The crosstalk between Dectin1 and TLR4 via NF-κB subunits p65/RelB in mammary epithelial cells.
The crosstalk between Dectin1 and TLR4 via NF-κB subunits p65/RelB in mammary epithelial cells.
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DOI：
10.1016/j.intimp.2014.09.004
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发表时间：
2014-12
影响因子：
5.6
通讯作者：
Wei Zhu;Nai-shuo Zhu;Dou Bai;J. Miao;S. Zou
中科院分区：
文献类型：
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作者：
Wei Zhu;Nai-shuo Zhu;Dou Bai;J. Miao;S. Zou
乳腺上皮细胞（MECs）作为乳腺功能单元的一部分，不仅负责乳中许多成分的合成，为后代提供必要的营养和免疫支持，而且在乳腺炎病原体的反应和免疫信号通路的启动中发挥重要作用。MEC对病原体相关分子模式（pathogen associated molecular patterns, PAMPs）如LPS、脂质胆酸（lipoteichoic acid， LTA）和β-葡聚糖的信号传导和产生有一定的贡献，但不同PAMPs之间的串扰对大鼠MEC信号传导和产生的影响有待进一步研究。在本研究中，我们通过大鼠mec中siDectin1和siTLR4的产生证实了β-葡聚糖直接上调Dectin1和LPS上调TLR4。然后我们的结果描述了β-葡聚糖或LPS都可以激活大鼠mec中的RelB和/或p65。此外，p65和RelB的关联分析表明，β-葡聚糖和LPS共同促进p65/RelB异源二聚体，在大鼠mec中产生炎症反应。综上所述，我们目前的研究结果表明β-葡聚糖可以被认为是一种潜在的免疫调节剂，它通过NF-κB亚基与TLR4一起启动和调节大鼠mec的先天免疫。
Mammary epithelial cells (MECs), as part of the functional unit of the udder, are not only responsible for the synthesis of many components in milk that provide necessary nutritional and immunological support to the offspring, but also playing essential roles in the reaction to mastitis pathogens and the initiation of the immune signaling pathway. There are contributions of MECs to the signaling and production of pathogen associated molecular patterns (PAMPs) such as LPS, lipoteichoic acid (LTA), and β-glucans, but the crosstalk of different PAMPs induces signalings and productions in rat MEC that need further study. In the present study, we have demonstrated that β-glucan up-regulates Dectin1 and LPS up-regulates TLR4 directly, as confirmed by generation of siDectin1 and siTLR4 in rat MECs. Then our results have described that either β-glucan or LPS can activate RelB and/or p65 in rat MECs. Furthermore, the association of p65 and RelB has been analyzed that collaboration of β-glucan and LPS promotes p65/RelB heterodimers, producing inflammatory responses in rat MECs. In conclusion, summary of our present results suggests that β-glucan can be considered as a potential immuno-modulator, which s with TLR4 via NF-κB subunits to initiate and regulate the innate immunity in rat MECs.