Exploration of the Shared Gene Signatures and Molecular Mechanisms between Chronic Bronchitis and Antineutrophil Cytoplasmic Antibody-associated Glomerulonephritis: Evidence from Transcriptome Data (2024)

Title:Exploration of the Shared Gene Signatures and Molecular Mechanismsbetween Chronic Bronchitis and Antineutrophil CytoplasmicAntibody-associated Glomerulonephritis: Evidence from Transcriptome Data

Volume: 30 Issue: 25

Author(s): Xiaojing Cai, Yueqiang Li, Qingquan Liu, Xiang Gao and Junhua Li*

Affiliation:

• Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan,China

Keywords: Chronic bronchitis, anti-neutrophil cytoplasmic antibody, crescent glomerulonephritis, vasculitis, bioinformatics, differentially expressed genes.

Abstract:

Background: Chronic Bronchitis (CB) is a recurrent and persistent pulmonary inflammation disease.Growing evidence suggests an association between CB and Anti-neutrophil Cytoplasmic Antibody-associatedGlomerulonephritis (ANCA-GN). However, the precise mechanisms underlying their association remainunclear.

Aims: The purpose of this study was to further explore the molecular mechanism of the occurrence of chronicbronchitis (CB) associated with anti-neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-GN).

Objective: Our study aimed to investigate the potential shared pathogenesis of CB-associated ANCA-GN.

Methods: Datasets of ANCA (GSE108113 and GSE104948) and CB (GSE151052 and GSE162635) were obtainedfrom the Gene Expression Omnibus (GEO) datasets. Firstly, GSE108113 and GSE151052 were analyzedto identify common differentially expressed genes (DEGs) by Limma package. Based on commonDEGs, protein-protein interaction (PPI) network and functional enrichment analyses, including GO, KEGG,and GSEA, were performed. Then, hub genes were identified by degree algorithm and validated inGSE104948 and GSE162635. Further PPI network and functional enrichment analyses were performed on hubgenes. Additionally, a competitive ceRNA network was constructed through miRanda and spongeScan. Transcriptionfactors (TFs) were predicted and verified using the TRRUST database. Furthermore, the CIBERSORTalgorithm was employed to explore immune cell infiltration. The Drug Gene Interaction Database(DGIDB) was utilized to predict small-molecular compounds of CB and ANCA-GN.

Results: A total of 963 DEGs were identified in the integrated CB dataset, and 610 DEGs were identified inthe integrated ANCA-GN dataset. Totally, we identified 22 common DEGs, of which 10 hub genes (LYZ, IRF1,PIK3CG, IL2RG, NT5E, ARG2, HBEGF, NFATC2, ALPL, and FKBP5) were primarily involved in inflammationand immune responses. Focusing on hub genes, we constructed a ceRNA network composed of323 miRNAs and 348 lncRNAs. Additionally, five TFs (SP1, RELA, NFKB1, HIF1A, and SP3) were identifiedto regulate the hub genes. Furthermore, immune cell infiltration results revealed immunoregulation in CBand ANCA-GN. Finally, some small-molecular compounds (Daclizumab, Aldesleukin, and NT5E) were predictedto predominantly regulate inflammation and immunity, especially IL-2.

Conclusion: Our study explores the inflammatory-immune pathways underlying CB-associated ANCA-GNand emphasizes the importance of NETs and lymphocyte differentiation, providing novel insights into theshared pathogenesis and therapeutic targets.

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Cai Xiaojing, Li Yueqiang, Liu Qingquan, Gao Xiang and Li Junhua*, Exploration of the Shared Gene Signatures and Molecular Mechanismsbetween Chronic Bronchitis and Antineutrophil CytoplasmicAntibody-associated Glomerulonephritis: Evidence from Transcriptome Data, Current Pharmaceutical Design 2024; 30 (25) . https://dx.doi.org/10.2174/0113816128297623240521070426

About this journal

Submission closes on: 30 July, 2024

Guest Editor(s): Dr. M Pinheiro

Submission closes on: 03 December, 2024

Guest Editor(s): Dr. Carlo Cervellati

Submission closes on: 18 September, 2024

Guest Editor(s): Dr. Sidharth Mehan

Submission closes on: 03 December, 2024

Guest Editor(s): Dr. Ali Yadollahpour,

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