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 pancreatitis. However, the effects of prior stress on pancreatic NF-kappaB activation 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 for up to 6 h prevents supramaximal caerulein-induced pancreatic IkappaB-alpha degradation and NF-kappaB activation in vivo. NF-kappaB activity is also inhibited in vitro in pancreatic acini prepared from water-immersed animals. TNF-alpha-induced NF-kappaB activation in pancreas or in pancreatic acini is unaffected by prior water immersion. Chelation of intracellular Ca(2+) by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate/acetoxymethyl ester has similar effects to water immersion in preventing caerulein but not TNF-alpha-induced NF-kappaB activation in pancreas. Both the spike response and the sustained rise in [Ca(2+)](i) in response to supramaximal caerulein stimulation are reduced markedly in acini prepared from water-immersed animals as compared with normal animals. Our findings indicate that, in addition to Ca(2+)-dependent mechanisms, Ca(2+)-independent signaling events also may lead to NF-kappaB activation in pancreatic acinar cells. Water immersion stress prevents supramaximal caerulein-induced NF-kappaB activation in pancreas in vivo and in vitro by affecting intracellular Ca(2+) homeostasis.