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. Key words: Trauma; Hemorrhagic Shock; Taumatic Brain Injury; Inflammation; Systems Biology