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Articles in PresS, published online ahead of print July 17, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00370.2001
Submitted on August 20, 2001
Accepted on May 23, 2002
1 Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: asaluja{at}bidmc.harvard.edu.
Cyclooxygenase-2 (COX-2), a widely distributed enzyme, plays an important role in inflammation. We have studied the role of COX-2 in acute pancreatitis and pancreatitis-associated lung injury using both the pharmacological inhibition of COX-2 and genetic deletion of COX-2. Pancreatitis was induced in mice by 12 hourly injections of caerulein. The severity of pancreatitis was assessed by measuring serum amylase, pancreatic trypsin activity, intrapancreatic sequestration of neutrophils, and acinar cell necrosis. The severity of lung injury was evaluated by measuring lactate dehydrogenase levels in the bronchoalveolar lavage fluid and by quantitating neutrophil sequestration in the lung. In both the pharmacologically inhibited and genetically altered mice, the severity of pancreatitis and pancreatitis-associated lung injury was reduced when compared to the non-inhibited strains of COX-2 sufficient mice. This reduction in injury indicates that COX-2 plays an important pro-inflammatory role in pancreatitis and its associated lung injury. Our findings support the concept that COX-2 inhibitors may play a beneficial role in the prevention of acute pancreatitis or in the reduction of its severity.
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