Toll-like receptor-4, but not toll-like receptor-2 mediates secretion of tumour necrosis factor α and interleukin-8 in lipopolysaccharide-stimulated mouse mammary epithelial cells
Toll-like receptor-4, but not toll-like receptor-2 mediates secretion of tumour necrosis factor α and interleukin-8 in lipopolysaccharide-stimulated mouse mammary epithelial cells
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DOI：
10.2478/bvip-2013-0068
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发表时间：
2013-09
影响因子：
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通讯作者：
C. He;Qiong Yi;Yuanfang Li;Hang Yang;Lu Wang
中科院分区：
文献类型：
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作者：
C. He;Qiong Yi;Yuanfang Li;Hang Yang;Lu Wang
摘要分离昆明种小鼠乳腺上皮细胞，用10 μg/mL的大肠杆菌脂多糖（LPS）体外刺激。ELISA法检测培养上清中肿瘤坏死因子α（TNF-α）和白细胞介素8（IL-8）的释放。此外，用Toll样受体2（TLR 2）和TLR 4抗体进行阻断实验以验证细胞因子分泌是否依赖于LPS诱导的TLR 2或TLR 4活化。结果显示，LPS刺激的小鼠MEC可显著分泌TNF-α和IL-8。阻断TLR 4通路可抑制TNF-α和IL-8的分泌，而阻断TLR 2通路则不能抑制LPS诱导的TNF-α和IL-8的分泌。因此，TLR 4可以介导LPS诱导的小鼠MEC中细胞因子如TNF-α和IL-8的表达。
Abstract Mammary epithelial cells (MECs) from Kunming mice were isolated and stimulated in vitro with 10 μg/mL of Escherichia coli lipopolysaccharide (LPS). The release of tumour necrosis factor α (TNF-α) and interleukin-8 (IL-8) into culture supernatants was 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-stimulated mouse MECs significantly secreted TNF-α and IL-8. Blocking of the TLR4 pathway inhibited the secretion of TNF-α and IL-8, while inhibition of LPS-induced TNF-α and IL-8 production was not observed when TLR2 was blocked. Thus, TLR4 can mediate the LPS-induced expression of cytokines such as TNF-α and IL-8 in mouse MECs.