Neutrophil activation in anti-proteinase 3-positive vasculitis--a prospective study

In vitro studies have demonstrated that antineutrophil cytoplasmic antibodies (ANCA) have the capacity to activate neutrophils. Whether circulating neutrophils in patients with vasculitis are activated is under debate. Eight consecutive patients with antiproteinase 3 (PR3) positive acute vasculitis were included in this prospective study. Neutrophil expression of adhesion molecules, Fc-receptors and the ANCA-antigen PR3 was analysed and clinical characteristics were documented at inclusion and after 1, 3, 6 and 9 months in the same individuals. As additional markers of inflammation and endothelial activation interleukin-8 and soluble vascular cell adhesion molecule-1 in serum were analysed at the same time points. The expression of adhesion molecules on circulating neutrophils, CD62L and CD11b after in vitro N-formyl-methionyl-leucyl-phenylalanine stimulation was significantly decreased at diagnosis and after 1 month but returned to normal levels after 3-9 months. The neutrophil expression of Fc-receptor IIIb (CD 16) was decreased at diagnosis but normalized after 1-9 months. The main finding was an activated neutrophil adhesion phenotype at diagnosis and after 1 month, with normalized expression of adhesion molecules at 3-9 months. A pathological regulation of adhesion molecules may have implications on the endothelial damage seen in vasculitis.