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<p>Severe acute pancreatitis (SAP) is an inflammatory pancreatic disease characterized by significant tissue damage and systemic inflammation, leading to multiple organ failure and even death. IL-22 has been shown to have anti-inflammatory properties, but whether it can exert a protective effect in cases of multiple organ failure in SAP remains unclear. Therefore, this study aimed to systematically evaluate the protective effect of recombinant Interleukin (IL)-22 (rIL-22) on SAP and secondary multiple organ injury and the underlying mechanism for this effect. Balb/c mice were i.p. injected with caerulein (CAE) to induce SAP, followed by i.p. administration of rIL-22. Histopathological changes were observed by H&amp;E staining. The serum levels of pancreatitis-related biomarkers and serum pro-inflammatory cytokines were measured. TUNEL assay was conducted to assess the number of apoptotic cells. The expression of pro-inflammatory cytokines, autophagy and apoptosis biomarkers were analyzed by IHC and Western blot. Rat pancreatic acinar cells (AR42J), Human non-small cell lung cancer cells (A549) and Human colon carcinoma cell lines (Caco-2) were stimulated with MDK83190 and Rapamycin to establish in vitro apoptosis and autophagy models. These models were then treated with rIL-22. Our data revealed pathological damage and dysfunction in the pancreas and multiple organs (including the liver, lungs, kidneys and colon), along with systemic inflammation, in CAE-induced SAP mice. Additionally, elevated levels of apoptosis and autophagy were detected in both the pancreas and multiple organs. Strikingly, rIL-22 alleviates SAP and secondary multiple organ damage, especially in the lungs and colon, by mitigating histopathological injury, reducing serum levels of pancreatitis-related biomarkers and pro-inflammatory cytokines (both in tissue and serum), and suppressing apoptosis and autophagy. Further study demonstrated that rIL-22 could reverse apoptosis and autophagy induced by MDK83190 and Rapamycin in vitro. These results suggest rIL-22 as a potential therapeutic candidate for SAP and its subsequent multiple organ injury.</p>

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rIL-22 Alleviates Severe Acute Pancreatitis and Secondary Multiple Organ Injury Induced by Caerulein in Mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月14日

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  • Hongli Yang,
  • Weijia Sun,
  • Peilin Cheng,
  • Feifei Zhou,
  • Rui Mo,
  • Qianqian Xu,
  • Cuiyu Zhu,
  • Ruofan Cao,
  • Haiyan Jing,
  • Heng Wang,
  • Bingjie Jin,
  • Fengyuan Yu,
  • Li Ge,
  • Hongwei Xu

摘要

Severe acute pancreatitis (SAP) is an inflammatory pancreatic disease characterized by significant tissue damage and systemic inflammation, leading to multiple organ failure and even death. IL-22 has been shown to have anti-inflammatory properties, but whether it can exert a protective effect in cases of multiple organ failure in SAP remains unclear. Therefore, this study aimed to systematically evaluate the protective effect of recombinant Interleukin (IL)-22 (rIL-22) on SAP and secondary multiple organ injury and the underlying mechanism for this effect. Balb/c mice were i.p. injected with caerulein (CAE) to induce SAP, followed by i.p. administration of rIL-22. Histopathological changes were observed by H&E staining. The serum levels of pancreatitis-related biomarkers and serum pro-inflammatory cytokines were measured. TUNEL assay was conducted to assess the number of apoptotic cells. The expression of pro-inflammatory cytokines, autophagy and apoptosis biomarkers were analyzed by IHC and Western blot. Rat pancreatic acinar cells (AR42J), Human non-small cell lung cancer cells (A549) and Human colon carcinoma cell lines (Caco-2) were stimulated with MDK83190 and Rapamycin to establish in vitro apoptosis and autophagy models. These models were then treated with rIL-22. Our data revealed pathological damage and dysfunction in the pancreas and multiple organs (including the liver, lungs, kidneys and colon), along with systemic inflammation, in CAE-induced SAP mice. Additionally, elevated levels of apoptosis and autophagy were detected in both the pancreas and multiple organs. Strikingly, rIL-22 alleviates SAP and secondary multiple organ damage, especially in the lungs and colon, by mitigating histopathological injury, reducing serum levels of pancreatitis-related biomarkers and pro-inflammatory cytokines (both in tissue and serum), and suppressing apoptosis and autophagy. Further study demonstrated that rIL-22 could reverse apoptosis and autophagy induced by MDK83190 and Rapamycin in vitro. These results suggest rIL-22 as a potential therapeutic candidate for SAP and its subsequent multiple organ injury.