DANIELA PERRONI FRIAS
Projetos de Pesquisa
Unidades Organizacionais
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
10 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 10
- Expression patterns of peroxiredoxin genes in bronchial epithelial cells exposed to diesel exhaust particles(2021) SERIANI, Robson; PAULA, Carla Peres de; CUNHA, Anderson Ferreira da; OLIVEIRA, Marcos Antonio de; KREMPEL, Paloma Gava; FRIAS, Daniela Perroni; NEGRI, Elnara Marcia; MAUAD, Thais; MACCHIONE, MariangelaSeveral mechanisms have been suggested to explain the adverse effects of air pollutants on airway cells. One such explanation is the presence of high concentrations of oxidants and pro-oxidants in environmental pollutants. All animal and plant cells have developed several mechanisms to prevent damage by oxidative molecules. Among these, the peroxiredoxins (PRDXs) are of interest due to a high reactivity with reactive oxygen species (ROS) through the functioning of the thioredoxin/thioredoxin reductase system. This study aimed to verify the gene expression patterns of the PRDX family in bronchial epithelial airway cells (BEAS-2B) cells exposed to diesel exhaust particles (DEPs) at a concentration of 15 mu g/mL for 1 or 2 h because this it is a major component of particulate matter in the atmosphere. There was a significant decrease in mRNA fold changes of PRDX2 (0.43 +/- 0.34; *p = 0.0220), PRDX5 (0.43 +/- 0.34; *p = 0.0220), and PRDX6 (0.33 +/- 0.25; *p = 0.0069) after 1 h of exposure to DEPs. The reduction in mRNA levels may consequently lead to a decrease in the levels of PRDX proteins, increasing oxidative stress in bronchial epithelial cells BEAS-2B and thus, negatively affecting cellular functions.
- Influence of particles from atmospheric pollution in female hormonal receptors in bronchi cells.>(2020) SMELAN, Juliana; ALMEIDA, Juliane; FRIAS, Daniela; BRENTANI, Mitzi; MACCHIONE, Mariangela
- Human bronchial epithelial cells exposed in vitro to diesel exhaust particles exhibit alterations in cell rheology and cytotoxicity associated with decrease in antioxidant defenses and imbalance in pro- and anti-apoptotic gene expression(2016) SERIANI, Robson; SOUZA, Claudia Emanuele Carvalho de; KREMPEL, Paloma Gava; FRIAS, Daniela Perroni; MATSUDA, Monique; CORREIA, Aristides Tadeu; FERREIRA, Marcia Zotti Justo; ALENCAR, Adriano Mesquita; NEGRI, Elnara Marcia; SALDIVA, Paulo Hilario Nascimento; MAUAD, Thais; MACCHIONE, MariangelaDiesel exhaust particles (DEPs) from diesel engines produce adverse alterations in cells of the airways by activating intracellular signaling pathways and apoptotic gene overexpression, and also by influencing metabolism and cytoskeleton changes. This study used human bronchial epithelium cells (BEAS-2B) in culture and evaluates their exposure to DEPs (15ug/mL for 1 and 2 h) in order to determine changes to cell rheology (viscoelasticity) and gene expression of the enzymes involved in oxidative stress, apoptosis, and cytotoxicity. BEAS-2B cells exposed to DEPs were found to have a significant loss in stiffness, membrane stability, and mitochondrial activity. The genes involved in apoptosis [B cell lymphoma 2 (BCL-2 and caspase-3)] presented inversely proportional expressions (p=0.05, p=0.01, respectively), low expression of the genes involved in antioxidant responses [SOD1 (superoxide dismutase 1); SOD2 (superoxide dismutase 2), and GPx (glutathione peroxidase) (p=0.01)], along with an increase in cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) (p=0.01). These results suggest that alterations in cell rheology and cytotoxicity could be associated with oxidative stress and imbalance between pro-and antiapoptotic genes.
