The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects.
Bottom Line: 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.
Affiliation: Department of Surgery.
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.
No MeSH data available.
Related in: MedlinePlus
Mentions: Further complicating the primary damage in acute trauma is the increased susceptibility to sepsis and Multiple Organ Dysfunction Syndrome (MODS), a poorly understood syndrome of sequential and gradual loss of organ function . MODS is the most frequent cause of late deaths post-injury, accounting for substantial morbidity and mortality [4, 5]. MODS is considered to be due, in part, to excessive or maladaptive activation of inflammatory pathways . Organs such as the liver and the gut not only become damaged or dysfunctional from trauma-induced inflammation, but in turn further perpetuate this inflammatory vicious cycle [7, 8, 21]. Furthermore, patients admitted to the intensive care unit following trauma and hemorrhage often become susceptible to infection “second hit” further complicating attempts at immunomodulation early in the clinical course  (Fig. 1).
No MeSH data available.