Unveiling the multidimensional cytokine landscape in acute pancreatitis.

In acute pancreatitis (AP), sudden epigastric pain is accompanied by intense release of inflammatory mediators that rapidly recruit and activate innate immune cells. Pro-inflammatory cytokines (e.g., IL-6, IL-1β, TNF-α) play a key role in amplifying inflammation and may contribute to systemic complications, while anti-inflammatory cytokines (e.g., IL-10) modulate this response. Therefore, the aim of the study was to evaluate cytokines in patients with AP. We measured circulating cytokines at a single time point in 50 AP patients and 40 healthy controls using multiplex ELISA kit (Bio-Plex Pro™ Human Cytokine Screening Panel). Statistically significant increases were observed for IL-1α, IL-1β, IL-6, IL-10 and other cytokines (IL-2Rα, IFN-γ, IL-1Rα, IL-16, IL-2, MIF, IFN-α, IL-5, IL-4, IL-3, IL-12[p40], IL-12[p70], IL-17, LIF, IL-18, IL-15, IL-13; all q ≤ 0.05), alongside decreases in TNF-β (p = 0.00550, q = 0.00600) and IL 9 (p = 0.01983, q = 0.02070). IL 2Rα (AUC = 0.918) and IFN-γ (AUC = 0.907) demonstrated high discriminatory power for AP and remained significant after FDR correction (p < 0.0001, q < 0.0001). Correlation analysis linked IL-6, IL-16, and IL-1Ra with hepatic steatosis, IL-18 and IL-1Ra with alcohol use disorder and revealed an inverse relationship between IL-1β levels and severity of pancreatic necrosis. The cytokine profile reflects concurrent activation of pro inflammatory pathways, compensatory anti-inflammatory mechanisms, and early lymphocytic suppression. IL-2Rα and IFN-γ appear to be sensitive early diagnostic biomarkers, and the inverse IL-1β necrosis relationship suggests that early IL-1β signaling may facilitate efficient tissue clearance. Multi cytokine profiling may improve early risk stratification and monitoring of immunological dynamics.