Single-Cell Analysis Reveals the Role of the Neuropeptide Receptor FPR2 in Monocytes in Kawasaki Disease: A Bioinformatic Study

Author:

Wang Tengyang123,Liu Guanghua123ORCID,Guo Xiaofeng123ORCID,Ji Wei123

Affiliation:

1. Fujian Branch of Shanghai Children’s Medical Center Affiliated to Shanghai Jiaotong University School of Medicine, No. 966 Hengyu Road, Jinan, Fuzhou City, Fujian Province, China

2. Fujian Children’s Hospital, No. 966 Hengyu Road, Jinan, Fuzhou City, Fujian Province, China

3. Fujian Maternity and Child Health Hospital, Affiliated Hospital of Fujian Medical University, No. 18 Daoshan Road, Gulou District, Fuzhou City, Fujian Province, China

Abstract

Exploring the role of neuropeptides in the communication between monocyte subtypes facilitates an investigation of the pathogenesis of Kawasaki disease (KD). We investigated the patterns of interaction between neuropeptide-associated ligands and receptors in monocyte subpopulations in KD patients. Single-cell analysis was employed for the identification of cell subpopulations in KD patients, and monocytes were classified into 3 subpopulations: classical monocytes (CMs), intermediate monocytes (IMs), and nonclassical monocytes (NCMs). Cell-cell communication and differential analyses were used to identify ligand-receptor interactions in monocytes. Five neuropeptide-related genes (SORL1, TNF, SORT1, FPR2, and ANXA1) were involved in cell-cell interactions, wherein FPR2, a neuropeptide receptor, was significantly highly expressed in KD. Weighted gene coexpression network analysis revealed a significant correlation between the yellow module and FPR2 ( p < 0.001 , CC = 0.43 ). Using the genes in the yellow module, we constructed a PPI network to assess the possible functions of the FPR2-associated gene network. Gene set enrichment analysis showed that increased FPR2 levels may be involved in immune system regulation. FPR2 in CMs mediates the control of inflammation in KD. The findings of this study may provide a novel target for the clinical treatment of KD.

Publisher

Hindawi Limited

Subject

Biochemistry (medical),Clinical Biochemistry,Genetics,Molecular Biology,General Medicine

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