Figure 1. Hypothetical model linking C. jejuni enteritis to acute pancreatitis through a hyperstimulation mechanism. In this model the normal feedback loop to eliminate the luminal stimulus of C. jejuni with increased fluid secretion (manifested by watery diarrhea) is blocked at the level of dysfunctional CFTR. Hyperstimulation of the pancreas leads to acinar cell stimulation but duct cell dysfunction limits digestive enzyme elimination from the duct. Trypsinogen activation within the pancreas leads to generalized digestive enzyme activation, pancreatic injury, and acute pancreatitis.