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Mechanism for uptake of silica particles by monocytic U937 cells

Department of Environmental Medicine, National Institute of Public Health, P.O. Box 4404, Torshov, N-0403 Oslo, Norway

E Namork

P E Schwarze

Department of Environmental Medicine, Institute of Public Health, Oslo, Norway

A Aase

Department of Vaccine, Institute of Public Health, Oslo, Norway

We examined the mechanism for uptake by monocytic cells of particles found in the atmosphere of some industrial work places. As a model system, irregular crystalline silica particles (SPs), sphere-like cryptocrystalline microsilica particles (MPs) and carbon particles (CPs) were exposed to pro-monocytic U937 cells. Plasma-treated SP and MP, but not CP, activated the alternative complement pathway, but bound little C3b. However, all particles adsorbed serum IgG, IgA and IgM unspecifically. Phenotyping of U937 cells for complement receptors (CRs) and Fc receptors (FcRs) showed that interferon (INF) increased expression of FcRI, CR3 (CD11b/CD18) and CR4 (CD11c/CD18) and that phorbol-12-myristate-13-acetate (PMA) increased expression of CR4. Scanning electron microscopy (SEM) demonstrated higher phagocytosis of plasma-treated SP than native SP by both PMA and INF-stimulated, but not unstimulated, cells. MP and CP could not be distinguished from cellular structures. Inhibition experiments in SEM revealed uptake of heparin-plasma-treated SP via Fc'yRI on INF-stimulated U937 cells, but could not exclude possible participation of CR3. The results indicate that plasma-treated SPs bind Ig and are internalized by differentiated monocytic cells via FcR1, which is known to trigger cellular production of toxic oxygen species that may induce pulmonary inflammation in vivo.

Key Words: silica • phagocytosis • monocytes • Fc receptor • complement receptor

Human & Experimental Toxicology, Vol. 19, No. 7, 412-419 (2000)
DOI: 10.1191/096032700678816106


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