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首页> 外文期刊>Cellular immunology >Mycobacterium bovis Bacillus Calmette-Guerin (BCG)-induced activation of PI3K/Akt and NF-kB signaling pathways regulates expression of CXCL10 in epithelial cells.
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Mycobacterium bovis Bacillus Calmette-Guerin (BCG)-induced activation of PI3K/Akt and NF-kB signaling pathways regulates expression of CXCL10 in epithelial cells.

机译：牛分枝杆菌卡介苗（BCG）诱导的PI3K / Akt和NF-kB信号通路的激活调节上皮细胞中CXCL10的表达。

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摘要

CXCL10 production is a critical step in limiting mycobacterial infection. Although induction of this chemokine by mycobacteria in epithelial cells has been reported, it is still unclear how CXCL10 is regulated in Mycobacterium bovis BCG-infected epithelial cells. In this study, we demonstrate that phosphatidylinoditol 3-kinase (PI3K)/Akt and the nuclear factor kB (NF-kB) signaling pathways play an important role in CXCL10 expression at the protein and mRNA level in A549 cells. We demonstrate that treatment of A549 cells with LY294002 and wortmannin, two PI3K inhibitors, inhibited M. bovis BCG-induced CXCL10 expression. In addition, treatment of A549 cells with an Akt inhibitor significantly blocked M. bovis BCG-induced CXCL10 production. Moreover, our data show that treatment of epithelial cells with CAPE, BAY 11-7082, and PDTC three selective inhibitors of NF-kB, significantly reduced the effect of M. bovis BCG on induced CXCL10 mRNA expression (74%, 69% and 83% inhibition by 8microM CAPE, 10microM BAY 11-7082 and 3microM PDTC as assessed by real-time PCR, respectively). In accordance with the gene induction, the production of CXCL10 was also significantly reduced by these inhibitors. Finally, the inhibition of PI3K affect NF-kB activation in M. bovis BCG-infected cells, indicating that PI3K activity is required for the M. bovis BCG-induced activation of NF-kB. The functional association between PI3K/Akt and NF-kB demonstrates another mechanism in the regulation of M. bovis BCG-induced CXCL10 in A549 cells.
机译：CXCL10的生产是限制分枝杆菌感染的关键步骤。尽管已经报道了分枝杆菌在上皮细胞中诱导这种趋化因子，但是仍不清楚在牛分枝杆菌BCG感染的上皮细胞中如何调节CXCL10。在这项研究中，我们证明磷脂酰肌醇3激酶（PI3K）/ Akt和核因子kB（NF-kB）信号通路在A549细胞中蛋白质和mRNA水平的CXCL10表达中起重要作用。我们证明用两种PI3K抑制剂LY294002和渥曼青霉素对A549细胞的治疗抑制了牛分枝杆菌BCG诱导的CXCL10表达。另外，用Akt抑制剂处理A549细胞显着阻断牛分枝杆菌BCG诱导的CXCL10产生。此外，我们的数据显示，用CAPE，BAY 11-7082和PDTC三种选择性NF-kB抑制剂处理上皮细胞，可显着降低牛分枝杆菌BCG对诱导的CXCL10 mRNA表达的影响（74％，69％和83）分别通过实时PCR评估的8microM CAPE，10microM BAY 11-7082和3microM PDTC的抑制百分比）。根据基因诱导，这些抑制剂也显着降低了CXCL10的产生。最后，PI3K的抑制影响牛分枝杆菌BCG感染的细胞中NF-kB的激活，表明PI3K活性是牛分枝杆菌BCG诱导的NF-kB激活所必需的。 PI3K / Akt和NF-kB之间的功能关联证明了在牛分枝杆菌BCG诱导的A549细胞中CXCL10调控的另一种机制。

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