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首页> 美国卫生研究院文献>PLoS Clinical Trials >Expression of SAA1, SAA2 and SAA4 genes in human primary monocytes and monocyte-derived macrophages
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Expression of SAA1, SAA2 and SAA4 genes in human primary monocytes and monocyte-derived macrophages

机译：SAA1，SAA2和SAA4基因在人原代单核细胞和单核细胞衍生的巨噬细胞中的表达

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Circulating serum amyloid A (SAA) is increased in various inflammatory conditions. The human SAA protein family comprises the acute phase SAA1/SAA2, known to activate a large set of innate and adaptive immune cells, and the constitutive SAA4. The liver synthesis of SAA1/SAA2 is well-established but there is still an open debate on extrahepatic SAA expression especially in macrophages. We aimed to investigate the ability of human primary monocytes and monocyte-derived macrophages to express SAA1, SAA2 and SAA4 at both the transcriptional and protein levels, as previous studies almost exclusively dealt with monocytic cell lines. Monocytes and derived macrophages from healthy donors were stimulated under various conditions. In parallel with SAA, pro-inflammatory IL1A, IL1B and IL6 cytokine expression was assessed. While LPS alone was non-effective, a combined LPS/dexamethasone treatment induced SAA1 and to a lesser extent SAA2 transcription in human monocytes and macrophages. In contrast, as expected, pro-inflammatory cytokine expression was strongly induced following stimulation with LPS, an effect which was dampened in the presence of dexamethasone. Furthermore, in monocytes polarized towards a pro-inflammatory M1 phenotype, SAA expression in response to LPS/dexamethasone was potentiated; a result mainly seen for SAA1. However, a major discrepancy was observed between SAA mRNA and intracellular protein levels under the experimental conditions used. Our results demonstrate that human monocytes and macrophages can express SAA genes, mainly SAA1 in response to an inflammatory environment. While SAA is considered as a member of a large cytokine network, its expression in the monocytes-macrophages in response to LPS-dexamethasone is strikingly different from that observed for classic pro-inflammatory cytokines. As monocytes-macrophages are major players in chronic inflammatory diseases, it may be hypothesized that SAA production from macrophages may contribute to the local inflammatory microenvironment, especially when macrophages are compactly organized in granulomas as in sarcoidosis.
机译：在各种炎症条件下，循环血清淀粉样蛋白A（SAA）都会增加。人SAA蛋白家族包含已知会激活大量先天性和适应性免疫细胞的急性期SAA1 / SAA2和组成型SAA4。 SAA1 / SAA2的肝脏合成已被公认，但关于肝外SAA表达，尤其是在巨噬细胞中，仍存在公开辩论。我们的目的是研究人类原代单核细胞和单核细胞衍生的巨噬细胞在转录和蛋白质水平上表达SAA1，SAA2和SAA4的能力，因为以前的研究几乎只涉及单核细胞系。在各种条件下刺激来自健康供体的单核细胞和衍生的巨噬细胞。与SAA并行，评估促炎性IL1A，IL1B和IL6细胞因子的表达。虽然单独使用LPS无效，但LPS /地塞米松联合治疗可诱导人单核细胞和巨噬细胞中的SAA1转录，并在较小程度上诱导SAA2转录。相反，如所预期的，LPS刺激后强烈诱导促炎性细胞因子表达，这种作用在地塞米松的存在下减弱。此外，在偏向促炎性M1表型的单核细胞中，响应LPS /地塞米松的SAA表达增强。主要针对SAA1的结果。但是，在使用的实验条件下，观察到SAA mRNA与细胞内蛋白质水平之间存在重大差异。我们的结果表明，人类单核细胞和巨噬细胞可以表达SAA基因，主要是对炎症环境做出反应的SAA1基因。虽然SAA被认为是大型细胞因子网络的成员，但它对LPS-地塞米松的反应在单核细胞-巨噬细胞中的表达与经典的促炎性细胞因子明显不同。由于单核细胞巨噬细胞是慢性炎性疾病的主要参与者，因此可以假设巨噬细胞产生的SAA可能有助于局部炎性微环境，尤其是当肉芽肿中巨噬细胞像结节病一样紧密组织时。

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