Published online Oct 14, 2021. doi: 10.3748/wjg.v27.i38.6489
Peer-review started: April 4, 2021
First decision: May 27, 2021
Revised: June 10, 2021
Accepted: August 27, 2021
Article in press: August 27, 2021
Published online: October 14, 2021
The clinical severity of acute pancreatitis (AP) is related to its prognosis. Excessive activation of inflammatory cells and their cytokines is one of the main mechanisms of pathogenesis of AP. Research on changes in inflammatory mediators in patients with different clinical severity of AP is important clinically. The interleukin (IL)-33/ST2L functional pathway is involved in the pathological process of AP. Soluble suppression of tumorigenicity 2 (sST2) is a secreted form of the ST2 receptor and acts as a decoy receptor for IL-33. In this study, we investigated whether the sST2 could serve as a novel inflammatory marker predicting the severity of acute pancreatitis.
In this study, the authors focused on the function of sST2 in predicting the severity of AP. The key issue to be solved is the association between IL-33/ST2L pathway and AP. The significance of solving these problems may constitute a new therapeutic target for regulating immune activation during the AP inflammatory storm.
The objective of this study was to investigate the role of sST2 in AP.
The authors assessed the association between sST2 and severity of AP in 123 patients enrolled in this study. The serum levels of sST2, C-reactive protein (CRP) and Th1- and Th2-related cytokines 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 patients was evaluated by the 2012 Atlanta Classification Criteria.
The serum sST2 Level was significantly increased in AP patients and significantly elevated in severe acute pancreatitis (SAP) patients compared to moderate severe acute pancreatitis and mild acute pancreatitis patients. The cutoff point of sST2 at 1190pg/mL was associated with SAP.
This study suggests that sST2 may be used as a novel inflammatory marker in predicting the severity of acute pancreatitis and that sST2 might regulate the function and differentiation of IL-33/ST2L mediated Th1 and Th2 lymphocytes in the homeostasis of acute pancreatitis.
It is necessary to determine the long-term predictive value of sST2 for the prognosis of AP in subsequent longitudinal studies. Additionally, the role of IL-33/ST2L in acute pancreatitis needs to be further verified in both in vivo and in vitro experiments.