Open Access
Article
Systemic inflammatory response following acute traumatic brain injury
Jia Lu1,Samantha Jianli Goh1,Priscilla Ying Lei Tng1,Yi Yu Deng1,Eng-Ang Ling1,Shabbir Moochhala1
1
Combat Care Laboratory, Defence Medical and Environmental Research Institute, DSO National Laboratories, 27 Medical Drive #09-01, Singapore. ljia@dso.org.sg
DOI: 10.2741/3489 Volume 14 Issue 10, pp.3795-3813
Published: 01 January 2009
(This article belongs to the Special Issue Animals in SIRS research)
Abstract

The early, delayed, and systemic effects of acute traumatic brain injury (TBI) are the result of inflammatory mediators which initiate systemic inflammatory response syndrome (SIRS), subsequent complement deficits and coagulopathy. Once SIRS is triggered by acute inflammation, it can detrimentally self-propagate. Systemic inflammation causes tissue damage leading to further inflammation and damage, leaving the body in a vicious cycle of hyperinflammation. Therefore, important inflammatory mediators like interleukin (IL)-1 beta, IL-6 and tumour necrosis factor (TNF) alpha, are targeted in compensatory anti-inflammatory response syndrome (CARS) in an attempt to control the development of SIRS. The hypothalamus-pituitary (HPA)-axis and sympathetic nervous system (SNS) efferent limbs in CARS provide negative feedback for the production of inflammatory mediators. However, in the case of acute TBI, the activation of CARS often leads to the complication of immunosuppression which may result in multi-organ dysfunction syndrome (MODS) and mortality. In light of this, the activation of the SIRS following acute TBI does not bode well. If left uncontrolled, multiple systems will be implicated making it difficult to remedy.

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Jia Lu, Samantha Jianli Goh, Priscilla Ying Lei Tng, Yi Yu Deng, Eng-Ang Ling, Shabbir Moochhala. Systemic inflammatory response following acute traumatic brain injury. Frontiers in Bioscience-Landmark. 2009. 14(10); 3795-3813.