- Relationship between Nrf2-Keap1 system and cell death in BEAS-2B exposed to Diesel Exhaust Particles(2017) FRIAS, Daniela; NUNES, Raquel; MATSUDA, Monique; YOSHIZAKI, Kelly; CARVALHO-OLIVEIRA, Regiani; PEREIRA, Daniela; VASCONCELLOS, Perola; MAUAD, Thais; MACCHIONE, Mariangela
- Fragrances as a trigger of immune responses in different environments(2024) MACCHIONE, M.; YOSHIZAKI, K.; FRIAS, D. P.; MAIER, K.; SMELAN, J.; PRADO, C. M.; MAUAD, T.Fragrances can cause allergic skin reactions, expressed as allergic contact dermatitis and reactions in the respiratory tract that range from acute temporary upper airway irritation to obstructive lung disease. These adverse health effects may result from the stimulation of a specific (adaptive) immune response. Th1 cells, which essentially produce interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), play a key role in allergic contact dermatitis and also on allergic sensitization to common allergens (e.g., nickel and fragrance). It has been shown that fragrance allergy leads to Th2/Th22 production of IL-4, IL-5 and IL-13, controlling the development of IgE and mediating hypersensitivity reactions in the lung, such as asthma. Cytokines released during immune response modulate the expression of cytochrome P450 (CYPs) proteins, which can result in alterations of the pharmacological effects of substances in inflammatory diseases. The mechanisms linking environment and immunity are still not completely understood but it is known that aryl hydrocarbon receptor (AhR) is a sensor with conserved ligand-activated transcription factor, highly expressed in cells that controls complex transcriptional programs which are ligand and cell type specific, with CYPs as targeted genes. This review focuses on these important aspects of immune responses of the skin and respiratory tract cells, describing some in vitro models applied to evaluate the mechanisms involved in fragrance-induced allergy.
- Anthracosis particulate matter causes changes in macrophages inflammatory response and in expression of genes related to xenobiotics metabolism in co-culture of macrophages with BEAS-2B airway cells(2023) FRIAS, Daniela Perroni; VIEIRA, Gabriela Lima; SMELAN, Juliana; LACERDA, Joao Paulo Amorim De; MAUAD, Thais; DOLHNIKOFF, Marisa; MACCHIONE, Mariangela
- Nrf2 positively regulates autophagy antioxidant response in human bronchial epithelial cells exposed to diesel exhaust particles(2020) FRIAS, Daniela Perroni; GOMES, Raquel Labiapari Nunes; YOSHIZAKI, Kelly; CARVALHO-OLIVEIRA, Regiani; MATSUDA, Monique; JUNQUEIRA, Mara de Souza; TEODORO, Walcy Rosolia; VASCONCELLOS, Perola de Castro; PEREIRA, Daniela Cristina de Almeida; CONCEICAO, Paulo Roberto da; SALDIVA, Paulo Hilario Nascimento; MAUAD, Thais; MACCHIONE, MariangelaDiesel exhaust particles (DEP) are known to generate reactive oxygen species in the respiratory system, triggering cells to activate antioxidant defence mechanisms, such as Keap1-Nrf2 signalling and autophagy. The aim of this study was to investigate the relationship between the Keap1-Nrf2 signalling and autophagy pathways after DEP exposure. BEAS-2B cells were transfected with silencing RNA (siRNA) specific to Nrf2 and exposed to DEP. The relative levels of mRNA for Nrf2, NQO1, HO-1, LC3B, p62 and Atg5 were determined using RT-PCR, while the levels of LCB3, Nrf2, and p62 protein were determined using Western blotting. The autophagy inhibitor bafilomycin caused a significant decrease in the production of Nrf2, HO-1 and NQO1 compared to DEPs treatment, whereas the Nrf2 activator sulforaphane increased the LC3B (p = 0.020) levels. BEAS-2B cells exposed to DEP at a concentration of 50 mu g/mL for 2 h showed a significant increase in the expression of LC3B (p = 0.001), p62 (p = 0.008), Nrf2 (p = 0.003), HO-1 (p = 0.001) and NQO1 (p = 0.015) genes compared to control. In siRNA-transfected cells, the LC3B (p < 0.001), p62 (p = 0.001) and Atg5 (p = 0.024) mRNA levels and the p62 and LC3II protein levels were decreased, indicating that Nrf2 modulated the expression of autophagy markers (R < 1). These results imply that, in bronchial cells exposed to DEP, the Nrf2 system positively regulates autophagy to maintain cellular homeostasis.
