Analysis of Immune Cell Infiltration Characteristics in Severe Acute Pancreatitis through Integrated Bioinformatics

Abstract

Abstract Objective: The etiopathogenesisof severe acute pancreatitis(SAP) remains poorly understood.We aim to investigate the role of immune cells Infiltration Characteristics during SAP progression. Methods/Design:Gene expression profiles of the GSE194331 dataset were retrieved from the GEO. Lasso regression and random forest algorithms were employed to select feature genes from genes related to SAP progression and immune responses. CIBERSORT was utilized to estimate differences in immune cell types and proportions and the relationship between immune cells and gene expression. We performed pathway enrichment analysis using GSEA to examine disparities in KEGG signaling pathways when comparing the two groups. Additionally, CMap analysis was executed to identify prospective small molecular compounds. Results: The three hub genes (CBLB,JADE2,RNF144A) were identified that can predict SAP progression. Analysis of CIBERSORT and TISIDB databases has shown that there are significant differences in immune cell expression levels between the normal and SAP groups, and three hub genes (CBLB,JADE2,RNF144A) were highly correlated with multiple immune cells, regulating the characteristics of immune cell infiltration in the microenvironment.Finally,drug prediction through the Connectivity Map database suggested that compounds such as Entecavir, KU-0063794, Y-27632, and Antipyrine have certain effects as potential targeted drugs for the treatment of SAP. Conclusion: CBLB, JADE2, and RNF144A are hub genes in SAP, potentially playing important roles in SAP progression. This finding further broadens the understanding of the etiopathogenesis of SAP and provides a feasible basis for future research on diagnostic and immunotherapeutic targets for SAP. Strengths and limitations of this study: To find new hub genes related to severe pancreatitis and to suggest the key role of immunoinfiltrating cells in the occurrence and development of severe acute pancreatitis. There is a lack of relevant basic experiments to further verify the pathogenesis of severe acute pancreatitis