Phagocytosis and intracellular killing of Staphylococcus aureus by polymorphonuclear cells from synovial fluid of patients with rheumatoid arthritis

Abstract

The phagocytosis and intracellular killing by synaivial fluid (SF) polymorphonuclear cells (PMN) of 10 patients with rheumatoid arthritis was studied. PMN phagocytosis was assessed by morphologic and microbliologic methods and intracellular killing was measured independently of continuous phagocytosis of Stuphylococcus uureus. Phagocytosis of S aureus by SF PMN or peripheral blood (PB) PMN was as effective in the presence of synovial fluid as in the presence of serum. On average, SF PMN ingested S uureus opsonizetl with synovial fluid and serum more efficiently than patient or donor PB PMN did. Enhanced ingestion of S aweus was associated with increased expression of C3 receptors on the membrane of SF PMN. In the presence of hleat-inactivated synovial fluid, the capacity of SF PMN to ingest S aumus was greater than that of patient or donor PB PMN. Under these conditions, phagocytic activity was correlated with Fc receptor expression. SF PMN was found to be as active in killing S aureus as PB PMPi from healthy donors.

Neutrophil Responsiveness to Chemoattractant Tripeptide in Rheumatoid Arthritis

“…Although previous chemotaxis studies are difficult to interpret because failure to control for known medication effects on neutrophil function ( 15) defective peripheral blood neutrophil responsiveness has been more consistently found in RA patients with Felty's syndrome than in those with RA alone (46,47). Moreover, recent studies have found no local defects in RA neutrophil migration (48) or in handling of the important pathogen Staphylococcus aureus (49). Our careful evaluation of neutrophil responsiveness to the well-defined bacterial chemoattractant f-Met-Leu-Phe supports these findings and describes a novel method for differentiating chemotactically distinct subpopulations of RA peripheral blood neutrophils.…”

A Risk-Benefit Assessment of Slow-Acting Antirheumatic Drugs in Rheumatoid Arthritis

“…[I04,105] Others have failed to confirm this. [106] The incidence of discontinuation of treatment because of leucopenia varies between 0.1 % for chloroquine and 1.5% for intramuscular gold. The likelihood of methotrexate, sulfasalazine and penicillamine being discontinued because of neutropenia is 1 %, while thrombocytopenia occurs most commonly with penicillamine (2.5%) and parenteral gold 0.1%»)107] The incidence of thrombocytopenia with gold therapy varies between o and 5%.…”

Activation of neutrophils by soluble and insoluble immunoglobulin aggregates from synovial fluid of patients with rheumatoid arthritis.

“…The mean age was 55 (21-80) years and the mean duration of disease was 7-6 (0. [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] cells/ml. Control suspensions contained no further additions and primed neutrophils were supplemented with 50 U/ml recombinant (r) GM-CSF.…”

“…Suspensions of neutrophils in RPMI 1640 medium (107/ml) were primed with 50 U/ml granulocytemacrophage colony stimulatingfactor (GM-CSF) for one hour at 37°C. After this incubation,5 ,ug/ml cytochalasin B was added to the suspensions before stimulation with 1 pMM fMet-Leu-Phe (0), 10% (v/v) of the supernatantfrom cell free synovialfluid (d), or 10% (v/v) the pelletfrom cellfree synovialfluid (0). The pellet and supernatant were obtained by centrifugation of cellfree synovialfluidfor two minutes at 11 600 g. After stimulation, 5X 105 cells were sampled at varying time points, the ceUs rapidly spun down, and the extracellular medium assayedfor myeloperoxidase activity.…”