- The effects of particulate matter on inflammation of respiratory system: Differences between male and female(2017) YOSHIZAKI, Kelly; BRITO, Jose Mara; SILVA, Luiz Fernando; LINO-DOS-SANTOS-FRANCO, Adriana; FRIAS, Daniela Perroni; SILVA, Renata Calciolari Rossi e; AMATO-LOURENCO, Luis Fernando; SALDIVA, Paulo Hilario Nascimento; TIBERIO, Iolanda de Fatima Lopes Calvo; MAUAD, Thais; MACCHIONE, MariangelaAir pollution is known to exacerbate respiratory diseases and epidemiological studies have shown that women present more chronic respiratory symptoms than man exposed to traffic pollution, however, the reason why is unclear. This study evaluated the inflammatory differences in BALB/c mouse males (n = 34) and females (n = 111) in three phases of the estrous cycle that were exposed to ambient air (AA) or concentrated ambient particles (CAPs). Tracheal hyperreactivity to methacholine, bronchoalveolar lavage fluid (BALF) and immunohistochemical of airways and lung parenchyma were studied. Hyperreactivity increased in CAPs-exposed female mice compared with AA-exposed mice in estrus (p < 0.05) and proestrus phases (p < 0.05) and decreased in CAPs-exposed males compared with those exposed to AA (p < 0.05). Males had increased numbers of total cells (p = 0.037) and macrophages (p = 0.028) compared to females. BALF levels of cyclooxygenase-2(COX-2) (p = 0.000), transforming growth factor alpha (TGF-alpha) (p = 0.001) and IL-8 receptor alpha (IL-8R alpha) (p = 0.014) were increased in males compared with proestrus, estrus and diestrus females, independent of exposure. Proestrus females exhibited significantly higher cadherin expression in lung parenchyma than did males (p = 0.005). CAPs exposure increased matrix metalloproteinase-9 (MMP-9) (p = 0.024) and isoprostane (p = 0.003) expression in the airways of both, males and females. The level of substance P (SP) (p = 0.001) increased in lung parenchyma in males compared with females, while IL-17 levels in airways (p = 0.042) and in lung parenchyma (p = 0.008) increased in females. MMP-9 levels (p = 0.024) were significantly lower in the lung parenchyma of CAPs-exposed females. TGF-alpha (p = 0.007) levels increased in the lung parenchyma of CAPs-exposed females compared to AA-exposed females. These results suggest that inflammatory markers differentially expressed in male mice were mostly linked to acute inflammation (IL-1 beta, IL-8R alpha, COX-2), whereas in females, markers that may lead to a chronic inflammatory process such as IL-17 and remodeling (MMP-9) were increased.
conferenceObject Anthrachosis Particulate Matter Causes Metabolic Changes in Macrophage and Airway Cells Culture(2022) FRIAS, D. P.; VIEIRA, G.; SMELAN, J.; LACERDA, J.; MACCHIONE, M.conferenceObject Expression of CYP450 Genes and Cytokine Secretion Following Exposure to Cinnamyl Alcohol of BEAS-2B and Dendritic Cells Co-Culture(2020) FRIAS, D. P.; YOSHIZAKI, K.; MAIER, K.; OLIVEIRA, L.; SANTILLO, B.; PRADO, C. M.; OSHIRO, T.; BARBUTO, J.; SALDIVA, P.; MAUAD, T.; MACCHIONE, M.