Epithelial and extracellular matrix injury in quartz-inflamed lung: role of the alveolar macrophage.
The bronchoalveolar leukocytes from quartz-inflamed lung were separated into macrophage-enriched and neutrophil-enriched populations on density gradients. Neutrophil-enriched populations showed the greatest activity in causing injury to epithelial cells and fibronectin in vitro. Inflammatory macrophage-enriched populations from quartz-exposed lung had the ability to cause fibronectin degradation but could not cause detachment injury to epithelial cells over and above that caused by control alveolar macrophages. Fibronectin damage in vivo could be an important factor in disordering the connective tissue scaffold of the lung, thereby favoring fibrosis. In vitro quartz stimulated more production of cytokines by alveolar macrophages than the inert particulate titanium dioxide. Cytokines could be important in upregulating adhesion molecules in the membranes of lung cells in vivo; this process could aid leukocyte/lung cell contact, allowing epithelial injury to be expressed, and could also be a factor leading to pathological change.
Donaldson
K
K
Institute of Occupational Medicine, Edinburgh, Scotland.
Brown
G M
GM
Brown
D M
DM
Slight
J
J
Li
X Y
XY
D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004848:Epithelium; D005109:Extracellular Matrix / Q000187:drug effects / Q000378:metabolism*; D005353:Fibronectins / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D055370:Lung Injury; D016676:Macrophages, Alveolar / Q000378:metabolism / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology*; D011791:Quartz / Q000009:adverse effects*; D051381:Rats; D012829:Silicosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*
D016207:Cytokines; D005353:Fibronectins; D011791:Quartz