velocity reached during a physical test) and assessed for pulmonary inflammation and remodeling, and cytokine levels in bronchoalveolar lavage (BAL). Results At 45 days post injury, compared to BLEO, BLEO+EX demonstrated reduced collagen deposition in the airways (p<0.001) and also in the lung parenchyma (p<0.001). In BAL, a decreased number of total leukocytes (p<0.01), eosinophils (p<0.001), lymphocytes (p<0.01), macrophages (p<0.01), and neutrophils (p<0.01), as well as reduced pro-inflammatory cytokines (CXCL-1; p<0.01), (IL-1 beta; p<0.001), (IL-5; p<0.01), (IL-6; p<0.001), (IL-13; p<0.01) and pro-fibrotic growth factor IGF-1 (p<0.001) were observed. Anti-inflammatory cytokine IL-10 was increased (p<0.001). Conclusion AE attenuated bleomycin-induced collagen deposition, inflammation and cytokines accumulation in the lungs of mice with a predominately Th2-background suggesting that therapeutic AE (15-44 days post injury) attenuates the pro-inflammatory, Th2 immune response and fibrosis in the bleomycin model.
- Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model(2019) ITO, Juliana Tiyaki; CERVILHA, Daniela Aparecida de Brito; LOURENCO, Juliana Dias; GONCALVES, Natalia Gomes; VOLPINI, Rildo Aparecido; CALDINI, Elia Garcia; LANDMAN, Gilles; LIN, Chin Jia; VELOSA, Ana Paula Pereira; TEODORO, Walcy Paganelli Rosolia; TIBERIO, Iolanda de Fatima Lopes Calvo; MAUAD, Thais; MARTINS, Milton de Arruda; MACCHIONE, Mariangela; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosBackground The imbalance between pro- and anti-inflammatory immune responses plays a pivotal role in chronic obstructive pulmonary disease (COPD) development and progression. To clarify the pathophysiological mechanisms of this disease, we performed a temporal analysis of immune response-mediated inflammatory progression in a cigarette smoke (CS)-induced mouse model with a focus on the balance between Th17 and Treg responses. Methods C57BL/6 mice were exposed to CS for 1, 3 or 6 months to induce COPD, and the control groups were maintained under filtered air conditions for the same time intervals. We then performed functional (respiratory mechanics) and structural (alveolar enlargement) analyses. We also quantified the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, or TGF-beta positive cells in peribronchovascular areas and assessed FOXP3 and IL-10 expression through double-label immunofluorescence. Additionally, we evaluated the gene expression of NF-kappa B and TNF in bronchiolar epithelial cells. Results Our CS-induced COPD model exhibited an increased proinflammatory immune response (increased expression of the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, and IL-6 markers) with a concomitantly decreased anti-inflammatory immune response (FOXP3, IL-10, and TGF-beta markers) compared with the control mice. These changes in the immune responses were associated with increased alveolar enlargement and impaired lung function starting on the first month and third month of CS exposure, respectively, compared with the control mice. Conclusion Our results showed that the microenvironmental stimuli produced by the release of cyto-kines during COPD progression lead to a Th17/Treg imbalance.
- Myofibroblasts are increased in the lung parenchyma in asthma(2017) BOSER, Stacey R.; MAUAD, Thais; ARAUJO-PAULINO, Bianca Bergamo de; MITCHELL, Ian; SHRESTHA, Grishma; CHIU, Andrea; BUTT, John; KELLY, Margaret M.; CALDINI, Elia; JAMES, Alan; GREEN, Francis H. Y.Background Increased airway smooth muscle is observed in large and small airways in asthma. Semi-quantitative estimates suggest that cells containing alpha smooth muscle actin (alpha-SMA) are also increased in the lung parenchyma. This study quantified and characterized alpha-SMA positive cells (alpha-SMA+) in the lung parenchyma of non-asthmatic and asthmatic individuals. Methods Post-mortem sections of peripheral lung from cases of fatal asthma (FA), persons with asthma dying of non-respiratory causes (NFA) and non-asthma control subjects (NAC) were stained for alpha-SMA, quantified using point-counting and normalised to alveolar basement membrane length and interstitial area. Results alpha-SMA+ fractional area was increased in alveolar parenchyma in both FA (14.7 +/- 2.8% of tissue area) and NFA (13.0 +/- 1.2%), compared with NAC (7.4 +/- 2.4%), p < 0.05 The difference was greater in upper lobes compared with lower lobes (p < 0.01) in both asthma groups. Similar changes were observed in alveolar ducts and alveolar walls. The electron microscopic features of the alpha-SMA+ cells were characteristic of myofibroblasts. Conclusions We conclude that in asthma there is a marked increase in alpha-SMA+ myofibroblasts in the lung parenchyma. The physiologic consequences of this increase are unknown.