The Nicotinic Receptor Polymorphism rs16969968 Is Associated with Airway Remodeling and Inflammatory Dysregulation in COPD Patients

COPD; airways; epithelial remodeling; inflammation; nicotinic receptors; rs16969968.

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Lynda Saber Cherif, Zania Diabasana, Jeanne-Marie Perotin, Julien Ancel, Laure M G Petit, Maëva A Devilliers, Arnaud Bonnomet, Nathalie Lalun, Gonzague Delepine, Uwe Maskos, Philippe Gosset, Myriam Polette, Anaëlle Muggeo, Thomas Guillard, Gaëtan Deslée, Valérian Dormoy

期刊 Cells
影响因子 6
起止号 2022 Sep 20;11(19):2937.
种属 Human
技术平台抗体芯片
应用领域免疫/内分泌
研究方向免疫/内分泌
细胞类型上皮细胞
检测蛋白 Adiponectin/Acrp30,IFN-gamma,CCL2/MCP-1,Angiogenin,IGFBP-2,CCL7/MCP-3,Angiopoietin-1,IGFBP-3,M-CSF,Angiopoietin-2,IL-1 alpha/IL-1F1,MIF,Apolipoprotein A1,IL-1 beta/IL-1F2,CXCL9/MIG,BAFF/BLyS/TNFSF13B,IL-1ra/IL-1F3,CCL3/CCL4 MIP-1 alpha/beta,BDNF,IL-2,CCL20/MIP-3 alpha,CD14,IL-3,CCL19/MIP-3 beta,CD30,IL-4,MMP-9,CD31/PECAM-1,IL-5,Myeloperoxidase,CD40 Ligand/TNFSF5,IL-6,Osteopontin (OPN),Chitinase 3-like,IL-8,PDGF-AA,Complement Component C5/C5a,IL-10,PDGF-AB/BB,Complement Factor D,IL-11,Pentraxin 3/TSF-14,C-Reactive Protein/CRP,IL-12 p70,CXCL4/PF4,Cripto-1,IL-13,RAGE,Cystatin C,IL-15,CCL5/RANTES,Dkk-1,IL-16,RBP4,DPPIV/CD26,IL-17A,Relaxin-2,EGF,IL-18 BPa,Resistin,CXCL5/ENA-78,IL-19,CXCL12/SDF-1 alpha,Endoglin/CD105,IL-22,Serpin E1/PAI-1,EMMPRIN,IL-23,SHBG,Fas Ligand,IL-24,ST2/IL1 R4,FGF basic,IL-27,CCL17/TARC,KGF/FGF-7,IL-31,TFF3,FGF-19,IL-32 alpha/beta/gamma,TfR,Flt-3 Ligand,IL-33,TGF-alpha,G-CSF,IL-34,Thrombospondin-1,GDF-15,CXCL10/IP-10,TIM-1,GM-CSF,CXCL11/I-TAC,TNF-alpha,CXCL1/GRO alpha,Kallikrein 3/PSA,uPAR,Growth Hormone (GH),Leptin,VCAM-1,HGF,LIF,VEGF,ICAM-1/CD54,Lipocalin-2/NGAL,Vitamin D BP

Abstract

Genome-wide association studies unveiled the associations between the single nucleotide polymorphism rs16969968 of CHRNA5, encoding the nicotinic acetylcholine receptor alpha5 subunit (α5SNP), and nicotine addiction, cancer, and COPD independently. Here, we investigated α5SNP-induced epithelial remodeling and inflammatory response in human COPD airways. We included 26 α5SNP COPD patients and 18 wild-type α5 COPD patients in a multi-modal study. A comparative histologic analysis was performed on formalin-fixed paraffin-embedded lung tissues. Isolated airway epithelial cells from bronchial brushings were cultivated in the air-liquid interface. Broncho-alveolar fluids were collected to detect inflammatory mediators. Ciliogenesis was altered in α5SNP COPD bronchial and bronchiolar epithelia. Goblet cell hyperplasia was exacerbated in α5SNP small airways. The broncho-alveolar fluids of α5SNP COPD patients exhibited an increase in inflammatory mediators. The involvement of the rs16969968 polymorphism in airway epithelial remodeling and related inflammatory response in COPD prompts the development of innovative personalized diagnostic and therapeutic strategies.Keywords:COPD; airways; epithelial remodeling; inflammation; nicotinic receptors; rs16969968.

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