ArticleFrontiers in immunology2022
Identification and validation of the common pathogenesis and hub biomarkers in Hirschsprung disease complicated with Crohn's disease.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 30 citations in OpenAlex.
- Crohn's Disease Developing After Hirschsprung's Disease in a Child With Down Syndrome: A Rare Clinical Overlap.Cureus · 2026Article
- Diagnostic and prognostic significance of Super-enhancer-associated genes in Crohn's disease and immune regulatory roles.European journal of medical research · 2025Article
- Clinicopathologic features of allied disorders of Hirschsprung disease and status update.World journal of gastrointestinal surgery · 2025Review
- Identification of ulcerative colitis diagnostic markers from differentially expressed genes shared with Hirschsprung disease.Scientific reports · 2025Article
- Article
- Bioinformatics Prediction for Network-Based Integrative Multi-Omics Expression Data Analysis in Hirschsprung Disease.Biomolecules · 2024Article
- A unicentric cross-sectional observational study on chronic intestinal inflammation in total colonic aganglionosis: beware of an underestimated condition.Orphanet journal of rare diseases · 2023Observational
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Although increasing evidence has supported that Hirschsprung disease (HSCR) is the risk factor for children developing Crohn's disease (CD), the common mechanism of its co-occurrence remains unknown. The purpose of this study is to further explore the underlying mechanism and biomarkers for the co-occurrence of HSCR and CD. Methods: The Gene Expression Omnibus (GEO) database was used to obtain gene expression profiles for CD (GSE95095) and HSCR (GSE98502). Following the identification of the shared differentially expressed genes (DEGs) of CD and HSCR, functional annotation, protein-protein interaction (PPI) network creation, and module assembly were performed to discover hub genes. RT-qPCR was performed to validate the expression of the hub genes in HSCR samples. The receiver operating characteristic (ROC) curve was utilized to assess the accuracy of the hub genes as biomarkers in predicting CD in both the training dataset and test dataset. Results: A total of 103 common DEGs (50 downregulated genes and 53 upregulated genes) were chosen for further investigation. The importance of chemokines and cytokines in these two disorders is highlighted by functional analysis. MCODE plug identified three important modules, which functionally enriched the immune system process. Finally, nine hub genes were identified using cytoHubba, including IL1B, IL10, CXCL10, ICAM1, EGR1, FCGR3A, S100A12, S100A9, and FPR1. The nine hub genes were mainly enriched in immune- and inflammation-related pathways. External data profiles and RT-qPCR confirmed the expression of the nine hub genes in HSCR and CD. ROC analysis revealed that the nine hub genes had a strong diagnostic value. Conclusion: Our study reveals the common pathogenesis of HSCR and CD. These hub genes and diagnostic models may provide novel insight for the diagnosis and treatment of HSCR complicated with CD.
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