LUIZ FERNANDO FERRAZ DA SILVA
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
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
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Resultados de Busca
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conferenceObject BRAIN DEATH PARADOXICALLY INDUCES LEUCOPENIA AND REDUCTION IN THE NUMBER OF BONE MARROW CELLS(2013) MENEGAT, Laura; BORELLI, Primavera; SIMAS, Rafael; CALIMAN, Julia Maria; SILVA, Luiz Fernando Ferraz; MOREIRA, Luiz Felipe; SANNOMIYA, Paulina- Anacardic Acids from Cashew Nuts Ameliorate Lung Damage Induced by Exposure to Diesel Exhaust Particles in Mice(2013) CARVALHO, Ana Laura Nicoletti; ANNONI, Raquel; TORRES, Larissa Helena Lobo; DURAO, Ana Carolina Cardoso Santos; SHIMADA, Ana Lucia Borges; ALMEIDA, Francine Maria; HEBEDA, Cristina Bichels; LOPES, Fernanda Degobbi Tenorio Quirino Santos; DOLHNIKOFF, Marisa; MARTINS, Milton Arruda; SILVA, Luiz Fernando Ferraz; FARSKY, Sandra Helena Poliselli; SALDIVA, Paulo Hilario Nascimento; ULRICH, Cornelia M.; OWEN, Robert W.; MARCOURAKIS, Tania; TREVISAN, Maria Teresa Salles; MAUAD, ThaisAnacardic acids from cashew nut shell liquid, a Brazilian natural substance, have antimicrobial and antioxidant activities and modulate immune responses and angiogenesis. As inflammatory lung diseases have been correlated to environmental pollutants exposure and no reports addressing the effects of dietary supplementation with anacardic acids on lung inflammation in vivo have been evidenced, we investigated the effects of supplementation with anacardic acids in a model of diesel exhaust particle-(DEP-) induced lung inflammation. BALB/c mice received an intranasal instillation of 50 mu g of DEP for 20 days. Ten days prior to DEP instillation, animals were pretreated orally with 50, 150, or 250mg/kg of anacardic acids or vehicle (100 mu L of cashew nut oil) for 30 days. The biomarkers of inflammatory and antioxidant responses in the alveolar parenchyma, bronchoalveolar lavage fluid (BALF), and pulmonary vessels were investigated. All doses of anacardic acids ameliorated antioxidant enzyme activities and decreased vascular adhesion molecule in vessels. Animals that received 50mg/kg of anacardic acids showed decreased levels of neutrophils and tumor necrosis factor in the lungs and BALF, respectively. In summary, we demonstrated that AAs supplementation has a potential protective role on oxidative and inflammatory mechanisms in the lungs.
conferenceObject Cd23+(fc epsilon rii - Low Affinity Ige Receptor) Cells In Large Airways And Bronchopulmonary Lymph Nodes Of Fatal Asthma(2013) CAGNONI, E. F.; FERREIRA, D. S.; SILVA, L. F. Ferraz da; CARVALHO, A. N.; SANTOS, A. B. G.; MEDEIROS, M. R.; DOLHNIKOFF, M.; RABE, K. F.; MAUAD, T.- Airway Dimensions in Fatal Asthma and Fatal COPD: Overlap in Older Patients(2013) SENHORINI, Aletea; FERREIRA, Diogenes S.; SHIANG, Christina; SILVA, Luiz F. F.; DOLHNIKOFF, Marisa; GELB, Arthur F.; MAUAD, ThaisIn some patients with chronic asthma clinical and physiological similarities with COPD may exist, such as partial reversibility to bronchodilators and persistent expiratory airflow obstruction. However, pathological data comparing both diseases in patients of similar age and disease severity are scarce. We compared large and small airway dimensions in 12 younger (mean age 32 yrs) and 15 older (mean age 65 yrs) non-smoker adult fatal asthma patients with 14 chronic smokers with severe, fatal COPD (mean age 71 yrs). Using H&E, Movat pentachrome staining and image analysis, we quantified large airway basement membrane (BM) thickness (mu m), submucosal gland area and large and small airway inner wall, smooth muscle and outer wall areas. Areas were normalized by BM perimeter (mu m(2)/mu m). Younger adult fatal asthma patients had thicker BM, smooth muscle, and outer wall areas in both small and large airways when compared to COPD patients. In older asthmatics there was an overlap in BM thickness and airway structure in small airways. Inner wall layer in large and small airway level and submucosal gland areas were similar among groups. In conclusion, there are airway histological structural similarities between fatal asthma and fatal COPD. Older fatal asthmatics present overlapping airway structural features with younger adult fatal asthmatics and severe COPD patients. Our data contributes to a better understanding of asthma pathology in the elderly.
