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

Autor: Pappa V; The Children's Hospital of Philadelphia Research Institute, 3401 Civic Center Blvd., Philadelphia, PA 19104, USA., Spitsin S; The Children's Hospital of Philadelphia Research Institute, 3401 Civic Center Blvd., Philadelphia, PA 19104, USA., Gaskill PJ; Drexel University College of Medicine, 245 N 15th St., Philadelphia, PA 19102, USA., Douglas SD; The Children's Hospital of Philadelphia Research Institute, 3401 Civic Center Blvd., Philadelphia, PA 19104, USA; Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, PA 19104, USA. Electronic address: douglas@email.chop.edu.
Jazyk: angličtina
Zdroj: Journal of neuroimmunology [J Neuroimmunol] 2021 Apr 15; Vol. 353, pp. 577524. Date of Electronic Publication: 2021 Feb 20.
DOI: 10.1016/j.jneuroim.2021.577524
Abstrakt: 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.
(Copyright © 2021 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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