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Systemically Administered Ligands of Toll-Like Receptor 2, -4, and -9 Induce Distinct Inflammatory Responses in the Murine Lung

机译:系统管理的配体 类似Toll的受体2,-4和-9诱导鼠肺明显的炎症反应

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摘要

Objective. To determine whether systemically administered TLR ligands differentially modulate pulmonary inflammation. Methods. Equipotent doses of LPS (20 mg/kg), CpG-ODN (1668-thioat 1 nmol/g), or LTA (15 mg/kg) were determined via TNF activity assay. C57BL/6 mice were challenged intraperitoneally. Pulmonary NFκB activation (2 h) and gene expression/activity of key inflammatory mediators (4 h) were monitored. Results. All TLR ligands induced NFκB. LPS increased the expression of TLR2, 6, and the cytokines IL-1αβ, TNF-α, IL-6, and IL-12p35/p40, CpG-ODN raised TLR6, TNF-α, and IL12p40. LTA had no effect. Additionally, LPS increased the chemokines MIP-1α/β, MIP-2, TCA-3, eotaxin, and IP-10, while CpG-ODN and LTA did not. Myeloperoxidase activity was highest after LPS stimulation. MMP1, 3, 8, and 9 were upregulated by LPS, MMP2, 8 by CpG-ODN and MMP2 and 9 by LTA. TIMPs were induced only by LPS. MMP-2/-9 induction correlated with their zymographic activities. Conclusion. Pulmonary susceptibility to systemic inflammation was highest after LPS, intermediate after CpG-ODN, and lowest after LTA challenge.
机译:目的。为了确定全身施用的TLR配体是否差异调节肺部炎症。方法。通过TNF活性测定法确定了等效剂量的LPS(20μg/ kg),CpG-ODN(1668-硫代1μnmol/ g)或LTA(15μmg/ kg)。 C57BL / 6小鼠腹膜内攻击。监测肺的NFκB活化(2 h)和关键炎症介质的基因表达/活性(4 h)。结果。所有TLR配体均诱导NFκB。 LPS增加TLR2、6和细胞因子IL-1αβ,TNF-α,IL-6和IL-12p35 / p40的表达,CpG-ODN升高TLR6,TNF-α和IL12p40的表达。 LTA无效。另外,LPS增加了趋化因子MIP-1α/β,MIP-2,TCA-3,嗜酸性粒细胞趋化因子和IP-10,而CpG-ODN和LTA没有。 LPS刺激后,髓过氧化物酶活性最高。 LMP上调MMP1、3、8和9,CpG-ODN和MMP2上调MMP2,LTA上调9。 TIMP仅由LPS诱导。 MMP-2 / -9诱导与其酶活性有关。结论。 LPS后,肺部对全身性炎症的敏感性最高,CpG-ODN后为中等,而LTA激发后的最低。

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