Vitronectin protects alveolar macrophages from silica toxicity.
Silicosis is an interstitial lung disease caused by the inhalation of crystalline silicon dioxide. Current concepts suggest that a crucial step in the development of silicosis is silica-induced injury of alveolar macrophages (AM). The adhesive protein vitronectin is a natural constituent of the lung, in which its function is largely unexplored. This study investigated a possible role for vitronectin in protecting AM from silica exposure. In this study, the concentration of vitronectin was shown to be increased in the bronchoalveolar lavage fluid of silica-treated rats. Vitronectin affinity for silica was shown both in vitro and in vivo by immunostaining. Vitronectin reduced silica-induced injury to cultured AM as determined with the (51)Cr release assay. Vitronectin reduced silica-induced free radical production as determined with a cell-free thiobarbituric acid assay. Additionally, vitronectin reduced the silica-induced respiratory burst in AM as determined with chemiluminescence. This study suggests that vitronectin may protect AM during the initial exposure to silica.
Wisniowski
P E
PE
Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Spech
R W
RW
Wu
M
M
Doyle
N A
NA
Pasula
R
R
Martin
W J
WJ
D000818:Animals; D015153:Blotting, Western; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002478:Cells, Cultured; D005609:Free Radicals / Q000378:metabolism; D007150:Immunohistochemistry; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016897:Respiratory Burst / Q000187:drug effects; D012822:Silicon Dioxide / Q000633:toxicity*; D019096:Vitronectin / Q000032:analysis / Q000276:immunology / Q000502:physiology*
D005609:Free Radicals; D019096:Vitronectin; D012822:Silicon Dioxide