caa a22 4500 477054579 CHVBK 20180405111344.0 cr unu---uuuuu 170330e19961201xx s 000 0 eng 10.1007/BF02602955 doi (NATIONALLICENCE)springer-10.1007/BF02602955 Priming of neutrophils with tumor necrosis factor-α measured as Fcγ receptor-mediated respiratory burst correlates with increased complement receptor 3 membrane density [Elektronische Daten] [B. Åsman, A. Gustafsson, K. Bergström] 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 FcγR-mediated respiratory burst, measured as chemiluminescence. Purified neutrophilic granulocytes from healthy volunteers were preincubated with recombinant human tumor necrosis factor-α. This had a priming effect, inqreasing both the Fcγ receptor-mediated luminol-enhanced chemiluminescence and the membrane expression of the C3bi receptor (CRB) (r=0.843). The membrane densities of FcγRII, FcγRIII, and CR1 were unaffected by tumor necrosis factor-α. The mechanism of increased chemiluminescence may involve redistribution of the Fcγ 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-α. In conclusion, a simultaneous increase in the FcγR-mediated respiratory burst and CR3 density after priming with tumor necrosis factor-α indicates a cooperation between FcγR and CR3. Springer-Verlag, 1996 Neutrophils nationallicence Respiratory burst nationallicence Tumor necrosis factor-α priming nationallicence Fcγ receptors nationallicence Complement receptors nationallicence Åsman B. Department of Laboratory Science and Technology, Division of Clinical Chemistry, Karolinska Institute, Huddinge University Hospital, S-141 86, Huddinge, Sweden aut Gustafsson A. Department of Laboratory Science and Technology, Division of Clinical Chemistry, Karolinska Institute, Huddinge University Hospital, S-141 86, Huddinge, Sweden aut Bergström K. Department of Laboratory Science and Technology, Division of Clinical Chemistry, Karolinska Institute, Huddinge University Hospital, S-141 86, Huddinge, Sweden aut International Journal of Clinical and Laboratory Research Springer-Verlag 26/4(1996-12-01), 236-239 0940-5437 26:4<236 1996 26 599 https://doi.org/10.1007/BF02602955 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02602955 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Åsman B. Department of Laboratory Science and Technology, Division of Clinical Chemistry, Karolinska Institute, Huddinge University Hospital, S-141 86, Huddinge, Sweden aut NATIONALLICENCE 700 1- Gustafsson A. Department of Laboratory Science and Technology, Division of Clinical Chemistry, Karolinska Institute, Huddinge University Hospital, S-141 86, Huddinge, Sweden aut NATIONALLICENCE 700 1- Bergström K. Department of Laboratory Science and Technology, Division of Clinical Chemistry, Karolinska Institute, Huddinge University Hospital, S-141 86, Huddinge, Sweden aut NATIONALLICENCE 773 0- International Journal of Clinical and Laboratory Research Springer-Verlag 26/4(1996-12-01), 236-239 0940-5437 26:4<236 1996 26 599 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer