A model depicting the mechanisms by which intraductal bile acids cause acute pancreatitis in the mouse. Bile acids bind to the bile acid receptor Gpbar1 expressed on the apical plasma membranes of acinar cells. This interaction causes increased 5-LO activity in the acinar cell, resulting subsequently in LTB4 synthesis and secretion from the cell. Increased pancreatic LTB4 concentrations can then bind to TRPV1 receptors expressed by a subclass of primary sensory afferent nerves innervating the pancreas, resulting in the peripheral release of proinflammatory neurotransmitters such as substance P, which subsequently causes neutrophil recruitment, edema, and necrosis, and acute pancreatitis.