Integrin β1 contributes to acute pancreatitis by mediating macrophage adhesion and inflammatory cascades.

Acute pancreatitis (AP) exhibits marked clinical heterogeneity. To investigate the molecular mechanisms involved in AP, we integrated bioinformatics analysis of public sequencing datasets, which identified differentially expressed genes (DEGs) significantly associated with AP. Subsequently, GO/KEGG enrichment analyses revealed robust involvement of these DEGs in cellular adhesion and MAPK signaling pathways. Protein-protein interaction (PPI) network analysis pinpointed integrin β1 (ITGB1) as the central hub gene, while single-gene gene set enrichment analysis (GSEA) across ontological databases confirmed its significant enrichment in pathways associated with adhesion and inflammation. These findings establish ITGB1 as a pivotal regulator coordinating cell adhesion and inflammatory responses in AP. In murine AP models, ITGB1 protein was significantly upregulated in the pancreas and co-localized specifically with macrophages. In vitro studies using bone marrow-derived macrophages (BMDMs) revealed that ITGB1 upregulation enhanced macrophage-endothelial adhesion and inflammatory cascades through p38 MAPK phosphorylation. Critically, clinical translation studies established the dual diagnostic value of ITGB1. The receiver operating characteristic (ROC) curve exhibited significant discriminatory power for distinguishing patients with AP from healthy controls, along with robust efficacy in stratifying disease severity. In conclusion, ITGB1 orchestrates macrophage-mediated inflammation through p38 MAPK-dependent mechanisms and can function as a biomarker for diagnosis and severity stratification in AP.