当前位置: X-MOL 学术Int. J. Med. Microbiol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
LincRNA-Cox2 regulates IL6/JAK3/STAT3 and NF-κB P65 pathway activation in Listeria monocytogenes-infected RAW264.7 cells
International Journal of Medical Microbiology ( IF 4.1 ) Pub Date : 2021-06-09 , DOI: 10.1016/j.ijmm.2021.151515
Yurong Zhu 1 , Ye Lu 2 , Lin Yuan 3 , Wei Ling 3 , Xugan Jiang 3 , Shengxia Chen 3 , Bing Hu 4
Affiliation  

Listeria monocytogenes (Lm) can lead to high mortality rates relative to other foodborne pathogens. Lm-induced inflammation is partly characterized by macrophage activation. Long non-coding RNAs (lncRNAs) have important roles in various biological processes. However, it is unknown how lncRNAs regulate the host response to Lm infection. To identify the role of lncRNA in Lm infection, we used in vitro and in vivo models. We found that lincRNA-Cox2 was highly expressed in Lm-infected RAW264.7 cells. LincRNA-Cox2 knockdown resulted in reduced proinflammatory cytokines, apoptosis, migration ability and enhanced phagocytosis of Lm. LincRNA-Cox2 knockdown also reduced the phosphorylation of Janus kinase 3 (JAK3) and signal transducer and activator of transcription (STAT3) and the nuclear translocation of nuclear factor (NF)-κB P65, which are known to be involved in inflammatory responses. Experimentally inhibiting the protein and phosphorylation levels of STAT3 resulted in reduced proinflammatory cytokines and enhanced phagocytosis of Lm by the RAW264.7 cells. Our research suggests that lincRNA-Cox2 plays important roles in inflammation, the phagocytic function and cell migration ability of RAW264.7 cells by activating interleukin (IL)-6/JAK3/STAT3 signaling, and lincRNA-Cox2 also regulates NF-κB P65 nuclear translocation. Our research provides new insights into the regulatory role of lincRNA-Cox2 in Lm infection.



中文翻译:

LincRNA-Cox2 调节单核细胞增生李斯特菌感染的 RAW264.7 细胞中的IL6/JAK3/STAT3 和 NF-κB P65 通路激活

李斯特菌(Lm) 可导致相对于其他食源性病原体的高死亡率。Lm 诱导的炎症部分以巨噬细胞激活为特征。长链非编码 RNA (lncRNA) 在各种生物过程中具有重要作用。然而,lncRNA 如何调节宿主对 Lm 感染的反应尚不清楚。为了确定 lncRNA 在 Lm 感染中的作用,我们使用了体外和体内模型。我们发现 lincRNA-Cox2 在 Lm 感染的 RAW264.7 细胞中高度表达。LincRNA-Cox2 敲低导致促炎细胞因子减少、细胞凋亡、迁移能力和 Lm 吞噬作用增强。LincRNA-Cox2 敲低还降低了 Janus 激酶 3 (JAK3) 和信号转导和转录激活因子 (STAT3) 的磷酸化以及核因子 (NF)-κB P65 的核易位,已知与炎症反应有关。通过实验抑制 STAT3 的蛋白质和磷酸化水平导致促炎细胞因子减少和 RAW264.7 细胞对 Lm 的吞噬作用增强。我们的研究表明 lincRNA-Cox2 通过激活白细胞介素 (IL)-6/JAK3/STAT3 信号传导在 RAW264.7 细胞的炎症、吞噬功能和细胞迁移能力中发挥重要作用,并且 lincRNA-Cox2 还调节 NF-κB P65 核易位。我们的研究为 lincRNA-Cox2 在 Lm 感染中的调节作用提供了新的见解。通过激活白细胞介素 (IL)-6/JAK3/STAT3 信号传导来调节 RAW264.7 细胞的吞噬功能和细胞迁移能力,lincRNA-Cox2 还调节 NF-κB P65 核转位。我们的研究为 lincRNA-Cox2 在 Lm 感染中的调节作用提供了新的见解。通过激活白细胞介素 (IL)-6/JAK3/STAT3 信号传导来调节 RAW264.7 细胞的吞噬功能和细胞迁移能力,并且 lincRNA-Cox2 还调节 NF-κB P65 核转位。我们的研究为 lincRNA-Cox2 在 Lm 感染中的调节作用提供了新的见解。

更新日期:2021-06-16
down
wechat
bug