Macrophages play a pivotal role in the pathogenesis of pancreatitis.
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Macrophages mainly differentiate into M1 macrophages that secrete proinflammatory cytokines and mediators, causing inflammatory cascade reaction and aggravating acute pancreatitis.
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Macrophages interact with pancreatic stellate cells in a cytokines-dependent manner to accelerate the formation of pancreatic fibrosis in chronic pancreatitis.
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Immunotherapy targeting macrophages has good application prospects in the treatment of pancreatitis.
Abstract
Macrophages play a crucial role in the pathogenesis of pancreatitis that is a common gastrointestinal disease. Particularly, macrophages differentiate into different phenotypes and exert diverse functions in acute pancreatitis (AP) and chronic pancreatitis (CP), respectively. In AP, macrophages in the pancreas and other related organs are mainly activated and differentiated into a pro-inflammatory M1 phenotype, and furthermore secrete inflammatory cytokines and mediators, causing local inflammation of the pancreas, and even intractable systemic inflammatory response or multiple organ failure. In CP, macrophages often exhibit a M2 polarisation and interact with pancreatic stellate cells (PSCs) in an autocrine and paracrine cytokine-dependent manner to promote the progression of pancreatic fibrosis. As the severity of pancreatic fibrosis aggravates, the proportion of M2/M1 macrophage cytokines in the pancreas increases. The discovery of macrophages in the pathogenesis of pancreatitis has promoted the research of targeted drugs, which provides great potential for the effective treatment of pancreatitis. This paper provides an overview of the roles of various macrophages in the pathogenesis of pancreatitis and the current research status of pancreatitis immunotherapy targeting macrophages. The findings addressed in this review are of considerable significance for understanding the pivotal role of macrophages in pancreatitis.
