Water immersion stress prevents caerulein-induced pancreatic acinar cell NF-kappa B activation by attenuating caerulein-induced intracellular Ca2+ changes

Prior stress ameliorates caerulein-induced pancreatitis in rats. NF-kappaB is a proinflammatory transcription factor activated during caerulein pancre atitis. However, the effects of prior stress on pancreatic NF-kappaB activa tion are unknown. In the current study, the effect of prior water immersion stress on caerulein and tumor necrosis factor-alpha (TNF-alpha)-induced NF -kappaB activation in the pancreas was evaluated. Water immersion of rats f or up to 6 h prevents supramaximal caerulein-induced pancreatic I kappaB-al pha degradation and NF-kappaB activation in vivo, NF-kappaB activity is als o inhibited in vitro in pancreatic acini prepared from water-immersed anima ls. TNF alpha -induced NF-kappaB activation in pancreas or in pancreatic ac ini is unaffected by prior water immersion. Chelation of intracellular Ca2 by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate/acetoxymethyl este r has similar effects to water immersion in preventing caerulein but not TN F-alpha -induced NF-kappaB activation in pancreas. Both the spike response and the sustained rise in [Ca2+], in response to supramaximal caerulein sti mulation are reduced markedly in acini prepared from water-immersed animals as compared with normal animals. Our findings indicate that, in addition t o Ca2+-dependent mechanisms, Ca2+-independent signaling events also may lea d to NF-kappaB activation in pancreatic acinar cells. Water immersion stres s prevents supramaximal caerulein-induced NF-kappaB activation in pancreas in vivo and in vitro by affecting intracellular Ca2+ homeostasis.