The Role of Macrophages in Acute Pancreatitis: From Inflammatory Drivers to Therapeutic Targets

Acute pancreatitis (AP) involves activation of the innate immune system and an imbalanced inflammatory response. Both pancreatic and systemic inflammation associated with AP are mediated by macrophages. This review summarizes research on macrophage functions in AP pathogenesis and treatment. Relevant studies investigating macrophage activation, phenotypes, autophagy, and their roles in local and systemic inflammation were analyzed. During AP, macrophages initially adopt a pro-inflammatory phenotype to amplify inflammation. Macrophages located in tissues including the pancreas, adipose tissue, liver, lung, and spleen play a role in this process. As the disease progresses, they transition to an M2 phenotype to promote resolution. Macrophage-centered modulation of the innate immune response represents a promising therapeutic strategy. However, further exploration of macrophage interactions with other immune cells and pancreatic acinar cells is still needed. Targeting specific macrophage functions may improve AP management, which is the focus of this review.