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Vera Luiza Capelozzi

Publications and source records attributed to Vera Luiza Capelozzi.

23 records · Page 2Linked to original sources

Ultrastructural acute features of active remodeling after chemical pleurodesis induced by silver nitrate or talc.

This study evaluated submicroscopic features of active pleural remodeling associated with chemical pleurodesis. Twenty seven rabbits received intrapleural injection of 0.5% silver nitrate (SN; N = 9) or 400 mg/kg talc slurry (N = 9) in 2 ml of saline solution; control rabbits (N = 9) received 2 ml of saline alone. The rabbits were sacrificed 15 minutes, 24 hours, or 7 days postinjection, and specimens of visceral pleura were obtained, fixed, and photographed for submicroscopic analysis. After 15 minutes of talc or SN exposure, prominent injury to the mesothelial cells and mesothelial cell-mesothelial basement membrane (MC-MBM) union was visible. There was focal remesothelialization of the denuded area through mesothelial cell migration, proliferation, and differentiation. After 24 hours, early wound healing, characterized by a superficial exudate, was evident where myofibroblasts had proliferated through a gap in the MC-MBM. After 7 days, proliferation of highly active myofibroblasts was observed; these cells produced abundant extracellular matrix components in a more organized distribution paralleling the surface. This third stage of remodeling was more evident with SN than talc-induced chemical pleurodesis. Our results suggest that ideal chemical pleurodesis results from injury to the MC-MBM union and abnormal wound healing, involving three essential steps: remesothelialization, fibroblastic proliferation, and extracellular matrix accumulation and remodeling.

Animals↗

Heterogeneous remodeling of lung vessels in idiopathic pulmonary fibrosis.

Recently, several reports suggest differences in the vascularization of the various histopathologic patterns of parenchymal remodeling seen in usual interstitial pneumonia (UIP). In this study, we sought to validate the importance of vascular remodeling in patients with idiopathic pulmonary fibrosis (IPF) and to examine the relationship between vascular remodeling and parenchymal remodeling or pulmonary function. Open lung biopsies were performed in 57 patients with IPF, and vascular changes in alternating areas of parenchymal remodeling (UIP histologic patterns) were studied. Quantitative analysis of the internal area, internal perimeter, wall thickness, and surrounding cellularity of medium or large pulmonary arteries, as well as their distribution according to air/parenchymal ratios, was performed. Semiquantitative analysis also was used to determine the grade of vascular occlusion. An inverse association was found between vascularization and UIP parenchymal remodeling (p < 0.05); that is, the decreased internal luminal area and perimeter as well as the increased wall thickness run in parallel with progression from alveolar collapse toward severe mural-organizing fibrosis with honeycombing. Vascular regression (diminished internal area and perimeter of vessels) was also associated with higher FEV(1), FVC, and RV values (r = 0.48, p< 0.05), reflecting a tight relationship between vascular remodeling and pulmonary function. A progressive regression of vascularization, reflected by different degrees of luminal occlusion after vascular remodeling, coincided with parenchymal remodeling (alveolar collapse, mural-organizing fibrosis, and honeycombing). This vascular regression may be responsible for the impaired wound healing and progressive fibroproliferation found in patients with IPF. Further studies are needed to determine whether this relationship is causal or consequential.

Humans↗

Nonhomogeneous density of CD34 and VCAM-1 alveolar capillaries in major types of idiopathic interstitial pneumonia.

Integrin-immunoglobulin family ligand (CAMs) interactions between lung parenchymal cells (fibroblasts and epithelial cells) and integrin-extracellular matrix component interactions may be involved in the pathogenesis of idiopathic interstitial pneumonia (IIP). Among these, CD34 immunoquantitation allows determination of the degree of vascular proliferation (angiogenesis), whereas VCAM-1 immunoquantitation allows evaluation of the degree of endothelial activity and is strong evidence of inflammation. To validate the importance of vascular proliferation and endothelial cell activity within the alveolar walls and to explore the quantitative relationship between this factor and organizing fibrosis after parenchymal remodeling, we studied surgical lung biopsies in major IIP histologic patterns. We evaluated alveolar vascularity and activity in relation to the various degrees of organizing fibrosis in surgical lung biopsies of diffuse alveolar damage, nonspecific interstitial pneumonia, and usual interstitial pneumonia. Alveolar capillary endothelial cells were intensely immunoreactive with CD34 and VCAM-1. Vascular activity progressively increased in no-organizing fibrotic areas (normal, collapsed, and inflammatory septal areas), whereas vascular density gradually decreased as the degree of organizing fibrosis increased and was lower than that in control lungs in the most extensively fibrotic lesions (mural organizing fibrosis of usual interstitial pneumonia). These results indicate the presence of temporal nonhomogeneic vascular remodeling indiopathic interstitial pneumonia.

