The secretion of digestive enzymes, as the natural function of pancreatic acinar cells, is blocked in acute pancreatitis. As a result, premature activation of trypsinogen, increase in cytosolic calcium and overproduction of reactive oxygen species (ROS) occur in acinar cells. ROS act as messengers to trigger the activation of signalling pathways which lead to the development of inflammatory response. Acinar cells have demonstrated to be able to produce cytokines, chemokines and adhesion molecules mediated by the activation of mitogen-activated protein kinases (MAPK), nuclear factor-kB (NF-kB), activator protein-1 (AP-1) and signal transducers and activators of transcription (STAT) factors family. In addition, expression of the leukocyte common antigen (CD45), with phosphatase activity, has been recently found in pancreatic acinar cells. CD45 expression has demonstrated to be sensitive to oxidative stress. It is down-regulated during acute pancreatitis in acinar cells as they produce inflammatory factors. Data suggest that in healthy conditions, CD45 exerts a negative feed-back to repress the inflammatory response by inhibiting the activation of the kinase cascade. In conclusion, depending on the redox cellular state, pancreatic acinar cells may have a key role in the secretion of digestive enzymes into duodenum or behave like typical inflammatory cells.