INTERLEUKIN-6 REGULATION OF CCK GASTRIN RECEPTORS AND AMYLASE SECRETION IN A RAT PANCREATIC ACINAR CELL-LINE (AR4-2J)

In necrotizing pancreatitis a high interleukin-6 (IL-6) serum level ha s been proposed as a prognostic criterium. However, literature does no t report any information about the role of IL-6 in the function of pan creatic acinar cells. Cholecystokinin, gastrin binding, amylase releas e and intracellular calcium measurement were performed on a rat pancre atoma cell line, AR4-2J, which has been recognized as a useful tool fo r studies on the long-term regulation of pancreatic acinar cells. The addition of IL-6 (400 pM) for 48hrs to the AR4-2J cells induced no cha nge in the binding affinities but there was a 2 fold increase in the b inding capacity of cholecystokinin (CCKA R) and gastrin (CCKB R) recep tors. Although IL-6 treatment did not change directly the secretory ca pacity and did not activate the intracellular calcium mobilization of AR4-2J, it indirectly increased the sensitivity of the cells to the st imulation of amylase release and the intracellular calcium mobilizatio n by cholecystokinin and gastrin. It is most likely this effect was du e to the IL-6-induced increase in the numbers of CCKA R and CCKB R. Th erefore this report suggests that the cytokine IL-6 acts on the CCK re gulation of pancreatic enzyme secretion.