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首页> 外文期刊>Infection and immunity >Host Response to Infection: the Role of CpG DNA in Induction of Cyclooxygenase 2 and Nitric Oxide Synthase 2 in Murine Macrophages
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Host Response to Infection: the Role of CpG DNA in Induction of Cyclooxygenase 2 and Nitric Oxide Synthase 2 in Murine Macrophages

机译：宿主对感染的反应：CpG DNA在小鼠巨噬细胞中环氧合酶2和一氧化氮合酶2诱导中的作用

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Depending on sequence, bacterial and synthetic DNAs can activate the host immune system and influence the host response to infection. The purpose of this study was to determine the abilities of various phosphorothioate oligonucleotides with cytosine-guanosine-containing motifs (CpG DNA) to activate macrophages to produce nitric oxide (NO) and prostaglandin E2 (PGE2) and to induce expression of NO synthase 2 (NOS2) and cyclooxygenase 2 (COX2). As little as 0.3 μg of CpG DNA/ml increased NO and PGE2production in a dose- and time-dependent fashion in cells of the mouse macrophage cell line J774. NO and PGE2 production was noted by 4 to 8 h after initiation of cultures with the CpG DNA, with the kinetics of NO production induced by CpG DNA being comparable to that induced by a combination of lipopolysaccharide and gamma interferon. CpG DNA-treated J774 cells showed enhanced expression of NOS2 and COX2 proteins as determined by immunoblotting, with the relative potencies of the CpG DNAs generally corresponding to those noted for the induction of NO and PGE2 production as well as to those noted for the induction of interleukin-6 (IL-6), IL-12, and tumor necrosis factor. Extracts from CpG DNA-treated cells convertedl-arginine to l-citrulline, but the NOS inhibitorN G-monomethyl-l-arginine (NMMA) inhibited this reaction. The COX2-specific inhibitor NS398 inhibited CpG DNA-induced PGE2 production and inhibited NO production to various degrees. The NOS inhibitors NMMA, 1400W, andN-iminoethyl-l-lysine effectively blocked NO production and increased the production of PGE2 in a dose-dependent fashion. Thus, analogues of microbial DNA (i.e., CpG DNA) activate mouse macrophage lineage cells for the expression of NOS2 and COX2, with the production of NO and that of PGE2occurring in an interdependent manner.
机译：根据序列，细菌和合成DNA可以激活宿主免疫系统并影响宿主对感染的反应。这项研究的目的是确定具有胞嘧啶-鸟苷基序（CpG DNA）的各种硫代磷酸酯寡核苷酸激活巨噬细胞产生一氧化氮（NO）和前列腺素E 2 （PGE > 2 ）并诱导NO合酶2（NOS2）和环氧合酶2（COX2）的表达。小鼠巨噬细胞系J774细胞中，低至0.3μgCpG DNA / ml会以剂量和时间依赖性方式增加NO和PGE 2 的产生。在开始用CpG DNA培养4至8小时后，观察到NO和PGE 2 的产生，CpG DNA诱导的NO产生的动力学与脂多糖和γ的组合诱导的动力学相当。干扰素。经免疫印迹测定，经CpG DNA处理的J774细胞显示NOS2和COX2蛋白表达增强，CpG DNA的相对效能通常也与诱导NO和PGE 2 产生的能力相对应。关于诱导白介素6（IL-6），IL-12和肿瘤坏死因子的那些。经CpG DNA处理的细胞的提取物将1-精氨酸转化为1-瓜氨酸，但NOS抑制剂 N G -单甲基-1-精氨酸（NMMA）抑制了该反应。 COX2特异性抑制剂NS398在不同程度上抑制了CpG DNA诱导的PGE 2 的产生，并抑制了NO的产生。 NOS抑制剂NMMA，1400W和 N -亚氨基乙基-1-赖氨酸可以有效地阻断NO的产生，并以剂量​​依赖的方式增加PGE 2 的产生。因此，微生物DNA的类似物（即CpG DNA）激活小鼠巨噬细胞谱系细胞表达NOS2和COX2，并以相互依赖的方式产生NO和PGE 2 。

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