Serum soluble suppression of tumorigenicity 2 as a novel inflammatory marker predicts the severity of acute pancreatitis

BACKGROUND Acute pancreatitis(AP) is an inflammatory disease in which the regulatory pathway is complex and not well understood. Soluble suppression of tumorigenicity 2(s ST2) protein receptor functions as a decoy receptor for interleukin(IL)-33 to prevent IL-33/suppression of tumorigenicity 2 L(ST2 L)-pathwaymediated T helper(Th)2 immune responses.AIM To investigate the role of s ST2 in AP.METHODS We assessed the association between s ST2 and severity of AP in 123 patients enrolled in this study. The serum levels of s ST2, C-reactive protein(CRP) and Th1-and Th2-related cytokines, including interferon(IFN)-γ, tumor necrosis factor(TNF)-α, IL-2, IL-4, IL-5 and IL-13, were measured by highly sensitive ELISA, and the severity of AP in patients was evaluated by the 2012 Atlanta Classification Criteria.RESULTS Serum s ST2 levels were significantly increased in AP patients, and further, these levels were significantly elevated in severe AP(SAP) patients compared to moderately severe AP(MSAP) and mild AP(MAP) patients. Logistic regression showed s ST2 was a predictor of SAP [odds ratio(OR): 1.003(1.001–1.006), P = 0.000]. s ST2 cutoff point was 1190 pg/m L, and s ST2 above this cutoff was associated with SAP. s ST2 was also a predictor of any organ failure and mortality during AP [OR: 1.006(1.003–1.009), P = 0.000, OR: 1.002(1.001–1.004), P = 0.012,respectively]. Additionally, the Th1-related cytokines IFN-γ and TNF-α in the SAP group were higher and the Th2-related cytokine IL-4 in the SAP group was significantly lower than those in MSAP and MAP groups.CONCLUSION s ST2 may be used as a novel inflammatory marker in predicting AP severity and may regulate the function and differentiation of IL-33/ST2-mediated Th1 and Th2 Lymphocytes in AP homeostasis.