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首页> 美国政府科技报告 >Interaction of Recombinant IL-1 and Recombinant Tumor Necrosis Factor in the Induction of Mouse Acute Phase Proteins
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Interaction of Recombinant IL-1 and Recombinant Tumor Necrosis Factor in the Induction of Mouse Acute Phase Proteins

机译：重组IL-1与重组肿瘤坏死因子在小鼠急性期蛋白诱导中的相互作用

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Recombinant mouse and human interleukin (alpha and beta forms), as well as Interleukin alpha when administered in vivo, induced the production of the mouse acute phase reactants: serum amyloid P-component (SAP), C3, and fibrinogen. The maximum in vivo response consisted of a 10-levels increase in SAP levels, a 2-fold increase in C3 levels, and a 3-fold increase in fibrinogen concentration. By contrast, rTNF alpha induced a much smaller acute phase (AP) protein response (4-fold increase in SAP) when administered in vivo. Administration of a combination f rIL-1 and rTNF resulted in an AP response that was additive for SAP, synergistic for fibrinogen, but resulted in only the same amount of C3 induced by IL-1 alone. Both recombinant monokines induced new SAP synthesis by isolated hepatocytes in vitro with an optimal response occuring with either 1 U of rIL-1/ml per 200,000 or .001 U/ml of rTNF. The hepatocyte response to IL-1 was of the same magnitude as the response of intact mice; however, the response to TNF was approximately 10,000 times more efficient in vitro. Findings indicate that both monokines directly trigger hepatocyte synthesis of SAP and that their combined effect probable accounts for a substantial portion of the synthesis of these AP proteins in mice. Keywords: Inflammation, Immunology, Reprints. (aw)

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