Immune responses are an integral part of the pathogenesis of pancreatitis. Studies applying the mouse model of pancreatitis induced by partial ligation of the pancreatic duct to explore the pancreatic immune microenvironment are still lacking. The aim of the present study is to explore the macrophage profile and associated regulatory mechanisms in mouse pancreatitis, as well as the correlation with human chronic pancreatitis (CP). In the present study, the mouse model of pancreatitis was induced by partial ligation of the pancreatic duct. Mice in the acute phase were sacrificed at 0, 4, 8, 16, 32, 72 h after ligation, while mice in the chronic phase were sacrificed at 7, 14, 21, 28 days after ligation. We found that the pancreatic pathological score, expression of TNF-α and IL-6 were elevated over time and peaked at 72h in the acute phase, while in the chronic phase, the degree of pancreatic fibrosis peaked at day 21 after ligation. Pancreatic M1 macrophages and pyroptotic macrophages showed a decreasing trend over time, whereas M2 macrophages gradually rose and peaked at day 21. IL-4 is involved in the development of CP and is mainly derived from pancreatic stellate cells (PSCs). The murine pancreatitis model constructed by partial ligation of the pancreatic duct, especially the CP model, can ideally simulate human CP caused by obstructive etiologies in terms of morphological alterations and immune microenvironment characteristics.

中文翻译：

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胰腺导管部分结扎诱导的小鼠慢性胰腺炎模型封装了人类慢性胰腺炎中巨噬细胞的分布。

免疫反应是胰腺炎发病机制的一个组成部分。目前尚缺乏应用胰管部分结扎诱导胰腺炎小鼠模型探索胰腺免疫微环境的研究。本研究的目的是探讨小鼠胰腺炎的巨噬细胞谱和相关调控机制，以及与人类慢性胰腺炎（CP）的相关性。本研究采用部分结扎胰管诱导小鼠胰腺炎模型。急性期小鼠于结扎后0、4、8、16、32、72 h处死，慢性期小鼠于结扎后7、14、21、28天处死。我们发现胰腺病理评分、TNF-α和IL-6的表达随时间升高，在急性期72h达到峰值，而在慢性期，胰腺纤维化程度在结扎后第21天达到峰值。胰腺M1巨噬细胞和焦亡巨噬细胞随时间呈下降趋势，而M2巨噬细胞逐渐上升并在第21天达到峰值。IL-4参与CP的发展，主要来源于胰腺星状细胞（PSCs）。胰管部分结扎构建的小鼠胰腺炎模型，特别是CP模型，可以从形态学改变和免疫微环境特征等方面理想地模拟梗阻性病因引起的人类CP。IL-4 参与 CP 的发展，主要来源于胰腺星状细胞 (PSC)。胰管部分结扎构建的小鼠胰腺炎模型，特别是CP模型，可以从形态学改变和免疫微环境特征等方面理想地模拟梗阻性病因引起的人类CP。IL-4 参与 CP 的发展，主要来源于胰腺星状细胞 (PSC)。胰管部分结扎构建的小鼠胰腺炎模型，特别是CP模型，可以从形态学改变和免疫微环境特征等方面理想地模拟梗阻性病因引起的人类CP。