Research Article: Unveiling the multidimensional cytokine landscape in acute pancreatitis
Abstract:
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-1?, TNF-?) 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-1?, IL-1?, IL-6, IL-10 and other cytokines (IL-2R?, IFN-?, IL-1R?, IL-16, IL-2, MIF, IFN-?, 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-? (p = 0.00550, q = 0.00600) and IL 9 (p = 0.01983, q = 0.02070). IL 2R? (AUC = 0.918) and IFN-? (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-1? 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-2R? and IFN-? appear to be sensitive early diagnostic biomarkers, and the inverse IL-1? necrosis relationship suggests that early IL-1? signaling may facilitate efficient tissue clearance. Multi cytokine profiling may improve early risk stratification and monitoring of immunological dynamics.
Introduction:
Acute pancreatitis (AP) is one of the most common causes of emergency hospitalizations for gastroenterological reasons ( 1 ). The ethology of the disease is varied and includes primarily gallstones and alcohol abuse. Less frequently, AP is caused by metabolic, drug-induced, iatrogenic, or idiopathic factors. Currently, a systematic increase in the number of AP cases is observed in developed countries ( 2 ). It is estimated that the annual incidence is approximately 30–40 cases per 100,000 people. Mortality may…
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