CHARACTERIZATION OF THE INFLAMMATORY RESPONSE DURING ACUTE AND POST-ACUTE PHASES AFTER SEVERE BURN

@article{Gauglitz2008CHARACTERIZATIONOT,
  title={CHARACTERIZATION OF THE INFLAMMATORY RESPONSE DURING ACUTE AND POST-ACUTE PHASES AFTER SEVERE BURN},
  author={Gerd G. Gauglitz and Juquan Song and David N. Herndon and Celeste C. Finnerty and Darren Boehning and José Moreno Barral and Marc G. Jeschke},
  journal={Shock},
  year={2008},
  volume={30},
  pages={503-507}
}
Severe burn causes a pronounced hypermetabolic response characterized by catabolism and extensive protein wasting. We recently found that this hypermetabolic state is driven by a severe inflammatory response. We characterized in detail the kinetics of serum levels of a panel of cytokines in a rat model, which may serve as reference for the development of therapeutic interventions applicable to humans. Male Sprague-Dawley rats (n = 8) received a full-thickness burn of 60% total body surface area… 
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129 Citations

The dynamics of the early inflammatory response in double-hit burn and sepsis animal models.

Cytokine expression profile over time in burned mice.

Comparison of the cytokine and chemokine dynamics of the early inflammatory response in models of burn injury and infection.

Long-term dynamic profiling of inflammatory mediators in double-hit burn and sepsis animal models.

Increased expression of cardiac IL-17 after burn

Early after burn, cardiac tissue is associated with significantly elevated levels of Th-17 cytokines, which appears to be specific for cardiac tissue and may promote myocardial inflammation and dysfunction associated with this form of trauma.

Hyperglycemia Exacerbates Burn-Induced Liver Inflammation via Noncanonical Nuclear Factor-κB Pathway Activation

Results indicate that burn injury to the skin rapidly activated canonical and noncanonical NF-κB pathways in the liver and was associated with increased expression of inflammatory markers and acute-phase proteins, and impaired glucose metabolism.

Inflammatory Response to Burn Trauma: Nicotine Attenuates Proinflammatory Cytokine Levels

This study confirms in a standardized burn model that stimulation of the nicotinic acetylcholine receptor is involved in the regulation of effectory molecules of the immune response.

Cimetidine enhances delayed-type hypersensitivity responses and serum interleukin (IL)-2, -10, -12, and IL-17 levels after burn injury in an animal model

Results here showed significant time-dependent changes in serum cytokines levels after burn injury and that cimetidine was able to significantly augment IL-2,IL-10, IL-12, and IL-17 levels as well as DTH responses that are normally suppressed following thermal trauma.

Age-related immune responses after burn and inhalation injury are associated with altered clinical outcomes

Parecoxib Reduces Systemic Inflammation and Acute Lung Injury in Burned Animals with Delayed Fluid Resuscitation

Evaluating the anti-inflammatory effects of Parecoxib in a delayed fluid resuscitation burned rat model suggests that it may have the potential to be used both as an analgesic and ameliorate the effects of lung injury following burn.
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References

SHOWING 1-10 OF 47 REFERENCES

CYTOKINE EXPRESSION PROFILE OVER TIME IN SEVERELY BURNED PEDIATRIC PATIENTS

After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis and the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.

The Early Acute Phase Response After Burn Injury in Mice

It is demonstrated that within the liver, the acute phase response after burn injury initially involves tumor necrosis factor-α and interleukin-1β, whereas interleukein-6 is not involved until later and that systemic serum amyloid A levels are not increased until interleucin- 6 is also increased.

The role of interleukin-10 in the regulation of the systemic inflammatory response following trauma-hemorrhage.

Deficient transforming growth factor beta and interleukin-10 responses contribute to the septic death of burned patients.

Major injury induces increased production of interleukin-10 by cells of the immune system with a negative impact on resistance to infection.

Comparing the production of interleukin-10 by peripheral blood mononuclear cells from injured patients and control subjects to determine the responsible cell types and to relate IL-10 production to the occurrence of sepsis found the CD4+ T-helper cells appear to be a major source of IL- 10 after injury.

Increased levels of circulating interleukin-8 in patients with large burns: relation to burn size and sepsis.

The increased IL-8 concentrations seem to be related to burn size and to have a role in the pathophysiology of sepsis in patients with large burns.

Interleukin-6 in the injured patient. Marker of injury or mediator of inflammation?

Interleukin-6 appears to play an active role in the postinjury immune response, making it an attractive therapeutic target in attempts to control hyperinflammatory provoked organ injury.

Marked increase in plasma interleukin-6 in burn patients.

It is suggested that interleukin-6 is released as an alarm signal and has a role for the wound healing in burn patients, and that the levels of interleuko-6 after injury is an indicator of the severity of burn.

Acute alcohol intoxication increases interleukin-18-mediated neutrophil infiltration and lung inflammation following burn injury in rats.

It is suggested that acute EtOH intoxication before burn injury upregulates IL-18, which in turn contributes to increased neutrophil infiltration and increased lung tissue edema following a combined insult of EtOH and burn injury.

Post burn muscle wasting and the effects of treatments.