conferenceObject Granzyme A Expression In Fatal Asthma(2013) SILVA, L. F.; SANTOS, F. E.; ANNONI, R.; NUSSBAUMER-OCHSNER, Y.; DOLHNIKOFF, M.; RABE, K. F.; MAUAD, T.; HIEMSTRA, P.conferenceObject Expression of CD1a cells and VCAM in large airways and thoracic lymph nodes of fatal asthma(2013) CAGNONI, Erika; FERREIRA, Diogenes; SILVA, Luiz Fernando; CARVALHO, Ana Laura; SANTOS, Angela; MEDEIROS, Maria Cristina; DOLHNIKOFF, Marisa; RABE, Klauss; MAUAD, Thais- Expression of acute-phase cytokines, surfactant proteins, and epithelial apoptosis in small airways of human acute respiratory distress syndrome(2013) PIRES-NETO, Ruy Camargo; MORALES, Maina Maria Barbosa; LANCAS, Tatiana; INFORSATO, Nicole; DUARTE, Maria Irma Seixas; AMATO, Marcelo Britto Passos; CARVALHO, Carlos Roberto Ribeiro de; SILVA, Luiz Fernando Ferraz da; MAUAD, Thais; DOLHNIKOFF, MarisaPurpose: Recent studies suggest a role for distal airway injury in acute respiratory distress syndrome (ARDS). The epithelium lining the small airways secretes a large number of molecules such as surfactant components and inflammatory mediators. There is little information on how these small airway secretory functions are altered in ARDS. Materials and Methods: We studied the lungs of 31 patients with ARDS (PaO2/fraction of inspired oxygen <= 200, 45 +/- 14 years, 16 men) and 11 controls (52 +/- 16 years, 7 men) submitted to autopsy and quantified the expression of interleukin (IL) 6, IL-8, surfactant proteins (SP) A and SP-B in the epithelium of small airways using immunohistochemistry and image analysis. In addition, an index of airway epithelial apoptosis was determined by the terminal deoxynucleotidyl transferase-mediated deoxyuridine-triphosphatase nick-end labeling assay, caspase 3, and Fas/Fas ligand expression. The density of inflammatory cells expressing IL-6 and IL-8 within the small airway walls was also quantified. Results: Acute respiratory distress syndrome airways showed an increase in the epithelial expression of IL-8 (P = .006) and an increased density of inflammatory cells expressing IL-6 (P = .004) and IL-8 (P < .001) compared with controls. There were no differences in SP-A and SP-B epithelium expression or in epithelial apoptosis index between ARDS and controls. Conclusion: Distal airways are involved in ARDS lung inflammation and show a high expression of proinflammatory interleukins in both airway epithelial and inflammatory cells. Apoptosis may not be a major mechanism of airway epithelial cell death in ARDS.
- Human Hemorrhagic Pulmonary Leptospirosis: Pathological Findings and Pathophysiological Correlations(2013) BRITO, Thales De; AIELLO, Vera Demarchi; SILVA, Luis Fernando Ferraz da; SILVA, Ana Maria Goncalves da; SILVA, Wellington Luiz Ferreira da; CASTELLI, Jussara Bianchi; SEGURO, Antonio CarlosBackground: Leptospirosis is a re-emerging zoonosis with protean clinical manifestations. Recently, the importance of pulmonary hemorrhage as a lethal complication of this disease has been recognized. In the present study, five human necropsies of leptospirosis (Weil's syndrome) with extensive pulmonary manifestations were analysed, and the antibodies expressed in blood vessels and cells involved in ion and water transport were used, seeking to better understand the pathophysiology of the lung injury associated with this disease. Principal Findings: Prominent vascular damage was present in the lung microcirculation, with decreased CD34 and preserved aquaporin 1 expression. At the periphery and even inside the extensive areas of edema and intraalveolar hemorrhage, enlarged, apparently hypertrophic type I pneumocytes (PI) were detected and interpreted as a non-specific attempt of clearence of the intraalveolar fluid, in which ionic transport, particularly of sodium, plays a predominant role, as suggested by the apparently increased ENaC and aquaporin 5 expression. Connexin 43 was present in most pneumocytes, and in the cytoplasm of the more preserved endothelial cells. The number of type II pneumocytes (PII) was slightly decreased when compared to normal lungs and those of patients with septicemia from other causes, a fact that may contribute to the progressively low PI count, resulting in deficient restoration after damage to the alveolar epithelial integrity and, consequently, a poor outcome of the pulmonary edema and hemorrhage. Conclusions: Pathogenesis of lung injury in human leptospirosis was discussed, and the possibility of primary non-inflammatory vascular damage was considered, so far of undefinite etiopathogenesis, as the initial pathological manifestation of the disease.
- Immune cell profile in infants' lung tissue(2013) SANTOS, Angela Batista Gomes dos; BINOKI, Daniella; SILVA, Luis Fernando F.; ARAUJO, Bianca Bergamo de; OTTER, Irene Den; ANNONI, Raquel; TSOKOS, Michael; STEIN, Renato T.; HIEMSTRA, Pieter S.; RABE, Klaus F.; DEBERTIN, Anette; TSCHERNIG, Thomas; MAUAD, ThaisLittle is known about the normal immune cell profile in the lungs of infants without pulmonary disease. Normal lung samples obtained at autopsy of 10 infants that died either due to incidental or inflicted causes or non-pulmonary diseases were stained for antibodies against B and T lymphocytes, macrophages, NK cells, cytotoxic cells, dendritic cells and mast cells. Cells were quantified in the airway epithelial layer, inner layer (between the epithelium and the outer smooth muscle border), outer layer (between the outer smooth muscle border and the external limits of the airway) and alveolar septa. Basement membrane or alveolar septa lengths were assessed by image analysis. Results were expressed as cells/mm. The median age of patients was 6.8 months, ranging from -11 to 840 days. The inner layer of the airways was the region with the smallest density of cells. There was a predominance of cells related to the innate immunity such as CD56+, Granzyme B+ and CD68+ cells in the epithelial layer and alveolar parenchyma. The outer layer and the lung parenchyma presented the highest cellular density. There were very few CD4+ T cells or dendritic cells in most of the lung compartments. The numbers of CD3+ T and granzyme B+ cells correlated positively with age. There was a compartmentalization of immune cells along airways and parenchyma, which may be related to the development of innate and acquired lung defense mechanisms.
conferenceObject Brain death induces leucopenia and reduction in the number of bone marrow cells(2013) CALIMAN, Julia M.; MENEGAT, Laura; BORELLI, Primavera; SIMAS, Rafael; SILVA, Luiz F. Ferraz da; MOREIRA, Luiz F.; SANNOMIYA, Paulina