Drug and rheumatoid factor effects on the uptake of immunoglobulin G aggregates by neurtrophil monolayers.
This study examines aggregate-cell interacations in a newly applied neutrophil monolayer system, as an in vitro model of rheumatoid inflammation. Insoluble and soluble immunoglobulin G (IgG) aggregates were combined with rheumatoid factor (RF) to produce IgG-RF complexes. The presence of RF did not significantly change the uptake of the insoluble aggregates by neutrophils as measured in the monolayer system. Neutrophils exposed to these aggregates showed significantly (P less than 0.005) greater uptake than those exposed to soluble aggregates, and the presence or absence of serum did not change these results. Increasing concentrations of radiolabeled aggregates to 1.5 mg/ml and cells to 5 X 10(6) neutrophils/ml increased cell-associated radioactivity. Addition of cytochalasin B to 5 mg/ml progressively depressed cell-associated radioactivity. Gold, but not aspirin, in therapeutic concentrations seemed to suppress aggregate uptake. This system offers a method for quantitatively assaying aggregate uptake which may be an important component of the rheumatoid inflammatory process.
D001241:Aspirin / Q000494:pharmacology*; D006046:Gold / Q000494:pharmacology*; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D012217:Rheumatoid Factor / Q000494:pharmacology*
D007074:Immunoglobulin G; D006046:Gold; D012217:Rheumatoid Factor; D001241:Aspirin