首页> 外文期刊>Bulletin of the Veterinary Institute in Pulawy >Toll-like receptor-4, but not toll-like receptor-2 mediates secretion of tumour necrosis factor alpha and interleukin-8 in lipopolysaccharide-stimulated mouse mammary epithelial cells
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Toll-like receptor-4, but not toll-like receptor-2 mediates secretion of tumour necrosis factor alpha and interleukin-8 in lipopolysaccharide-stimulated mouse mammary epithelial cells

机译:Toll样受体4,但不是Toll样受体2介导脂多糖刺激的小鼠乳腺上皮细胞中肿瘤坏死因子α和白介素8的分泌

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摘要

Mammary epithelial cells (MECs) from Kunming mice were isolated and stimulated in vitro with 10 mug/mL of Escherichia coli lipopolysacchande (LPS). The release of tumour necrosis factor a (TNF-alpha) and interleukin-8 (IL-8) into culture supernatantswas measured by ELISA. Furthermore, blocking experiments with Toll-like receptor 2 (TLR2) and TLR4 antibodies were performed to verify whether cytokine secretion depended on LPS-induced activation of TLR2 or TLR4. The results revealed that LPS-stimulatedmouse MECs significantly secreted TNF-alpha and IL-8. Blocking of the TLR4 pathway inhibited the secretion of TNF-alpha and IL-8, while inhibition of LPS-induced TNF-alpha and IL-8 production was not observed when TLR2 was blocked. Thus, TI.R4 can mediate the LPS-induced expression of cytokines such as TNF-alpha and IL-8 in mouse MECs.
机译:分离来自昆明小鼠的乳腺上皮细胞(MEC),并用10杯/ mL的大肠杆菌脂多糖(LPS)体外刺激。通过ELISA测定了肿瘤坏死因子α(TNF-α)和白介素8(IL-8)向培养上清液中的释放。此外,进行了使用Toll样受体2(TLR2)和TLR4抗体的阻断实验,以验证细胞因子的分泌是否依赖于LPS诱导的TLR2或TLR4的激活。结果表明,LPS刺激的小鼠MEC显着分泌TNF-α和IL-8。 TLR4途径的阻滞抑制了TNF-α和IL-8的分泌,而当TLR2被阻滞时未观察到LPS诱导的TNF-α和IL-8产生的抑制作用。因此,TI.R4可以介导小鼠MEC中LPS诱导的细胞因子(如TNF-α和IL-8)的表达。

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