caa a22 4500 465764134 CHVBK 20180323111908.0 cr unu---uuuuu 170327e19900601xx s 000 0 eng 10.1007/BF00915814 doi (NATIONALLICENCE)springer-10.1007/BF00915814 IL-1 and IL-6 mediate increased production and synthesis by hepatocytes of acute-phase reactant mouse serum amyloid P-component (SAP) [Elektronische Daten] [Bih-Fen Lin, Nam-On Ku, Kamyar Zahedi, Alexander Whitehead, Richard Mortensen] Primary mouse hepatocytes exposed to the inflammatory cytokines IL-1 and IL-6 in vitro displayed an increase in the production of the major acute-phase reactant, serum amyloid P-component (SAP). Antiserum to recombinant human IL-6 selectively neutralized the SAP-inducing activity secreted by human diploid fibroblasts. Purified mouse interferon-Β-(IFN-Β), but not IFN-α, also induced SAP production. Addition of 0.05 ng/ml of recombinant mouse IL-1α induced a 10-fold increase in SAP production, whereas recombinant human and recombinant mouse IL-6 displayed optimal SAP-inducing activity of four-fold and seven-fold at 10 ng/ ml and 1 unit/ml/2×105 mouse hepatocytes, respectively. The SAP-inducing activity was neutralized by antibodies to each of the recombinant cytokines. The kinetics of the SAP response in vitro was similar for all of the cytokines. Addition of a mixture of IL-1 and IL-6 to the hepatocytes resulted in SAP production that was not synergistic, but additive, over a range of concentrations for each cytokine. The increase in SAP production mediated by the cytokines was in part the result of an increase in the level of SAP mRNA. Metabolic incorporation of [35S]methionine into mouse SAP occurred in response to both IL-1 and IL-6. Therefore, mouse SAP should be classified among the subset of acute-phase proteins that can be induced by the direct action of either IL-1 or IL-6 on hepatocytes. Plenum Publishing Corporation, 1990 Lin Bih-Fen Department of Microbiology, The Ohio State University, 484 W.12 Avenue, 43210, Columbus, Ohio aut Ku Nam-On Department of Microbiology, The Ohio State University, 484 W.12 Avenue, 43210, Columbus, Ohio aut Zahedi Kamyar Division of Immunology, The Children's Hospital, USA aut Whitehead Alexander Division of Immunology, The Children's Hospital, USA aut Mortensen Richard Department of Microbiology, The Ohio State University, 484 W.12 Avenue, 43210, Columbus, Ohio aut Inflammation Kluwer Academic Publishers-Plenum Publishers 14/3(1990-06-01), 297-313 0360-3997 14:3<297 1990 14 10753 https://doi.org/10.1007/BF00915814 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00915814 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Lin Bih-Fen Department of Microbiology, The Ohio State University, 484 W.12 Avenue, 43210, Columbus, Ohio aut NATIONALLICENCE 700 1- Ku Nam-On Department of Microbiology, The Ohio State University, 484 W.12 Avenue, 43210, Columbus, Ohio aut NATIONALLICENCE 700 1- Zahedi Kamyar Division of Immunology, The Children's Hospital, USA aut NATIONALLICENCE 700 1- Whitehead Alexander Division of Immunology, The Children's Hospital, USA aut NATIONALLICENCE 700 1- Mortensen Richard Department of Microbiology, The Ohio State University, 484 W.12 Avenue, 43210, Columbus, Ohio aut NATIONALLICENCE 773 0- Inflammation Kluwer Academic Publishers-Plenum Publishers 14/3(1990-06-01), 297-313 0360-3997 14:3<297 1990 14 10753 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer