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.