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Elevated CXCL1 expression contributes to the development of pediatric Crohn's disease and serves as a diagnostic
1Department of Gastroenterology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, No. 56, Nanlishi Road, Xicheng District, Beijing 100045, China.
Insights
CXCL1 is elevated in pediatric Crohn's disease (PCD) and may serve as a diagnostic marker. This finding could lead to improved treatment strategies for children with PCD.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Pediatric Crohn's disease (PCD) is a severe condition lacking efficient diagnostic markers.
- Understanding molecular mechanisms is crucial for developing better diagnostic and treatment approaches.
Purpose of the Study:
- To identify novel diagnostic markers for PCD.
- To explore the molecular mechanisms underlying PCD.
- To investigate potential therapeutic targets for PCD.
Main Methods:
- Downloaded and analyzed PCD datasets from the Gene Expression Omnibus (GEO) database.
- Identified differentially expressed genes (DEGs) and hub genes using bioinformatics analyses (Limma, GO, KEGG, GSEA, PPI).
- Validated CXCL1 expression in patient samples using qRT-PCR and assessed its diagnostic value via ROC analysis.
Main Results:
- Identified 71 DEGs and 15 hub genes, with CXCL1 significantly upregulated in PCD intestinal tissues.
- CXCL1 expression correlated with immune infiltration and was enriched in IL-17 and NF-kappa B signaling pathways.
- CXCL1 demonstrated high diagnostic accuracy (AUC > 0.90) in distinguishing PCD patients.
Conclusions:
- CXCL1 is implicated in PCD pathogenesis and shows potential as a valuable diagnostic biomarker.
- Targeting CXCL1 may offer new therapeutic avenues for pediatric Crohn's disease.
- Further research into CXCL1's role can enhance PCD management and treatment outcomes.
Purpose:
Pediatric Crohn's disease (PCD), which is a severe illness impacting the physical health of children. Nevertheless, there is still a lack of highly efficient diagnostic markers. Here, we aim to develop efficient diagnostic and treatment approaches, gaining a deeper understanding of the molecular mechanisms and potential targets causing PCD.
Methods:
PCD datasets were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between PCD and normal were screened by Limma package. DEGs were subjected to further analyses utilizing GO, KEGG, GSEA and PPI analysis. The CIBERSORT analysis aimed at examining the correlation between CXCL1 and immune infiltration. The clinical diagnostic value of CXCL1 and drugs targeting CXCL1 were analyzed through ROC and CMap database. Additionally, intestinal mucosal tissue samples from PCD patients were collected to conduct qRT-PCR for detecting the expression of CXCL1.
Results:
Overall, 71 DEGs were selected from GSE101794 and GSE93624. A total of 15 hub genes were identified by the constructed PPI network, among which CXCL1 was significantly increased in intestinal tissue in the PCD patients. DEGs between high- and low-CXCL1 expression were mainly enriched in the IL-17 and NF-kappa B signaling pathways. ROC analysis showed that AUC values of CXCL1 were 0.908, 0.945 and 0.890 based on GSE101794, GSE93624 and GSE57945, the similar results was obtained using qRT-PCR. The immune infiltration results indicate that CXCL1 could potentially play a regulatory role in the immune response of PCD.
Conclusions:
We have determined that CXCL1 might have a crucial involvement in the advancement of PCD, thus having the potential to be a diagnostic marker in order to enhance treatment choices for PCD.
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