神经激肽-1 受体信号诱导 CD16+单核细胞中促炎转录组特征。
Neurokinin-1 receptor signaling induces a pro-inflammatory transcriptomic profile in CD16+ monocytes.
机构信息
The Children's Hospital of Philadelphia Research Institute, 3401 Civic Center Blvd., Philadelphia, PA 19104, USA.
Drexel University College of Medicine, 245 N 15th St., Philadelphia, PA 19102, USA.
出版信息
J Neuroimmunol. 2021 Apr 15;353:577524. doi: 10.1016/j.jneuroim.2021.577524. Epub 2021 Feb 20.
Neurokinin-1 receptor (NK1R) signaling can be immunomodulatory and it can lead to preferential transmigration of CD14+CD16+ monocytes across the blood brain barrier, potentially promoting the development of inflammatory neurological diseases, such as neuroHIV. To evaluate how NK1R signaling alters monocyte biology, RNA sequencing was used to define NK1R-mediated transcriptional changes in different monocyte subsets. The data show that NK1R activation induces a greater number of changes in CD14+CD16+ monocytes (152 differentially expressed genes), than in CD14+CD16- monocytes (36 genes), including increases in the expression of NF-κB and components of the NLRP3 inflammasome pathway. These results suggest that NK1R may alter the inflammatory state of CD14+CD16+ monocytes, influencing the development of neuroinflammation.
神经激肽-1 受体（NK1R）信号具有免疫调节作用，它可以导致 CD14+CD16+单核细胞优先穿过血脑屏障，从而可能促进炎症性神经疾病的发展，如神经 HIV。为了评估 NK1R 信号如何改变单核细胞生物学，我们使用 RNA 测序来定义 NK1R 介导的不同单核细胞亚群的转录变化。数据表明，NK1R 激活诱导 CD14+CD16+单核细胞（152 个差异表达基因）的变化比 CD14+CD16-单核细胞（36 个基因）更多，包括 NF-κB 的表达增加和 NLRP3 炎症小体途径的组成部分。这些结果表明，NK1R 可能改变 CD14+CD16+单核细胞的炎症状态，影响神经炎症的发展。
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