Priming of neutrophils with tumor necrosis factor-alpha measured as Fc gamma receptor-mediated respiratory burst correlates with increased complement receptor 3 membrane density.

Hyperactive or primed neutrophils which damage tissue via cytokines and membrane receptors may be implicated in the pathogenesis of inflammatory conditions. The purpose of this study was to elucidate the priming mechanism in neutrophils by assessing changes in membrane receptors and the Fc gamma R-mediated respiratory burst, measured as chemiluminescence. Purified neutrophilic granulocytes from healthy volunteers were preincubated with recombinant human tumor necrosis factor-alpha. This had a priming effect, increasing both the Fc gamma receptor-mediated luminol-enhanced chemiluminescence and the membrane expression of the C3bi receptor (CRB) (r = 0.843). The membrane densities of Fc gamma RII, Fc gamma RIII, and CR1 were unaffected by tumor necrosis factor-alpha. The mechanism of increased chemiluminescence may involve redistribution of the Fc gamma receptors and cooperation with upregulated CR3, facilitating crosslinking of the receptors. The experiments were performed in a buffer without divalent cations, since these increased the background activity and abolished the priming effect of tumor necrosis factor-alpha. In conclusion, a simultaneous increase in the Fc gamma R-mediated respiratory burst and CR3 density after priming with tumor necrosis factor-alpha indicates a cooperation between Fc gamma R and CR3.