Please use this identifier to cite or link to this item:
|Title:||Chemokines as therapeutic targets in systematic inflammatory response syndrome||Authors:||HE MIN||Keywords:||chemokines, sepsis, acute pancreatitis||Issue Date:||16-Dec-2008||Citation:||HE MIN (2008-12-16). Chemokines as therapeutic targets in systematic inflammatory response syndrome. ScholarBank@NUS Repository.||Abstract:||Exaggerated systemic inflammatory response syndrome may lead to multiple organ dysfunction, organ failure and eventually death. Chemokines, a large family of small chemotactic cytokines, are critical inflammatory mediators in the development of both acute pancreatitis and sepsis. The present study has shown that blockage of CCR1 by a small molecule CCR1 antagonist has protective effect against acute lung injury in animal models of acute pancreatitis and sepsis. Depletion of mast cells by compound 48/80 has also attenuated acute pancreatitis-associated lung injury and sepsis-associated lung injury by attenuating the levels of chemokines. Treatment with an exogenous CX3C chemokine FTK has shown pro-inflammatory effect in acute pancreatitis-associated lung injury and anti-inflammatory effect against sepsis-associated lung injury. These promising findings validate that manipulating chemokine system may have protective effect in systemic inflammatory response syndrome.||URI:||http://scholarbank.nus.edu.sg/handle/10635/16626|
|Appears in Collections:||Ph.D Theses (Open)|
Show full item record
Files in This Item:
|HeM.pdf||2.84 MB||Adobe PDF|
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.