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 non-human 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.
Original language | English |
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Pages (from-to) | 97-103 |
Number of pages | 7 |
Journal | Libyan journal of medicine |
Volume | 4 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2009 |
Keywords
- Trauma
- Hemorrhagic Shock
- Traumatic Brain Injury
- Inflammation
- Systems Biology
- NECROSIS-FACTOR-ALPHA
- TRANSLATIONAL SYSTEMS BIOLOGY
- REDUCED MATHEMATICAL-MODEL
- ORGAN DYSFUNCTION SYNDROME
- HEMORRHAGIC-SHOCK
- IN-SILICO
- CYTOKINE PRODUCTION
- CLINICAL-TRIALS
- NITRIC-OXIDE
- CEREBROSPINAL-FLUID