Neuropeptide Y, a potential marker for lupus, promotes lupus development.

Lupus NPY Relationship

Journal

International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259

Informations de publication

Date de publication:
24 Nov 2023
Historique:
received: 22 09 2023
revised: 17 11 2023
accepted: 18 11 2023
medline: 26 11 2023
pubmed: 26 11 2023
entrez: 25 11 2023
Statut: aheadofprint

Résumé

Relationship between neuropeptide Y (NPY) serum levels, NPY genetic mutation with systemic lupus erythematosus (SLE) pathogenesis is yet to be clarified, and role of NPY in development of SLE needs elucidation. This study included 460 SLE patients, 472 non-SLE cases, 500 healthy volunteers. Serum NPY, matrix metalloproteinase-1 (MMP-1) and MMP-8 levels were tested by ELISA. Genotyping 7 NPY single nucleotides polymorphisms (SNPs) (rs5573, rs5574, rs16129, rs16138, rs16140, rs16147, rs16478) was obtained by Kompetitive Allele-Specific PCR (KASP) method. Pristane-induced lupus mice were treated with NPY-Y1 receptor antagonist, and histological analysis, serological changes of the mice were evaluated. NPY serum concentrations were significantly increased in SLE patients when compared to that in healthy volunteers, non-SLE cases. Rs5573 G allele, rs16129 T allele, rs16147 G allele frequencies were significantly different between SLE cases and healthy controls. Rs5574 TT + TC genotypes were related to levels of IgG, C3, C4 and erythrocyte sedimentation rate, and rs16138 GG + GC genotypes correlated with SLE cases with anti-double-stranded deoxyribonucleic acid antibody (anti-dsDNA) (+). Serum MMP-1, MMP-8 concentrations were higher in SLE patients, and NPY levels were significantly related to MMP-1, MMP-8 levels. After treatment of lupus mice with NPY-Y1 receptor antagonist, damage of liver, spleen and kidney was alleviated, production of autoantibodies (anti-nuclear antibody (ANA), total IgG, anti-dsDNA) and MMP-1, MMP-8 was down-regulated, and differentiation of CD3 NPY may be a biomarker for lupus, which may promote occurrence and development of lupus.

Identifiants

pubmed: 38006754
pii: S1567-5769(23)01599-0
doi: 10.1016/j.intimp.2023.111272
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

111272

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Da-Cheng Wang (DC)

Department of Evidence-Based Medicine, Southwest Medical University, 1 Xianglin Road, Luzhou, Sichuan 646000, China.

Wang-Dong Xu (WD)

Department of Evidence-Based Medicine, Southwest Medical University, 1 Xianglin Road, Luzhou, Sichuan 646000, China.

Yang-Yang Tang (YY)

Department of Evidence-Based Medicine, Southwest Medical University, 1 Xianglin Road, Luzhou, Sichuan 646000, China.

Chan Yang (C)

Department of Evidence-Based Medicine, Southwest Medical University, 1 Xianglin Road, Luzhou, Sichuan 646000, China.

Rong Li (R)

Department of Evidence-Based Medicine, Southwest Medical University, 1 Xianglin Road, Luzhou, Sichuan 646000, China.

Guo-Cui Wu (GC)

School of Nursing, Anhui Medical University, 15 Feicui Road, Hefei, Anhui 230601, China.

An-Fang Huang (AF)

Department of Rheumatology and Immunology, Affiliated Hospital of Southwest Medical University, 25 Taiping Road, Luzhou, Sichuan 646000, China. Electronic address: loutch211@163.com.

Classifications MeSH