Defective responsiveness to ascorbic acid of neutrophil random and chemotactic migration in Felty's syndrome and systemic lupus erythematosus

Abstract

Polymorphonuclear (PMN) leukocytes from 4 patients with untreated systemic lupus erythematosus (SLE) showed defective random migration (P < 0.05) and depressed chemotactic responses to C5a and kallikrein (P < 0.01) compared to PMN leukocytes from normal subjects, or patients with rheumatoid arthritis (4) or Felty's syndrome (4) when examined at a standardized cell concentration with a micropore filter radioassay but not with a conventional Boyden technique. Normal in vitro enhancement of PMN leukocyte random and chemotactic migration by sodium ascorbate was absent in SLE and Felty's syndrome, but sodium ascorbate gave normal stimulation of hexose monophosphate shunt activity in the PMN leukocytes precluding a defect in ascorbate transport.