Phagocytosis and intracellular killing by polymorphonuclear cells from patients with rheumatoid arthritis and Felty's syndrome.
The present in vitro study concerned the phagocytosis and intracellular killing by polymorphonuclear cells (PMN) of 5 patients with rheumatoid arthritis (RA) and 12 patients with Felty's syndrome (FS). PMN phagocytosis was assessed by microbiologic and morphologic methods, and intracellular killing was measured independently of continuous phagocytosis of viable bacteria (Staphylococcus aureus). PMN from patients with RA or FS ingested S aureus opsonized with immunoglobulins and complement as effectively as did PMN from healthy donors. However, the capacity of patient PMN to ingest S aureus opsonized with sera lacking complement activity, e.g., heat-inactivated donor serum and the sera of 2 patients with FS, was lower than that of healthy donor PMN. This decreased ingestion is associated with diminished expression of Fc receptors on the membrane of PMN from patients who have RA or FS. As with sera lacking complement activity, decreased capacity to ingest S aureus was observed after preloading donor PMN with immune aggregates, which also decreased the expression of Fc receptors. PMN from patients with RA or FS were found to be as active in killing S aureus as cells from healthy donors.
D000328:Adult; D000368:Aged; D000936:Antigen-Antibody Complex / Q000032:analysis; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001770:Blood Bactericidal Activity; D003165:Complement System Proteins / Q000032:analysis; D005258:Felty Syndrome / Q000276:immunology*; D005260:Female; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D010587:Phagocytosis; D011961:Receptors, Fc / Q000032:analysis; D013211:Staphylococcus aureus
D000936:Antigen-Antibody Complex; D007136:Immunoglobulins; D011961:Receptors, Fc; D003165:Complement System Proteins