Antigens, CD34↗

Structural features of epithelial remodeling in usual interstitial pneumonia histologic pattern.

Epithelial remodeling probably contributes to parenchymal deterioration in usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF), but understanding its mechanisms is still a challenge. The aim of our study was to examine apoptosis and the epithelial changes in the histologic pattern of UIP. After immunohistochemical staining we quantified the content of type I cells, type II cells, surfactant-A protein, bcl-2, and Fas-ligand (Fas-L) in control and alveolar collapse, fibroblastic foci, and honeycomb in UIP areas of 23 open lung biopsies. A significant association was found between epithelial changes and parenchymal deterioration (p < 0.05). Type I epithelial cell density was similar between control (1.7 +/- 0.7%) and UIP alveolar collapse areas (1.8 +/- 0.6%) but decreased progressively in fibroblastic foci zones (0.8 +/- 0.4%) and honeycomb changes (0.4 +/- 0.3%). Type II cell density increased from control (25.6 +/- 8.3%) to areas of alveolar collapse (34.5 +/- 11.4%), then decreased toward fibroblastic foci (15.4 +/- 6.0%) and honeycomb change areas (23.1 +/- 8.6%). The surfactant-A protein increased from control (6.7 +/- 3.2%) to areas of alveolar collapse (31.1 +/- 9.5%) and decreased toward fibroblastic foci (14.5 +/- 4.9%) and honeycomb change areas (21.1 +/- 8.9%). Fas-L positive epithelial cell density presented a progressive decline from control (48.5 +/- 9.5%), alveolar collapse (37.9 +/- 12.4%), fibroblastic foci (27.4 +/- 6.8%), and honeycomb change areas (21.9 +/- 6.5%). A similar decline in density was found for bcl-2 positive epithelial cells from control (20.4 +/- 2.7%), alveolar collapse (18.9 +/- 5.1%), and fibroblastic foci areas (13.8 +/-2.9%), then increased honeycomb change areas (16.3 +/- 2.8%). We conclude that loss of the nuclear (bcl-2) and membrane (Fas-L) regulation of normal cell population density and suppression of cell death by apoptosis in UIP may be a determinant of the abnormal epithelial/parenchymal remodeling in UIP.

Aged↗

Diffuse panbronchiolitis: an underdiagnosed disease? Study of 4 cases in Brazil.

BACKGROUND: Diffuse panbronchiolitis is a clinical pathologic condition characterized by chronic inflammation of respiratory bronchioles, with clinical features that position it as a differential diagnosis among the sinopulmonary syndromes. METHODS AND RESULTS: We present 4 cases (1 Black, 2 Japanese descendants, and 1 Japanese), living in Brazil, in which the diagnosis was made by the clinical and radiological features and confirmed by transbronchial biopsy. The clinical findings included chronic sinusitis, productive cough, rhonchi, and wheezes. The pulmonary function tests showed an obstructive pattern. High resolution computerized tomography showed a diffuse nodular pattern, airway ectasia, and airway wall thickening. The biopsy showed interstitial accumulation of foam cells and lymphoid cells in the walls of respiratory bronchioles: 2 of our cases had bronchus-associated lymphoid tissue hyperplasia. We searched for the HLA Bw54 in all of our patients, but only 1 was positive. A low dose macrolide treatment was introduced, resulting in with clinical and functional improvement. A score that rated the extent of nodules, airway ectasia, mucus plugging, and airway wall thickening was applied on pre- and post-treatment High resolution computerized tomography results, revealing an improvement in tomographic pattern related to that observed in the pulmonary function tests. CONCLUSION: We conclude that diffuse panbronchiolitis is a systemic disease that is not exclusive to the Asian population, whose clinical and radiological features should be better known by occidental pulmonary physicians.

Adult↗