Please use this identifier to cite or link to this item:
|Title:||Preprotachykinin-A gene deletion protects mice against acute pancreatitis and associated lung injury||Authors:||Bhatia, M.
Multiple organ dysfunction syndrome
Systemic inflammatory response syndrome
|Issue Date:||1-May-2003||Citation:||Bhatia, M.,Slavin, J.,Cao, Y.,Basbaum, A.I.,Neoptolemos, J.P. (2003-05-01). Preprotachykinin-A gene deletion protects mice against acute pancreatitis and associated lung injury. American Journal of Physiology - Gastrointestinal and Liver Physiology 284 (5 47-5) : G830-G836. ScholarBank@NUS Repository.||Abstract:||Impaired lung function in severe acute pancreatitis is the primary cause of morbidity and mortality in this condition. Preprotachykinin-A (PPT-A) gene products substance P and neurokinin (NK)-A have been shown to play important roles in neurogenic inflammation. Substance P acts primarily (but not exclusively) via the NK1 receptor. NKA acts primarily via the NK2 receptor. Earlier work has shown that knockout mice deficient in NK1 receptors are protected against acute pancreatitis and associated lung injury. NK1 receptors, however, bind other peptides in addition to substance P, not all of which are derived from the PPT-A gene. To examine the role of PPT-A gene products in acute pancreatitis, the effect of PPT-A gene deletion on the severity of acute pancreatitis and the associated lung injury was investigated. Deletion of PPT-A almost completely protected against acute pancreatitis-associated lung injury, with a partial protection against local pancreatic damage. These results show that PPT-A gene products are critical proinflammatory mediators in acute pancreatitis and the associated lung injury.||Source Title:||American Journal of Physiology - Gastrointestinal and Liver Physiology||URI:||http://scholarbank.nus.edu.sg/handle/10635/108069||ISSN:||01931857|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Aug 16, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.