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Transforming growth factor-beta (TGF-beta) in silicosis.

Authors
Jagirdar-J; Begin-R; Dufresne-A; Goswami-S; Lee-TC; Rom-WN
Source
Am J Respir Crit Care Med 1996 Oct; 154(4):1076-1081
NIOSHTIC No.
00238706
Abstract
The role of transforming growth factor beta (TGFb) in human silicosis was examined. The study material consisted of lung tissue samples obtained at autopsy from 11 men who had been exposed to crystalline silica (14808607) during their working lifetimes and from two controls. All lung tissue samples from the silica exposed workers had histological evidence of silicosis. Seven had simple silicosis, three had pulmonary massive fibrosis (PMF), and one had evidence of acute or accelerated silicosis. Silicotic nodules were found in tissue samples from eight workers. Silica particle concentrations in lungs from the exposed subjects varied from 0.37x10(6) to 9.204x10(6) particles per milligram (mg) dry lung tissue. The highest concentrations were found in lungs from those with PMF. Silica concentrations in control lungs were below 0.3x10(6) particle/mg. In lung tissue from controls, small amounts of TGFb staining were found in the bronchial epithelium, macrophages, and bronchial and vascular smooth muscle. In samples from the silicotics, minimal to moderate staining for TGFb was seen in early silicotic peribronchiolar lesions. Central hyalinized areas in the nodular lesions contained the most intense TGFb staining. Fibroblasts in the periphery of the nodules also stained for TGFb. In lung tissue from the patient with acute silicosis, staining of hyperplastic alveolar epithelium was observed. Intense staining of macrophages was seen in three patients. Large areas of scar tissue in the PMF lesions also stained for TGFb. The authors conclude that TGFb may play a major role in the etiology of silicosis, particularly in the formation of silicotic lesions and development of PMF.
Keywords
NIOSH-Publication; NIOSH-Cooperative-Agreement; Pulmonary-system-disorders; Silica-dusts; Lung-tissue; Humans; Postmortem-examination; Histopathology; Immunochemistry; Lung-fibrosis
CODEN
AJCMED
CAS No.
14808-60-7
Publication Date
19961001
Document Type
Journal Article
Funding Type
Cooperative Agreement
Fiscal Year
1997
NTIS Accession No.
NTIS Price
Identifying No.
Cooperative-Agreement-Number-U60-CCU-206153
Issue of Publication
4
ISSN
1073-449X
Priority Area
Pulmonary-system-disorders
Source Name
American Journal of Respiratory and Critical Care Medicine
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