Interleukin 13 inhibits macrophage inflammatory protein-1 alpha production from human alveolar macrophages and monocytes
Interleukin 13 inhibits macrophage inflammatory protein-1 alpha production from human alveolar macrophages and monocytes
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DOI：
10.1165/ajrcmb.15.3.8810643
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发表时间：
1996-09-01
影响因子：
6.4
通讯作者：
Chung, KF
中科院分区：
文献类型：
--
作者：
Berkman, N;John, M;Chung, KF
白细胞介素13 （IL-13）是最近发现的一种由活化的T细胞分泌的蛋白，是人类单核细胞和b细胞功能的有效体外调节剂。IL-13与IL-4具有一些生物学特性和结构相似性。巨噬炎性蛋白1 α (MIP-1 α)是单核细胞和巨噬细胞活化的产物，是T细胞、单核细胞和巨噬细胞的重要激活因子。我们检测了人重组IL-13对外周血单核细胞（PBM）和肺泡巨噬细胞（AM）中脂多糖（LPS）和IL-1 β诱导的MIP-1 α mRNA和蛋白表达的影响。在PBM中，基础MIP-1 α蛋白为20 +/- 7 pM，在LPS和IL-1 β后增加至1,520 +/- 193 pM （P < 0.001）和233 +/- 50 pM （P < 0.003）。IL-13 （25 ng/ml）分别使这些数值降低了55 +/- 10%[无统计学意义（NS）]、43 +/- 9% （P < 0.03）和44 +/- 15% （NS）。LPS和IL-1 β诱导的MIP-1 α mRNA表达分别降低43 +/- 5% （P < 0.01）和41 +/- 4% （NS）。在AM中，IL-13使lps诱导的2030 +/- 242 pM的MIP-1 α蛋白释放减少32 +/- 8% (P < 0.05)， MIP-1 α mRNA释放减少27 +/- 1% （NS）。对于PBM和AM， IL-13对MIP-1 α蛋白的抑制作用在24 h时达到最大，呈剂量依赖性，在100 ng/ml时达到最大效果，与IL-4相似，但效力略低于IL-4。在PBM中，IL-13的抑制作用需要从头合成蛋白质，而不是由于mRNA衰变增强。因此，IL-13对单核细胞和巨噬细胞的MIP-1 α转录具有抑制作用，并且与IL-4和IL-10一样，可能是抑制炎症反应的重要介质。
Interleukin 13 (IL-13) is a recently described protein secreted by activated T cells and is a potent in vitro modulator of human monocyte and B-cell functions. IL-13 shares some biologic properties as well as structural similarities with IL-4. Macrophage-inflammatory protein 1 alpha (MIP-1 alpha) is a product of activated monocytes and macrophages and an important activator of T cells, monocytes, and macrophages. We determined the effect of human recombinant IL-13 on lipopolysaccharide (LPS)- and IL-1 beta-induced MIP-1 alpha mRNA and protein expression from peripheral blood monocytes (PBM) and alveolar macrophages (AM). In PBM, basal MIP-1 alpha protein was 20 +/- 7 pM and increased following LPS and IL-1 beta to 1,520 +/- 193 (P < 0.001) and 233 +/- 50 (P < 0.003) pM. IL-13 (25 ng/ml) reduced these values by 55 +/- 10% [not significant (NS)], 43 +/- 9% (P < 0.03), and 44 +/- 15% (NS), respectively. LPS- and IL-1 beta-induced MIP-1 alpha mRNA expression was reduced by 43 +/- 5% (P < 0.01) and 41 +/- 4% (NS). In AM, IL-13 reduced LPS-induced MIP-1 alpha protein release of 2,030 +/- 242 pM by 32 +/- 8% (P < 0.05) and MIP-1 alpha mRNA by 27 +/- 1% (NS). For both PBM and AM, the inhibitory effect of IL-13 on MIP-1 alpha protein was maximal at 24 h, was dose dependent with a maximal effect at 100 ng/ml, and was similar to, although slightly less potent than, that seen with IL-4. In PBM, the inhibitory effect of IL-13 required de novo protein synthesis and was not due to enhanced mRNA decay. Thus, IL-13 has inhibitory effects on the transcription of MIP-1 alpha from monocytes and macrophages, and as is the case with IL-4 and IL-10, may be an important mediator for suppressing inflammatory responses.