The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects.
Bottom Line: The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's).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: Cytokines are a broad class of protein hormones that mediate inflammatory and immune responses in a complex, context-sensitive manner [12, 88] (Fig. 3]. Not surprisingly, cytokines play a major role in the body's response to T/HS and TBI [107, 109]. Major cytokines that participate in the response to trauma include tumor necrosis factor–alpha (TNF-α), interleukin-1 beta (IL-1β), IL-2, IL-6, IL-8 [20, 24, 25], IL-4  and recently IL-18 . On the other hand, the cytokine IL-10 counteracts the effects of the pro-inflammatory cytokines IL-1, IL-6 and TNF-α in various contexts , including severe hemorrhagic shock . Unlike septic shock, where the cascade of cytokines is well defined, the role of cytokines in trauma and hemorrhagic shock is not well elucidated, the experimental and clinical data are conflicting , and the response in humans (as opposed to animal models of T/HS) is still poorly understood . Circulating levels of cytokines have been detected in animal models and in patients with severe sepsis, and these levels have some correlation with outcome . Production of the free radical nitric oxide (NO), which is produced in inflammatory settings by the enzyme inducible NO synthase (iNOS) , was shown to be a central mediator of post-T/HS inflammation in mice . In human trauma patients, circulating NO reaction products reflect the severity of injury during the first two hours after the traumatic insult, suggesting that increased NO production might play a role in the very early post injury period .
No MeSH data available.