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The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects.

Namas R, Ghuma A, Hermus L, Zamora R, Okonkwo DO, Billiar TR, Vodovotz Y - Libyan J Med (2009)

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.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery.

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.

No MeSH data available.


Related in: MedlinePlus

The inflammatory response to tissue injury. Traumatic injury signals various cell types to produce cytokines, chemokines, and DAMPs. In turn, DAMPs re-activate and further propagate the production of inflammatory mediators, setting in motion a positive feedback loop of inflammation→damage→inflammation.
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Figure 0002: The inflammatory response to tissue injury. Traumatic injury signals various cell types to produce cytokines, chemokines, and DAMPs. In turn, DAMPs re-activate and further propagate the production of inflammatory mediators, setting in motion a positive feedback loop of inflammation→damage→inflammation.

Mentions: However, hemorrhage and trauma, perhaps combined with failed attempts at therapy [13, 14], can induce a dysregulated acute inflammatory response that affects several organ systems and sets in motion a vicious cycle of inflammation damage inflammation [12, 15–18] driven by cytokines, chemokines, and products of damaged, dysfunctional, or stressed tissue (Fig. 2; see below).


The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects.

Namas R, Ghuma A, Hermus L, Zamora R, Okonkwo DO, Billiar TR, Vodovotz Y - Libyan J Med (2009)

The inflammatory response to tissue injury. Traumatic injury signals various cell types to produce cytokines, chemokines, and DAMPs. In turn, DAMPs re-activate and further propagate the production of inflammatory mediators, setting in motion a positive feedback loop of inflammation→damage→inflammation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3066737&req=5

Figure 0002: The inflammatory response to tissue injury. Traumatic injury signals various cell types to produce cytokines, chemokines, and DAMPs. In turn, DAMPs re-activate and further propagate the production of inflammatory mediators, setting in motion a positive feedback loop of inflammation→damage→inflammation.
Mentions: However, hemorrhage and trauma, perhaps combined with failed attempts at therapy [13, 14], can induce a dysregulated acute inflammatory response that affects several organ systems and sets in motion a vicious cycle of inflammation damage inflammation [12, 15–18] driven by cytokines, chemokines, and products of damaged, dysfunctional, or stressed tissue (Fig. 2; see below).

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.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery.

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.

No MeSH data available.


Related in: MedlinePlus