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Am. J. Respir. Crit. Care Med., Volume 162, Number 2, August 2000, 733-739

Vitronectin Protects Alveolar Macrophages from Silica Toxicity

PAUL E. WISNIOWSKI, ROBERT W. SPECH, MIN WU, NICHOLAS A. DOYLE, RAJAMOULI PASULA, and WILLIAM J. MARTIN II

Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana

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 51Cr 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.




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