Complement activation on immunoglobulin G-coated hydrophobic surfaces enhances the release of oxygen radicals from neutrophils through an actin-dependent mechanism

Neutrophil granulocytes are among the first cells to encounter a plasma pro tein-coated implant and may through frustrated phagocytosis release toxic o xidative species. We used two model surfaces, hydrophobic and hydrophilic g lass, to investigate the effects of plasma immunoglobulin G (IgG)-complemen t interactions for neutrophil adhesion and respiratory burst. The respirato ry burst was measured with luminol-amplified chemiluminescence and cell adh esion was determined by labeling neutrophils with 2', 7'-bis-(carboxy-ethyl )-5(6)-carboxyfluorescein. We demonstrate that the IgG-triggered neutrophil adhesion and oxygen radical production is augmented in the presence of nor mal human serum, in particular on hydrophobic surfaces, indicating that com plement factors enhance the neutrophil activation. We propose that the comp lement factors C3, C5a, and Clq are especially important fur this amplifica tion, but factor B is probably not. Disturbance of the actin filament dynam ics with cytochalasin B or jasplakinolide blocked the neutrophil radical ge neration on all surfaces. However, these drugs did not affect the number of adherent neutrophils. We suggest that there is a synergistic interaction b etween adsorbed IgG, and the complement system, which amplifies the neutrop hil acute inflammatory responses through a dynamic actin cytoskeleton on sy nthetic surfaces. (C) 2000 John Wiley & Sons, Inc.