The early IL‐6 and IL‐10 response in trauma is correlated with injury severity and mortality

Stensballe, Jakob; Christiansen, Michael; Tønnesen, Else; Espersen, Kurt; Lippert, Freddy; Rasmussen, Lars S.

doi:10.1111/j.1399-6576.2008.01801.x

Cited by 103 publications

(105 citation statements)

References 26 publications

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Section: Traumamentioning

confidence: 94%

“…In this early study patients who died from injury or developed posttraumatic complications due to multiple organ dysfunction syndrome had elevated IL-10 levels in comparison with injured patients with an uneventful posttraumatic course [16]. Thus, trauma causes an enhanced release of IL-10 dependent on the severity of injury and because increased IL-10 levels are significantly related to posttraumatic complications, IL-10 may be involved in their pathogenesis [16]. A significant increase of both IL-6 and IL-10 concentrations was found over time in a reported study, with a significant correlation between the Injury Severity Score and the levels of both IL-6 and IL-10 at all sampling points [16].…”

Section: Traumamentioning

confidence: 99%

“…Serum concentrations of IL-6 and IL-10 were significantly higher in patients not surviving 30 days. The early systemic inflammatory response measured as IL-6 and IL-10 in serum is correlated with injury severity and 30-day mortality following trauma [16].…”

Section: Traumamentioning

confidence: 99%

“…Thus, trauma causes an enhanced release of IL-10 dependent on the severity of injury and because increased IL-10 levels are significantly related to posttraumatic complications, IL-10 may be involved in their pathogenesis [16]. A significant increase of both IL-6 and IL-10 concentrations was found over time in a reported study, with a significant correlation between the Injury Severity Score and the levels of both IL-6 and IL-10 at all sampling points [16]. Serum concentrations of IL-6 and IL-10 were significantly higher in patients not surviving 30 days.…”

Section: Traumamentioning

confidence: 99%

“…Interleukin-10 (IL-10) can markedly inhibit lymphocyte and phagocytic functions, essential for an adequate immune response [16]. In this early study patients who died from injury or developed posttraumatic complications due to multiple organ dysfunction syndrome had elevated IL-10 levels in comparison with injured patients with an uneventful posttraumatic course [16]. Thus, trauma causes an enhanced release of IL-10 dependent on the severity of injury and because increased IL-10 levels are significantly related to posttraumatic complications, IL-10 may be involved in their pathogenesis [16].…”

Section: Traumamentioning

confidence: 99%

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Nursing Education, Trauma and Care in the Intensive Care

Frieri¹

2017

Int Arch Nurs Health Care

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Section: Traumamentioning

confidence: 94%

Section: Traumamentioning

confidence: 99%

Section: Traumamentioning

confidence: 99%

Section: Traumamentioning

confidence: 99%

Section: Traumamentioning

confidence: 99%

See 3 more Smart Citations

Nursing Education, Trauma and Care in the Intensive Care

Frieri¹

2017

Int Arch Nurs Health Care

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Tissue influx of neutrophils and monocytes is delayed during development of trovafloxacin‐induced tumor necrosis factor‐dependent liver injury in mice

Giustarini

Kruijssen

Roest

et al. 2018

J of Applied Toxicology

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Idiosyncratic drug-induced liver injury (iDILI) has a poorly understood pathogenesis. However, iDILI is often associated with inflammatory stress signals in human patients as well as animal models. Tumor necrosis factor (TNF) and neutrophils play a key role in onset of trovafloxacin (TVX)-induced iDILI, but the exact role of neutrophils and other leukocytes remains to be defined. We therefore set out to study the kinetics of immunological changes during the development of TVX-induced iDILI in the established murine model of acute liver injury induced by administration of TVX and TNF. Initially, TNF stimulated the appearance of leukocytes, in particular neutrophils, into the liver of TVX-treated mice, but even more so in control mice treated with the non-DILI inducing analogue levofloxacin (LVX) or saline as vehicle (Veh). This difference was apparent at 2 hours after TNF administration, but at 4 hours, the relative neutrophil amounts were reduced again in Veh- and LVX-treated mice whereas the amounts in TVX-treated mice remained at the same increased level as at 2 hours. The influx of monocytes/macrophages, which was unaffected in Veh- and LVX-treated mice was markedly reduced or even absent in TVX-treated mice. Unlike controls, mice receiving TVX + TNF display severe hepatotoxicity with clear pathology and apoptosis, coagulated hepatic vessels and increased alanine aminotransferase levels and interleukin 6/10 ratios. Findings indicate that TVX delays the acute influx of neutrophils and monocytes/macrophages. Considering their known anti-inflammatory functions, the disruption of influx of these innate immune cells may hamper the resolution of initial cytotoxic effects of TVX and thus contribute to liver injury development.

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Experimental blunt chest trauma impairs fracture healing in rats

Recknagel

Bindl

Kurz

et al. 2010

Journal Orthopaedic Research

108

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In poly-traumatic patients a blunt chest trauma is an important trigger of the posttraumatic systemic inflammatory response. There is clinical evidence that fracture healing is delayed in such patients, however, experimental data are lacking. Therefore, we investigated the influence of a thoracic trauma on fracture healing in a rat model. Male Wistar rats received either a blunt chest trauma combined with a femur osteotomy or an isolated osteotomy. A more rigid or a more flexible external fixator was used for fracture stabilization to analyze whether the thoracic trauma influences regular healing and mechanically induced delayed bone healing differently. The blunt chest trauma induced a significant increase of IL-6 serum levels after 6 and 24 h, suggesting the induction of a systemic inflammation, whereas the isolated fracture had no effect. Under a more rigid fixation the thoracic trauma considerably impaired fracture healing after 35 days, reflected by a significantly reduced flexural rigidity (three-point-bending test), as well as a significantly diminished callus volume, moment of inertia, and relative bone surface (mCT analysis). In confirming the clinical evidence, this study reports for the first time that a blunt chest trauma considerably impaired bone healing, possibly via the interaction of the induced systemic inflammation with local inflammatory processes. ß

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The early IL‐6 and IL‐10 response in trauma is correlated with injury severity and mortality

Abstract: The early systemic inflammatory response measured as IL-6 and IL-10 in serum is correlated with injury severity and 30-day mortality following trauma.

Cited by 103 publications

References 26 publications

Nursing Education, Trauma and Care in the Intensive Care

Nursing Education, Trauma and Care in the Intensive Care

Tissue influx of neutrophils and monocytes is delayed during development of trovafloxacin‐induced tumor necrosis factor‐dependent liver injury in mice

Experimental blunt chest trauma impairs fracture healing in rats

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