Neurokinin-1 receptor signaling induces a pro-inflammatory transcriptomic profile in CD16+monocytes

被引：4

作者：

Pappa, Vasiliki ^{[1
]}

Spitsin, Sergei ^{[1
]}

Gaskill, Peter J. ^{[2
]}

Douglas, Steven D. ^{[1
,3
]}

机构：

[1] Childrens Hosp Philadelphia, Res Inst, 3401 Civ Ctr Blvd,Abramson Bldg,Room 1208A, Philadelphia, PA 19104 USA

[2] Drexel Univ, Coll Med, 245 N 15th St, Philadelphia, PA 19102 USA

[3] Univ Penn, Perelman Sch Med, 3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2021年 / 353卷

基金：

美国国家卫生研究院;

关键词：

Neurokinin-1; receptor; Substance P; Monocyte subsets; CD16; RNA sequencing; SUBSTANCE-P; GLYCOLYSIS; MONOCYTES; REPLICATION;

D O I：

10.1016/j.jneuroim.2021.577524

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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-kappa B 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.

引用

页数：5

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