caa a22 4500 465764460 CHVBK 20180323111909.0 cr unu---uuuuu 170327e19900401xx s 000 0 eng 10.1007/BF00917454 doi (NATIONALLICENCE)springer-10.1007/BF00917454 Recombinant interleukin-1 β interacts with high-affinity receptors to activate neutrophil leukotriene B4 synthesis [Elektronische Daten] [Larry Borish, Raymond Rosenbaum, Brian Mcdonald, Lanny Rosenwasser] The capacity of interleukin-1 (IL-1) to function as a neutrophil (PMN) activator has been the subject of controversy. While IL-1 purified from mononuclear cell supematants induced PMN activation, these observations have not been confirmed with recombinant IL-1. To document a cellular basis for a putative PMN-IL-1 interaction, we investigated the presence of IL-1 receptors on the PMN. Using an [35S]methionine-labeled preparation, specific binding of IL-1 to PMNs was demonstrated. Through Scatchard analysis PMNs were calculated to have a mean of 469 ±337 receptors per PMN with an affinity(K d) of 0.32±0.09 nM. As IL-1 frequently activates arachidonic acid metabolism in other cell types, we investigated eicosanoid production as a putative consequence of the IL-1-PMN interaction. HPLC analysis of extracted supernatants of IL-1-treated PMNs demonstrated the release of leukotriene B4 (LTB4), its oxidative products, and 5-hydroxyeicosatetraenoic acid (5-HETE). Production of LTB4 was quantified using a commercial RIA. LTB4 secretion increased from 17.2±1.1 to 96.7+-16.4 ng, also with 10.0 ng of IL-1. In time-course studies, it was shown that maximal eicosanoid secretion required a 30-min incubation with IL-1. These observations confirm the proinflammatory activity of IL-1 on neutrophils and resolve the controversy concerning a direct effect of IL-1 on neutrophils. In conclusion, recombinant IL-1β interacts with neutrophils through the presence on the PMN of a high-affinity receptor and results in the secretion of arachidonate metabolites. Plenum Publishing Corporation, 1990 Borish Larry Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut Rosenbaum Raymond Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut Mcdonald Brian Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut Rosenwasser Lanny Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut Inflammation Kluwer Academic Publishers-Plenum Publishers 14/2(1990-04-01), 151-162 0360-3997 14:2<151 1990 14 10753 https://doi.org/10.1007/BF00917454 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00917454 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Borish Larry Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut NATIONALLICENCE 700 1- Rosenbaum Raymond Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut NATIONALLICENCE 700 1- Mcdonald Brian Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut NATIONALLICENCE 700 1- Rosenwasser Lanny Department of Medicine New England Medical Center, Tufts Medical School, 750 Washington St., 02111, Boston, Massachusetts aut NATIONALLICENCE 773 0- Inflammation Kluwer Academic Publishers-Plenum Publishers 14/2(1990-04-01), 151-162 0360-3997 14:2<151 1990 14 10753 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer