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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Silicosis is a chronic lung disease induced by the inhalation of crystalline silica. Exposure of cultured macrophages to crystalline silica leads to cell death; however, the mechanism of cell-particle interaction, the fate of particles, and the cause of death are unknown. Time-lapse imaging shows that mouse macrophages avidly bind particles that settle onto the cell surface and that cells also extend protrusions to capture distant particles. Using confocal optical sectioning, silica particles were shown to be present within the cytoplasmic volume of live cells. In addition, electron microscopy and elemental analysis showed silica in internal cellular sections. To further examine the phagocytosis process, the kinetics of particle uptake was quantified using an assay in which cells were exposed to ovalbumin (OVA)-coated particles, and an anti-OVA antibody was used to distinguish surface-bound from internalized particles. Fc receptor-mediated uptake of antibody-coated silica particles was nearly complete within 5 minutes. In contrast, no OVA-coated particles were internalized at this time. After 30 minutes, 30% of bound silica was internalized and uptake continued slowly thereafter. OVA-coated latex beads, regardless of surface charge, were internalized at a similarly slow rate. These results demonstrate that macrophages internalize silica and that nonopsonized phagocytosis occurs by a temporally, and possibly mechanistically, distinct pathway from Fc receptor-mediated phagocytosis. Eighty percent of macrophages die within 12 hours of silica exposure. Neither OVA coating nor tetramethylrhodamine isothiocyanate labeling has any effect on cell death. Interestingly, antibody coating dramatically reduces silica toxicity. We hypothesize that the route of particle entry and subsequent phagosome trafficking affects the toxicity of internalized particles.
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PMID:The phagocytosis of crystalline silica particles by macrophages. 1855 90

Chronic inhalation of silica in various occupational settings results in the development of silicosis, a disease characterized by lung fibrosis. Uptake of silica particles by alveolar macrophages results in cell death and this is one of the contributing factors to the development of silicosis. We have characterized the uncoated or protein-coated (non-opsonized) and Fc receptor-mediated (antibody-opsonized) routes of silica phagocytosis and toxicity. Numerous microscopy techniques and fluorescent probes are outlined in this chapter to carefully measure particle uptake, by macrophages, phagosome maturation, phagosomal reactive oxygen species generation, phagolysosomal leakage, and cell death.
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PMID:Single Cell Analysis of Phagocytosis, Phagosome Maturation, Phagolysosomal Leakage, and Cell Death Following Exposure of Macrophages to Silica Particles. 2781 73