Review
English
Namas R1, Ghuma A1, Hermus L2, Zamora R1, Okonkwo DO3, Billiar TR1, Vodovotz Y1,4
1-Department of Surgery, University of Pittsburgh, Pittsburgh, PA. 2-Martini Hospital, Department of Surgery, Groningen, Netherlands. 3-Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA. 4-Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA.
Libyan J Med 2009; 4(3):C136-148
Abstract
Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP’s).
DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and nonhuman primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.
Keywords: Trauma, Hemorrhagic Shock, Traumatic Brain Injury, Inflammation, Systems Biology
Link/DOI: http://2657.indexcopernicus.com/fulltxt.php?ICID=883955