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首页> 外文期刊>Infection and immunity >Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages
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Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages

机译：Toll样受体2和4激动剂的信号转导在小鼠巨噬细胞中的差异基因表达。

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Lipopolysaccharide (LPS) derived from the periodontal pathogenPorphyromonas gingivalis has been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation of P. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants. More importantly, TLR2 stimulation by this P. gingivalis LPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages by Escherichia coli LPS. These data suggest that (i) P. gingivalis LPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively. Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.
机译：据报道，来自牙周病原菌牙龈卟啉单胞菌的脂多糖（LPS）在结构和功能上与肠杆菌脂多糖不同。这些研究表明，与不含蛋白质的肠细菌LPS相比，类似纯化的 P制剂。牙龈脂多糖具有强效的Toll样受体2（TLR2），而不是TLR4激动剂活性，可引起鼠巨噬细胞和转染子的基因表达和细胞因子分泌。更重要的是，此 P刺激TLR2。牙龈炎 LPS制备可导致一组基因的差异表达，这些基因通常是大肠杆菌 LPS在鼠巨噬细胞中诱导的。这些数据表明（i） P。牙龈炎LPS不能通过TLR4发出信号，并且（ii）通过TLR2和通过TLR4发出信号在数量和质量上都不同。我们的数据支持以下假设，即由TLR2和TLR4激动剂引起的共享信号通路必须分开，以解释炎症基因表达的不同模式。

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