Alterations of the complement system occurring during continuous‐flow filtration leukapheresis (CFFL) and intermittent‐flow centrifugation leukapheresis (IFCL) were assessed in 16 donors. Five blood samples were obtained at timed intervals during each cytaphere‐sis, three directly from each donor and two from the efferent lines returning blood from the leukapheresis machines to the donors. Components measured were C1, C2, C4, C3, C3‐C9 and CH50 of the classical, and factor B, properdin and properdin convertase of the alternative pathways. Changes in concentrations of components were compared to baseline values present in donor blood obtained prior to cytapheresis. During the first 10 minutes of CFFL, C2, C4, C3‐9 and CH50 were decreased (p < 0.05) in machine efferent fluids, but returned towards normal as the procedure continued. Changes in donor venous blood, decreased factor B, properdin and C3‐C9, were demonstrated only at the end of cytapheresis. During IFCL, significant (p < 0.05) decreases of C1, C2, C3‐C9 and factor B occurred in donor blood after 60 minutes of cytapheresis, however, all deficiencies except B corrected spontaneously as cytapheresis continued. In contrast, concentrations of C2, C4, C3‐C9, CH50 and factor B remained decreased in machine efferent fluids throughout the procedure. The data support those of previous studies that have demonstrated complement activation at the filter site during CFFL. Changes in donor venous blood are a new finding that may indicate in vivo activation of the alternative pathway. Profound changes of the complement system occur during IFCL also, but complement activation seems a less likely explanation. Instead, complement proteins may be lost by adsorption onto the surfaces of the IFCL software.

The reduction of nitroblue tetrazolium dye by human neutrophils was measured in the presence of serum in which the complement system had been activated through the alternate pathway by interaction with inulin. Neutrophils incubated with serum inulin supernatants reduced the dye and showed a general increase in oxidative metabolism. The oxidation of glucose-1–14-C by supernatant prepared from selectively depleted sera indicated that the neutrophil-stimulating factor(s) was generated through the alternate pathway of complement activation. The possibility that inulun had been ingested as a particle was ruled out by light microscopy and radiolabeling studies. The failure of neutrophils stimulated by the serum-inulun supernatants to migrate after exposure to a chemotactic agent suggested that the site of neutrophil-complement interaction was on the cell membrane. It is concluded from these results that biologically active fragments generated through the alternative pathway of complement activation can stimulate neutrophil metabolism in the absence of phagocytosis. Interaction of such fragments with circulating neutrophils in vivo and the subsequent metabolic activation of these cells is one explanation for the spontaneous reduction of nitroblue tetrazolium dye in vitro by neutrophils from patients with certain infections and inflammatory disorders.

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