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Fas/FasL pathway-mediated alveolar macrophage apoptosis involved in human silicosis.

Authors
Yao-S-Q; Rojanasakul-LW; Chen-Z-Y; Xu-Y; Bai-Y-P; Chen-G; Zhang-X-Y; Zhang-C-M; Yu-Y-Q; Shen-F-H; Yuan-J-X; Chen-J; He-Q-C
Source
Apoptosis 2011Dec; 16(12):1195-1204
NIOSHTIC No.
20040056
Abstract
In vitro and in vivo studies have demonstrated that lung cell apoptosis is associated with lung fibrosis; however the relationship between apoptosis of alveolar macrophages (AMs) and human silicosis has not been addressed. In the present study, AM apoptosis was determined in whole-lung lavage fluid from 48 male silicosis patients, 13 male observers, and 13 male healthy volunteers. The relationships between apoptosis index (AI) and silica exposure history, soluble Fas (sFas)/membrane-bound Fas (mFas), and caspase-3/caspase-8 were analyzed. AI, mFas, and caspase-3 were significantly higher in lung lavage fluids from silicosis patients than those of observers or healthy volunteers, but the level of sFas demonstrated a decreasing trend. AI was related to silica exposure, upregulation of mFas, and activation of caspase-3 and -8, as well as influenced by smoking status after adjusting for confounding factors. These results indicate that AM apoptosis could be used as a potential biomarker for human silicosis, and the Fas/FasL pathway may regulate this process. The present data from human lung lavage samples may help to understand the mechanism of silicosis and in turn lead to strategies for preventing or treating this disease.
Keywords
Respiratory-system-disorders; Pulmonary-system-disorders; Pulmonary-function; Lung-cells; Lung-disease; Lung-disorders; Lung-fibrosis; Lung-function; Cell-damage; Cell-function; Cellular-function; Cellular-reactions; Alveolar-cells; Silicosis; Men; Smoking; Biomarkers; Humans; Pathology; Author Keywords: Silicosis; Alveolar macrophages; Apoptosis; Soluble Fas; Membrane-bound Fas; Caspase
Contact
Q. He, Division of Pneumoconiosis, School of Public Health, China Medical University, 92 North 2nd Road, Heping District, Shenyang 110001, China
CODEN
APOPFN
CAS No.
7631-86-9; 14808-60-7
Publication Date
20111201
Document Type
Journal Article
Email Address
qche@mail.cmu.edu.cn
Fiscal Year
2012
NTIS Accession No.
NTIS Price
Identifying No.
B12212011
Issue of Publication
12
ISSN
1360-8185
NIOSH Division
HELD
Priority Area
Manufacturing
Source Name
Apoptosis: An International Journal on Programmed Cell Death
State
WV
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